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Tofranil (Imipramine)

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Generic Tofranil is a member of the family of drugs called tricyclic antidepressants. Generic Tofranil is used to treat depression. Generic Tofranil is also used on a short-term basis, along with behavioral therapies, to treat bed-wetting in children aged 6 and older. Sometimes Generic Tofranil is prescribed to treat bulimia, attention deficit disorder in children, obsessive-compulsive disorder and panic disorder.

Other names for this medication:

Similar Products:
Pamelor, Norpramin, Silenor, Zonalon, Aventyl, Norpress, Elavil


Also known as:  Imipramine.


Generic Tofranil is used to treat depression. Generic Tofranil is also used on a short-term basis, along with behavioral therapies, to treat bed-wetting in children aged 6 and older. Sometimes Generic Tofranil is prescribed to treat bulimia, attention deficit disorder in children, obsessive-compulsive disorder and panic disorder.

Generic Tofranil is a member of the family of drugs called tricyclic antidepressants.

Tofranil is also known as Imipramine, Antideprin, Deprenil, Deprimin, Deprinol, Depsonil, Dynaprin, Eupramin, Imipramil, Irmin, Janimine, Melipramin, Surplix, Antidep, Apo-Imipramine, Chrytemin, Daypress, Depsol, Ethipramine, Fronil, Imidol, Imimine, Imine, Imiprex, Imiprin, Impril, Medipramine, Melipramine, Mipralin, Novopramine, Primonil, Pryleugan, Sermonil, Sipramine, Talpramin, Tofnil, Tofranil-PM, Venefon.

Generic name of Generic Tofranil is Imipramine hydrochloride.

Brand names of Generic Tofranil are Tofranil, Tofranil-PM.


Take Generic Tofranil orally.

Take Generic Tofranil with or without food.

For adults

The usual starting dose is 75 mg a day. The maximum daily dose is 200 mg.

For children

Total daily dosages for children should not exceed 2.5 mg for each 2.2 pounds of the child's weight. Doses usually begin at 25 mg per day. This amount should be taken an hour before bedtime. If needed, this dose may be increased after 1 week to 50 mg (ages 6 through 11) or 75 mg (ages 12 and up), taken in one dose at bedtime or divided into 2 doses, 1 taken at mid-afternoon and 1 at bedtime.

Aged people

The usual dosage should start with 25 to 50 mg per day. The dose may be increased as necessary, but effective dosages usually do not exceed 100 mg a day.

If you want to achieve most effective results do not stop taking Generic Tofranil suddenly.


If you overdose Generic Tofranil and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Tofranil overdosage: agitation, bluish skin, convulsions, difficulty breathing, dilated pupils, drowsiness, heart failure, high fever, involuntary writhing or jerky movements, irregular or rapid heartbeat, lack of coordination, low blood pressure, overactive reflexes, restlessness, rigid muscles, shock, stupor, sweating, vomiting.


Store at room temperature between 20 and 25 degrees C (68 and 77 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Tofranil are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Generic Tofranil if you are allergic to Generic Tofranil components.

Be very careful with Generic Tofranil if you are pregnant, planning to become pregnant, or are breast-feeding.

Do not take Generic Tofranil if you are recovering from a recent heart attack or take MAO inhibitors, such as the antidepressants Nardil and Parnate.

Be very careful with Generic Tofranil if you have diabetes, hypoglycemia, a history of mental disorders.

Be very careful with Generic Tofranil if you are taking albuterol (Proventil, Ventolin), antidepressants that act on serotonin, including Prozac, Paxil and Zoloft, antipsychotic drugs such as Mellaril and chlorpromazine, barbiturates such as Nembutal and Seconal, blood pressure medications such as Catapres, Carbamazepine (Tegretol), cimetidine (Tagamet), decongestants such as Sudafed, drugs that control spasms, such as Cogentin, Epinephrine (EpiPen), Flecainide (Tambocor), Guanethidine, Methylphenidate (Ritalin), Norepinephrine, other antidepressants such as Elavil and Pamelor, Phenytoin (Dilantin), Propafenone (Rythmol), Quinidine, thyroid medications such as Synthroid, tranquilizers and sleep aids such as Halcion, Xanax, and Valium.

Avoid alcohol.

Do not participate in any activities that require full alertness if you are unsure about your ability.

Try to stay out of the sun as much as possible.

It can be dangerous to stop Generic Tofranil taking suddenly.

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The potential effectiveness of imipramine hydrochloride (up to 5 mg/kg/d) was investigated in 53 prepubertal children suffering from major depressive disorder. Two complementary strategies were used simultaneously: a five-week, double-blind, placebo-controlled design (N = 38), and a plasma level/clinical response study (N = 30). Fifteen of the 16 children randomly assigned to active drug in the first study also participated in the second. Subjects were assessed using the Schedule for Affective Disorders and Schizophrenia for School Age Children and diagnosed according to unmodified Research Diagnostic Criteria. Response rates in the double-blind study were similar in both groups (imipramine, 56%; placebo, 68%). In the plasma level study, total maintenance plasma level (imipramine plus desipramine) was found to positively and linearly predict clinical response of the depressive syndrome (P less than .003). No evidence of a curvilinear relationship was found. Depressive hallucinations during the episode negatively predicted clinical response (P less than .05). Weight-corrected imipramine dosage did not predict either clinical response or plasma level in the individual subject. No predictors of response were found in the placebo group. These results suggest that the mean imipramine dosage was too low, and that future double-blind, placebo-controlled studies of imipramine in prepubertal major depression should include plasma level titration to above 150 ng/mL and an initial placebo washout period.

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The clinical significance of research findings is an important issue that, until recently, was often neglected. Statistical methods are available, however, to evaluate the meaningfulness of pre- to post-treatment change. The clinical significance of the National Institute of Mental Health Treatment of Depression Collaborative Research Program Data was evaluated. A substantial number of clients receiving treatment for depression made reliable improvements and had posttreatment scores that fell within a functional distribution. A small number of clients reliably deteriorated despite undergoing 12 sessions of treatment. No differences in clinical significance rates among treatment groups existed for measures of depressive symptoms. Treatments differed in terms of clinical significance on a measure of general symptom severity. There was substantial agreement among diverse methods of measurement regarding the identification of individuals making clinically significant change.

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Depression is one of the most prevalent mental illnesses, and causes a constant feeling of sadness and lose of interest, which often leads to suicide. Evidence suggests that depression is associated with aberrant MEK/ERK signaling. However, studies on MEK/ERK signaling in depression have only been done in a few brain regions, such as the hippocampus and mesolimbic reward pathways. Recent studies also implicate the involvement of the prefrontal cortex in depression. Thus, we examined the changes in MEK/ERK signaling in subregions of the prefrontal cortex of C57BL/6 mice by immunohistochemistry using phospho-MEK1/2 (Ser 217/221) and ERK1/2 (Thr202/Tyr204) antibodies. Mice were subjected to 21 consecutive days of restraint stress (for 2h daily), and depression-like behavior was evaluated using a sociability test and tail suspension test. The antidepressant, imipramine (20mg/kg) was injected intraperitoneally 30min before restraint stress exposure. Chronic/repeated restraint stress produced depressive-like behavior, such as increased social avoidance in the social interaction test, and enhanced immobility time in the tail suspension test. This depressive behavior was ameliorated by imipramine. The behavioral changes well corresponded to a decrease in MEK/ERK immunoreactivity in the medial orbital (MO) cortex and dorsal endopiriform nuclei (DEn), which was averted by imipramine, but not in cingulate, prelimbic, infralimbic, and motor cortex. These results suggest that MEK/ERK signaling is disrupted in the DEn and MO subregions of the prefrontal cortex in the depressive phenotype, and that blocking a decrease in activated MEK/ERK is inherent to the antidepressant imipramine response.

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The effects of neferine, an alkaloid of Nelumbo nucifera Gaertner embryos, on immobility in the forced swimming test, which is used to evaluate antidepressants, were investigated in mice. The administration of neferine from 25 to 100 mg/kg i.p. elicited anti-immobility effects in mice. The molecular dose effects of neferine in the forced swimming test were almost equal to those of the typical antidepressants maprotiline and imipramine. The involvement of the 5-HT receptor subtypes was also studied using 5-HT receptor antagonists. Anti-immobility effects of neferine are antagonized by the serotonin1A (5-HT1A) receptor antagonist, N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N-(2-pyridinyl)cyclohexanecarboxamide (WAY 100635). However, the 5-HT1B receptor antagonist, 3-[3-(dimethylamino)propyl]-4-hydroxy-N-[4-(4-pyridinyl)phenyl] benzamide dihydrochloride (GR 55562), the 5-HT2 receptor antagonist, 6-methyl-1-(methylethyl)-ergoline-8beta-carboxylic acid 2-hydroxy-1-methylpropyl ester (LY 53857), the 5-HT3 receptor antagonist, ondansetron and the 5-HT4 receptor antagonist, 4-amino-5-chloro-2-methoxy-benzoic acid 2-(diethylamino)ethyl ester (SDZ 205,557) did not affect the anti-immobility effects of neferine. The anti-immobility effect of the selective 5-HT1A receptor agonist, 8-hydroxy-2-(di-n-propylamino)tetaralin (8-OH-DPAT) was also antagonized by WAY 100635. Furthermore, co-administration of subactive doses of neferine (10 mg/kg) and 8-OH-DPAT (0.1 mg/kg) produced synergistic antidepressant-like effects. These results suggest that neferine shows antidepressant-like effects in mice similar to typical antidepressants and that these effects are mediated by the 5-HT1A receptor. Therefore, the central effects of neferine are likely to be linked to serotonergic neurotransmission.

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In vitro data indicate that imipramine (IMI), a widely used tricyclic antidepressant drug, is N-demethylated by several isoforms of cytochrome P450, which include CYP3A4. The aim of this study was to investigate the role of CYP3A in the in vivo N-demethylation of IMI.

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Therapeutic approaches via transcript regulation, allowing a modulation of LOX-1, may be an easier and safer strategy than a blockade of the receptor. Considering the wide distribution of LOX-1 on different tissues, research on the mechanisms of LOX-1 modulation by drugs and natural products applying "omic"-technologies will not only allow a better understanding of the role of LOX-1 in the processes of atherosclerosis, inflammation and longevity but also support the development of specific LOX-1 modulators, avoiding the initiation of molecular mechanisms which lead to adverse events.

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This report describes a middle-aged female who received imipramine for 7 days, developed severe cholestatic jaundice with features similar to primary biliary cirrhosis, and then improved clinically over the next 12 mo. Biochemical and histologic abnormalities persisted over a 14-yr period of follow-up, though subsequent administration of haloperidol may have influenced the long-term course. High levels of circulating immune complexes were also found 14 yr later, which raises questions about the relationship of primary biliary cirrhosis to drug-induced liver injury. A review of the literature on imipramine- and phenothiazine-related hepatic injuries reveals multiple similarities, and this case provides further evidence for a common hepatic reaction to the two drugs.

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To determine the flow-corrected luminal permeability, P(c), of lipophilic drugs measured by the in situ brain perfusion method under circumstances where the traditional Crone-Renkin equation (CRE) method, using diazepam as a flow marker, often fails.

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A kinetic model capable of predicting the effect of the rate of intraportal imipramine infusion in rats on the steady-state concentrations of imipramine and its active metabolite, desipramine, was developed by using kinetic parameters obtained from in vitro studies. A nonlinear relationship was observed between steady-state concentrations of imipramine and desipramine (formed from imipramine) and the intraportal infusion rate of imipramine. Biliary and urinary excretion rates of both compounds were negligible compared with the corresponding infusion rate, and the free fractions of imipramine and desipramine in blood were constant over the concentration range used in this investigation. In vitro studies revealed that imipramine and desipramine 2-hydroxylations were mediated by a high-affinity and low-capacity (saturable) enzyme(s), while N-demethylation of imipramine (which formed desipramine) was mediated by a low-affinity and high-capacity (not saturable) enzyme(s). The adequate prediction of the steady-state concentrations of imipramine and desipramine by the proposed model was possible only after incorporating the mutual competitive inhibition between 2-hydroxylations of imipramine and desipramine, in addition to the incorporation of saturable kinetics of imipramine and desipramine 2-hydroxylations. Furthermore, the steady-state concentrations of desipramine were predicted to also be affected by the formation rate of desipramine, which increased nonlinearly with the increase in the rate of intraportal infusion of imipramine.

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Artificially ventilated anesthetized dogs were given imipramine 7.5 mg/kg/hr i.v. In the first group (n = 6) mechanical cardiac activity was no longer detectable after a cumulative dose of 20.0 +/- 6.6 mg/kg (mean +/- sd). When aortic flow had decreased to 75% of its initial value, in a second group (n = 5) of experiments dopamine 10 micrograms/kg/min and in a third group (n = 5) isoproterenol 1 microgram/kg/min were administered i.v.. The doses of dopamine and isoproterenol were doubled when aortic flow had again decreased to 75% and 100%, respectively, of the original values. Cardiac mechanical activity was not detectable after a cumulative dose of 43.8 +/- 13.3 in the dopamine and 42.5 +/- 8.0 mg imipramine/kg in the isoproterenol group. These values differed significantly from that in the reference group (both 0.01 greater than p greater than 0.001). In the first group plasma imipramine concentrations at the end of the experiments were 3.06 +/- 0.66, in the second 3.36 +/- 0.66 and in the third 3.32 +/- 1.10 mg/1. Desipramine concentrations were 0.078 +/- 0.06, 0.162 +/- 0.076 and 0.383 +/- 0.09 mg/1 respectively. Dopamine induced a hemodynamic profile of low output and high pressure and isoproterenol one of low pressure and high output. It is concluded that dopamine combined with isoproterenol might be effective in counteracting the cardiodepressant action of imipramine.

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Mice were treated with either a sham procedure or focal hippocampal irradiation to disrupt cell proliferation before being confronted with 5 weeks of UCMS. From the third week onward, we administered monoaminergic ADs (imipramine, fluoxetine), the corticotropin-releasing factor 1 (CRF(1)) antagonist SSR125543, or the vasopressin 1b (V(1b)) antagonist SSR149415 daily. The effects of UCMS regimen, AD treatments, and irradiation were assessed by physical measures (coat state, weight), behavioral testing (Splash test, Novelty-Suppressed feeding test, locomotor activity), and hippocampal BrdU labeling.

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Brahmi exhibited significant decrease in duration of immobility in FST and reduced the shock induced decrease in activity in SID models. It didn't show any activity in the TST model.

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Adult fowl of both sexes injected with the monoamine oxidase inhibitor pargyline showed elevated circulating prolactin concentrations and reduced growth hormone concentrations. Young cockerels injected with the serotonin agonist quipazine and the antagonist methysergide showed responses consistent with a serotoninergic stimulatory control of prolactin. Injection of the serotonin precursor tryptophan and the serotonin re-uptake blocker imipramine resulted in elevated prolactin and reduced growth hormone levels. The similarities and differences in the control of prolactin and growth hormone in birds and mammals were discussed.

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In recent years, many Ayurvedic formulations are being researched to provide an effective antidepressant and anxiolytic drug in the field of psycho-pharmacology. The present study was planned to evaluate the anti-depressant and anxiolytic activity of Rasayana Ghana Tablet comprising three herbs Guduchi (Tinospora cordifolia Miers), Aamalaki (Emblica officinalis Garten) (RGT) and Gokshura (Tribulus terrestris Linn). Swiss albino mice were divided into four groups of six animals each, comprising of both male and female in each group. Group I received water served as normal control (WC), group II received vehicle and served as vehicle control (VC), group III received Rasayana Ghana tablet and group IV received standard drug diazepam (2 mg/kg) for anxiolytic study in elevated plus maze and standard antidepressant imipramine (5 mg/kg) for anti-depressant activity in behavior despair test. Rasayana Ghana tablet along with ghee and honey as vehicle is found to be having antidepressant and anxiolytic activity in experimental animals. Thus, this formulation can be used in prevention and treatment of depression and anxiety.

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Abnormalities of sphingolipid turnover in the brain during normal aging and age-related neurological disorders were associated with the neurons loss and cognitive malfunction. Calorie restriction (CR) prevented age-related deficits in hippocampal long-term potentiation and improved cognitive function at old age. In the paper we investigated the ceramide and sphingomyelin (SM) levels in the brain regions, which are critical for learning and memory of 3- and 24-month-old rats, as well as the correction of sphingolipid turnover in the brain of old rats, by means of the CR diet and modulators of SM turnover. Using the [methyl-(14)C-choline]SM, the neutral, but not the acid SMase activity has been observed to increase in both the hippocampus and brain cortex of 24-month-old rats with respect to 3-month-old animals. Age-dependent changes of neutral SMase activities were associated with ceramide accumulation and SM level drop in the brain structures studied. Treatment of the rats with the CR diet or N-acetylcysteine (NAC) or α-tocopherol acetate, but not an inhibitor of acid SMase imipramine, reduced the ceramide content and neutral SMase activity in the hippocampus of 24-month-old animals with respect to control rats of the same age. These results suggest that redox-sensitive neutral SMase plays important role in SM turnover dysregulation in both the hippocampus and neocortex at old age and that the CR diet can prevent the age-dependent accumulation of ceramide mainly via neutral SMase targeting.

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Assessment of an elderly depressed patient with an imipramine-induced tremor led to the conclusions that imipramine tremor (1) can be severe and incapacitating, (2) is most pronounced early in the treatment, (3) does not seem to be dose-related, and (4) is readily reversible with a beta-adrenergic blocking agent.

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The pharmacological concept that inhibition of the drug efflux pump P-glycoprotein (P-gp) enhances brain distribution of the antidepressant imipramine in the rat has recently been demonstrated. To determine if these findings are relevant to humans, the present study investigated if imipramine is a transported substrate of human P-gp. Furthermore, additional experiments were carried out to determine if findings in relation to imipramine and human P-gp would apply to other antidepressants from a range of different classes. To this end, bidirectional transport experiments were carried out in the ABCB1-transfected MDCKII-MDR1 cell line. Transported substrates of human P-gp are subjected to net efflux in this system, exhibiting a transport ratio (TR) ≥ 1.5, and directional efflux is attenuated by co-incubation of a P-gp inhibitor. Imipramine was identified as a transported substrate of human P-gp (TR = 1.68, attenuated by P-gp inhibition). However, the antidepressants amitriptyline, duloxetine, fluoxetine and mirtazapine were not transported substrates of human P-gp (TR ≤ 1.16 in all cases). These results offer insight into the role of P-gp in the distribution of antidepressants, revealing that rodent findings pertaining to imipramine may translate to humans. Moreover, the present results highlight that other antidepressants may not be transported substrates of human P-gp.

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Recent studies have demonstrated a scrutinized association of diabetes mellitus with depressive symptoms and major depression. Glycogen synthase kinase-3 (GSK-3) is a protein kinase enzyme constitutively active in non-stimulated cells and in multiple signalings. Independent lines of research provide a converging evidence for an involvement of GSK-3 in the regulation of behavior and hyperglycemia. The present study revealed that streptozotocin (STZ)-induced diabetic rats were found to show lengthened duration of immobility in the forced-swimming test (FST) and reduced locomotor and exploratory activities in the open-field test (OFT). Imipramine (15 mg/kg), Paroxetine (10 mg/kg) and lithium carbonate (36.94 mg/kg) for 14 days reduced immobility behavior in FST. Paroxetine and lithium carbonate increased the locomotor and exploratory activities, while imipramine decreased the locomotor activity in the OFT. Imipramine and lithium carbonate reduced the blood glucose level while paroxetine didn't alter it. STZ-induced diabetes increased GSK-3 gene expression which was determined using the reverse transcription-quantitative polymerase chain reaction test, while the three drugs decreased its expression. It can be concluded that lithium carbonate and imipramine can control both hyperglycemia and the associated symptoms of depression at the same time by inhibiting GSK-3 activity. On the other hand, paroxetine may only manage the depressive-like symptoms associated with diabetes through modulating the enzyme GSK-3, without changing blood glucose levels.

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The dexamethasone suppression test (DST) was performed in panic disorder (PD) patients with (n = 32) or without (n = 31) agoraphobia and in normal controls (n = 49). Postdexamethasone serum cortisol levels were significantly higher in agoraphobic PD patients (105.3 +/- 19.3 nmol/L) both when compared to PD patients without agoraphobia (47.3 +/- 7.7 nmol/L; p less than 0.01) and when compared to healthy controls (51.7 +/- 8.3 nmol/L; p less than 0.01). The rate of nonsuppressors (i.e., subjects displaying postdexamethasone cortisol levels greater than 138 nmol/L) was 28% and 3% in agoraphobic and nonagoraphobic PD patients, respectively, and 12% in controls. In patients, the postdexamethasone cortisol levels did not correlate with the number of panic attacks per week, baseline anxiety as measured using the Hamilton Anxiety Scale, depressive symptoms as measured using the Montgomery-Asberg Depression scale, or duration of illness. Data from eight patients in whom a second DST was performed after treatment with imipramine or clomipramine for three months indicate that a marked reduction of the number of anxiety attacks is not necessarily accompanied by a normalization of a pathological DST. In conclusion, it is suggested that the elevated postdexamethasone cortisol levels sometimes observed in agoraphobic PD patients are more closely related to the agoraphobic behavior than to the panic attacks per se.

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Daytime melatonin was measured by radioimmunoassay in 113 depressed outpatients before and after treatment with imipramine, mianserin, phenelzine, and placebo. At baseline, elevation of daytime melatonin values above expected levels suggests nonspecificity of the assay. After 6 weeks of treatment, melatonin levels were somewhat lower in patients on imipramine, mianserin, and placebo and slightly increased in patients treated with phenelzine. Changes in melatonin levels during treatment were significantly different for phenelzine compared with the other treatments. These findings are consistent with alterations in beta-adrenergic functioning or changes in serotonin levels.

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It has been suggested that tachykinin NK(2) receptor antagonists may have therapeutic utility in anxiety and/or depressive disorders.

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Daily administration of thyrotropin-releasing hormone (TRH) (20 mg/kg) for 10 days in 2 equally divided doses increased 5-hydroxytryptamine and/or 5-hydroxyindoleacetic acid levels in certain brain areas. Chronic imipramine treatment (10 mg/kg) for 10 days significantly decreased the levels of brain 5-hydroxytryptamine and 5-hydroxyindoleacetic acid. When TRH was administered concurrently with imipramine (10 mg/kg), this neuropeptide significantly potentiated the effects of imipramine on lowering of endogenous levels of 5-hydroxytryptamine (striatum, hypothalamus) and 5-hydroxyindoleacetic acid (striatum, midbrain, pons-medulla). Our data provide a possible neurochemical basis for the reported potentiation of tricyclic antidepressant action by TRH.

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Reduction of tertiary amine N-oxides by the mitochondrial fraction of rat liver was investigated. NADPH was required as a cofactor. The rate of reaction was faster with the NADPH-generating system than with NADPH. Isocitrate in the NADPH-generating system revealed the maximum stimulation. A little less activity was observed when NADH was used as a cofactor instead of NADPH. The reductase activity was markedly inhibited under aerobic conditions. The rates of mitochondrial tertiary amine N-oxide reduction expressed in nanomoles per milligram of protein per minute were: N,N-dimethylaniline N-oxide, 4.3; tiaramide N-oxide, 0.47; and imipramine N-oxide, 0.14. The activity for N,N-dimethylaniline N-oxide was comparable to the microsomal activity, but the activity for imipramine N-oxide was much less than that in microsomes. Isocitrate and alpha-ketoglutarate were found to stimulate mitochondrial tertiary amine N-oxide reduction more efficiently than other Krebs cycle intermediates. Oxalacetate, on the other hand, was the least effective intermediate. ATP together with NADPH and NADP stimulated the reaction efficiently, probably due to the energy-dependent intramitochondrial transhydrogenation. Antimycin, rotenone and cyanide had little or no effect on isocitrate-dependent N-oxide reduction, whereas an inhibitory effect was observed on succinate-supported N-oxide reductase. N-oxide reductase activity in mitochondria was partially suppressed under an atmosphere of carbon monoxide, althouth no increase of the activity was observed by phenobarbital pretreatment, nor inhibition by 2,4-dichloro-6-phenylphenoxyethylamine. Experiments with digitonin-treated mitochondria demonstrated that mitochondrial N-oxide reductase was bound to mitochondrial inner membrane or its matrix.

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Chronic (14 day) administration of several pharmacologically-distinct antidepressant drugs resulted in marked reductions in the serotonin2 (5-HT2)-mediated quipazine-induced head shake response which were accompanied by significant reductions in the density of cortical beta-adrenergic and 5-HT2 binding sites. Noradrenergic (DSP4[N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine]-induced) and serotonergic (5,7-DHT[5,7-dihydroxytryptamine]-induced) lesions either attenuated or blocked antidepressant-induced reductions in 5-HT2-mediated behavior. DSP4- and 5,7-DHT lesions did not alter the down-regulation of 5-HT2 binding sites produced by imipramine, desipramine, phenelzine or iprindole. To a large extent, the antagonism of antidepressant-induced reductions in 5-HT2-mediated behavior was coincident with the blockade of down-regulation of beta-adrenergic binding sites by both noradrenergic and serotonergic denervation. The functional interrelationship of 5-HT2 and beta-adrenergic receptors suggested by the present findings may provide insight into a common mechanism underlying the action of pharmacologically-distinct antidepressant drugs.

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The basic compound N-N-N'-trimethyl-N'-(2-hydroxy-3-methyl-5-iodobenzyl)-1,3- propanediamine (HIPDM) accumulates in human and rabbit lungs, where it forms a slowly effluxable pool. In isolated perfused rat lung, HIPDM is taken up by a saturable, energy-independent mechanism, which is competitively inhibited by imipramine, chlorpromazine and propranolol. To ascertain whether beta-adrenergic receptors are involved in the binding process of HIPDM to lung tissue, the ability of unlabelled HIPDM to displace the beta-adrenergic receptor ligand [125I]iodocyanopindolol (ICYP) from rabbit lung beta-receptors was examined. Lung microsomal membrane fractions (75 micrograms ml-1) were incubated at 37 degrees C for 3 h with 68 pM ICYP (with or without 1 microM of (+/-)-propranolol) in the presence of HIPDM (10(-10)-10(-3) M). Bound and free radioactivity were separated through glass-fibre filters and the retained radioactivity was counted in a gamma-spectrometer. HIPDM competed with ICYP for beta-adrenoceptors (13% displacement at 10(-5) M. 50% at 5 x 10(-5) M, and 90% at 2 x 10(-4) M). The inhibition curve of ICYP binding by HIPDM was similar to that observed for (-)-noradrenaline. Although the results of the in vitro studies cannot be extrapolated to in vivo conditions, they suggest that beta-adrenergic receptors may be involved in the observed lung uptake of the basic amine HIPDM.

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tofranil cost 2017-07-17

Forty-one panic disorder patients receiving placebo were investigated in a double-blind comparison of alprazolam, imipramine and placebo in panic disorder. A significantly higher drop-out rate was found in the placebo group than buy tofranil in the active treatment groups, but placebo response was found in 34% of the patients, defined as reduction of panic attacks to zero, and in 23%, defined as a score of greater than or equal to 8 on the Physician Global Improvement Scale (0-10 points). Several predictors of response to placebo were found. The responders had fewer panic attacks than the nonresponders at baseline. They also reported less psychopathology and were less help-seeking than the nonresponders. The implications for psychopathology and possible response to psychotherapy among responders and nonresponders are discussed. It is hypothesized that the responders show more signs of realistic processing of internal and external stimuli and fewer signs of subjective distress than the nonresponders. Responders will therefore probably be more responsive to psychotherapy than nonresponders.

tofranil 25 mg 2016-07-24

To compare response rates among patients with major depressive disorder (MDD) treated with either moclobemide, an buy tofranil antidepressant thought to simultaneously enhance both noradrenergic and serotonergic neurotransmission, or selective serotonin reuptake inhibitors (SSRIs).

tofranil online 2015-10-15

At steady-state, the mean serum imipramine concentration was significantly higher in transgenic mice than buy tofranil in control mice (859.0 vs. 319.9 ng/ml). In contrast, the mean steady-state brain imipramine concentration was significantly lower in transgenic mice (3,862.6 vs. 7,307.7 ng/g). Similarly, in transgenic mice, the mean steady-state serum desipramine concentration was significantly higher (176.7 vs. 39.0 ng/ml) while the mean brain desipramine concentration was lower (243.0 vs. 393.5 ng/g). The serum unbound fraction of imipramine was 3-fold lower in transgenic mice (0.03 vs. 0.09).

tofranil drug study 2017-01-21

Many cationic drugs are administered during pregnancy and might enter the fetal circulation by transplacental passage. This study was performed to characterize the apical uptake of choline and several cationic drugs at cultured epithelial cells of the human placenta. Total uptake of [3H]choline in BeWo cells was H(+)-independent and to 65% Na(+)-independent. Uptake rates into both cell lines were saturable with Michaelis-Menten constants (Kt) of 108 microM (BeWo) and 206 microM (JEG-3), respectively. Cationic drugs such as etilefrine, clonidine, ranitidine, diphenhydramine, imipramine and butylscopolamine strongly inhibited the [3H]choline uptake in BeWo cells and in JEG-3 cells, with Ki values ranging from 0.18 to 3.3 mM. In contrast, tetraethylammonium had only little inhibitory effect on [3H]choline uptake. Using high-performance capillary electrophoresis for quantitative analyses, uptake of etilefrine and diphenhydramine into JEG-3 or BeWo cells was measured. Diphenhydramine was transported into JEG-3 cells in a saturable manner with a Kt value of 0.75 mM. In the presence of sodium, diphenhydramine uptake at BeWo cells was inhibited to 69% by the addition of 50 mM choline chloride. Like choline uptake, total diphenhydramine uptake was to 68% Na(+)-independent in BeWo cells. We conclude that in addition to choline, several cationic drugs, in particular diphenhydramine, are buy tofranil taken up by placental epithelial cells from the maternal blood by carrier-mediated processes. Etilefrine, clonidine, ranitidine, diphenhydramine and butylscopolamine interact with the Na(+)-independent placental choline transport system.

tofranil maximum dosage 2017-02-23

One-way analysis of variance followed by Newman-Keuls multiple comparison test was employed to analyze the results. P < 0.05 was considered statistically significant as compared to control. CT at 400 mg/kg produced an antianxiety effect equivalent to lorazepam, in the elevated plus maze, open field, and social interaction tests among selected doses of the CT. CT at 400 mg/kg also induced an antidepressant activity similar to imipramine, in the behavioral despair, learned helplessness test, and tail suspension among selected doses of the CT. Moreover, CT at 400 mg/kg produced a significant antistress effect comparable to W. somnifera in water immersion-restraint stress by decreasing ulcer index, adrenal gland weight, and by normalizing the plasma levels of corticosterone, glucose, cholesterol, and triglyceride buy tofranil levels when related to stress control.

tofranil tablet uses 2015-06-02

A large number of studies suggest that individual characteristics of psychotherapists affect the outcome of psychosocial treatments for psychiatric illness, but little work has been done to see if this is also the case for pharmacotherapy. In the context of a multicenter study that compared psychosocial and medication treatments for panic disorder, we assessed whether such characteristics as age of the psychiatrist, number of years of experience, and gender influence the outcome of treatment with the antipanic drug imipramine. Data were examined by multiple and logistic regression analyses for eight psychiatrists who treated a total of 57 patients with panic disorder. More physician experience, measured as years since completing residency, was associated with better response to imipramine on one of two main dichotomous measures (the buy tofranil Clinical Global Impression-Improvement Scale) and on six of nine continuous measure rating scales. Associations between psychiatrist age and outcome and between psychiatrist gender and outcome were also present but on fewer measures. Although these are post-hoc analyses that were not planned when the multicenter study was originally designed and therefore there are limitations in the information available about the psychiatrists' characteristics, the findings suggest that even in the context of a clinical trial that employs a specific protocol and single medication, physician experience may influence patient outcome. Depression and Anxiety 17:88-93, 2003.

tofranil 5 mg 2016-03-26

Cholinesterases are divided into two classes based on differences in their substrate specificity and tissue distribution: acetylcholinesterase (AChE) and butyrylcholinesterase (BChE). These enzymes may be inhibited by several compounds, such as buy tofranil antidepressants. The antidepressants paroxetine, imipramine, clomipramine and sertraline inhibited both venom AChE as well as human serum BChE in a concentration-dependent manner but had no effect on AChE in the rat brain striatum. The IC(50) of venom calculated for imipramine was 0.3 mM, paroxetine 0.38 mM, clomipramine 0.34 mM and sertraline 0.35 mM. Analysis of kinetic data indicated that the inhibition caused by sertraline and paroxetine was mixed, i.e. K(m) values increased and V(max) decreased in a concentration dependent manner. Imipramine and clomipramine exhibited competitive inhibition, i.e. K(m) values increased and V(max) remained constant. The present results suggest that these therapeutic agents used for depression can also be considered as inhibitors of snake venom and human serum cholinesterase.

tofranil 200 mg 2015-03-19

Recently we identified GANT61, a small-molecule antagonist of Gli transcription factors, which are the final effectors of the mammalian Hedgehog (HH) signaling pathway. Here we describe a diamine substructure of GANT61 that carries the biological activity and show that this part of the molecule is structurally related to trans-1,4-bis(2-chlorobenzaminomethyl)cyclohexane dihydrochloride (AY9944), an inhibitor of the enzymatic activity and transcriptional inducer of 7-dehydrocholesterol-reductase (Dhcr7, EC Treatment of cells with the GANT61 diamine, AY9944, or overexpression of DHCR7 results in the attenuation of Smoothened-dependent and -independent HH signaling. Whereas GANT61 function is independent of Dhcr7, AY9944 does require up-regulation of endogenous Dhcr7. In line with these findings, buy tofranil Dhcr7-modulating antipsychotic (clozapine, chlorpromazine, haloperidol) and antidepressant (imipramine) drugs regulate HH signaling in vitro and in vivo. Modulation of HH signaling may represent a hitherto undiscovered biological (side) effect of therapeutics used to treat schizophrenia and depression.

tofranil drug 2017-01-06

The effect of chronic mild stress (CMS) and chronic treatment with the tricyclic antidepressant drug imipramine (10 mg/kg/day for 5 weeks) on neuronal responsiveness to the alpha 1-noradrenergic agonist phenylephrine and serotonin (5-HT) was examined ex vivo, in the CA1 cell layer of the rat hippocampal slice buy tofranil preparation. We corroborated some previous findings that CMS, which had been used as an animal model of depression, decreased the consumption of a 1% sucrose solution and that that effect was reversed by chronic administration of imipramine. Imipramine did not change the sucrose consumption in control animals. In both control and stressed animals, phenylephrine (5 microM) and 5-HT (10 microM) attenuated the amplitude of the population spikes evoked in the CA1 pyramidal cell layer by stimulation of Schaffer collateral/commissural fibers. Those inhibitory effects of phenylephrine and 5-HT were significantly potentiated by chronic treatment with imipramine. The imipramine-induced potentiation was similar in slices from control and stressed animals. These results suggest that the imipramine-induced functional changes in alpha 1-noradrenergic and serotonergic receptors in the hippocampus are not involved in the anti-anhedonic effect of chronic imipramine administration in the CMS model of depression.

tofranil medication information 2015-06-17

St John's wort (Hypericum perforatum) is a popular over-the-counter antidepressant. Its antidepressive effect has been buy tofranil attributed in part to inhibition of monoamine transporters and monoamine oxidase, on the basis of in vitro studies.

tofranil user reviews 2017-06-25

Regulation of tyrosine hydroxylase expression by antidepressant treatments was investigated in the locus coeruleus (LC), the major noradrenergic nucleus in brain. Rats were treated chronically with various antidepressants, and tyrosine hydroxylase levels were measured in the LC by immunoblot analysis. Representatives of all major classes of antidepressant medication-including imipramine, nortriptyline, tranylcypromine, fluvoxamine, fluoxetine, bupropion, iprindole, and electroconvulsive seizures-were found to decrease levels of tyrosine hydroxylase immunoreactivity by 40-70% in the LC. Decreased levels of enzyme immunoreactivity were shown to be associated with equivalent decreases in enzyme mRNA levels. Antidepressant regulation of LC buy tofranil tyrosine hydroxylase appeared specific to these compounds, inasmuch as chronic treatment of rats with representatives of other classes of psychotropic drugs, including haloperidol, diazepam, clonidine, cocaine, and morphine, failed to decrease levels of this protein. The results demonstrate that chronic antidepressants dramatically downregulate the expression of tyrosine hydroxylase in the LC and raise the possibility that such regulation of the enzyme represents an adaptive response of LC neurons to antidepressants that mediates some of their therapeutic actions in depression and/or other psychiatric disturbances.

tofranil drug classification 2016-09-12

Clitoral priapism is a rare condition that is associated with an extended duration of clitoral erection due to local engorgement of clitoral tissue resulting in pain. Although the pathophysiology is not completely understood, it has been associated with buy tofranil specific classes of medications, diseases that alter clitoral blood flow or others associated with small to large vessel disease. We present a case report of a 26-year-old patient who developed clitoral priapism without a clear medication or disease related etiology. The patient was treated with opiates, imipramine, non-steroidal anti-inflammatory medication, and local ice packs. She recovered uneventfully.

tofranil 150 mg 2016-04-15

We describe the clinical and electrophysiologic findings in seven patients referred for evaluation of excessive daytime somnolence. These patients had none of the usual causes of excessive daytime somnolence but during sleep exhibited stereotypic body movements, tachycardia, respiratory disturbances, somniloquy, and transient arousals in a repetitive fashion. These episodes induced fragmentation of sleep. The polysomnograms revealed an increase in wakefulness and stage I decreased rapid eye movement during sleep in Cotrimoxazole Bactrim Dosage addition to the episodes of abnormal body movements. No epileptiform features were present either in the electroencephalogram or in the nocturnal polysomnogram. Four of the seven patients were treated with anticonvulsants, with both subjective and objective improvement on subsequent follow-up polysomnograms. Because of the pronounced functional deficits associated with the sleep disorder in these patients, it is of great importance to recognize the disorder and treat it appropriately.

tofranil dosage information 2015-07-19

Clinical experience has firmly established the usefulness of imipramine in the management of enuresis. Our report describes the serious dose-related cardiac and central nervous system toxic effects of imipramine. Comparison of the human and Luvox Good Reviews animal toxicity data is presented and recommendations are given for safe human dose ranges.

tofranil diet pill 2016-10-30

The present study showed that continued forced swimming for 7 days caused chronic fatigue-induced anxiety-like behavior as assessed in mirror chamber, plus maze tests, and impairment in locomotor activity followed by oxidative damage (as evidenced by increased lipid peroxidation, nitrite levels, depleted reduced glutathione, and catalase activity) in animals. Seven days pretreatment with citalopram (5 and 10 mg/kg) and imipramine (10 and 20 mg/kg Epivir Cost ) significantly improved behavioral and biochemical alterations. Further, L-nitro-arginine methyl ester (L-NAME,5 mg/kg) and methylene blue (MB, 10 mg/kg) pretreatment with citalopram (5 mg/kg) or imipramine (10 mg/kg) potentiated their protective effect. However, l-arginine (100 mg/kg) pretreatment with citalopram (5 mg/kg) or imipramine (10 mg/kg) reversed their protective effect as compared with their effect per se (P < 0.05).

recommended tofranil dosage 2016-11-20

Tricyclic antidepressants (TA) often used in the supportive care of cancer patients exhibit cytostatic properties on human renal cancer cells in vitro. Complete growth inhibition was observed with imipramine and clomipramine at concentrations similar to that of nitrogen mustard. Clinical side effects of TA (cardiotoxicity, agranulocytosis) and their binding to nucleotides may point to Duricef Mg a mechanism of action similar to that of anthracyclines. Careful recording of TA applications during cancer chemotherapy or better randomized studies with or without TA should define the antineoplastic influence of TA in cancer chemotherapy.

tofranil tablets 2016-04-26

1. The present study shows the effects of imipramine in a single dose (10 mg kg(-1), p.o.) or following repeated (14 days, twice a day) treatment on the level of mRNA coding for D2 dopamine receptors in the rat caudate putamen (CP). Repeated administration of imipramine resulted in the increase of the level Rulide Medicine of mRNA coding for D2 dopamine receptors. 2. Radioligand binding studies with the D2 receptor agonist, [3H]-N-0437, indicated, that following imipramine administration, the affinity of the agonist for the D2 dopamine receptor significantly increased, though without any alterations in the Bmax. 3. Pharmacological manipulations (by use of forskolin, GppNHp and quinpirole) of the cyclic AMP generating system, ex vivo following administration of imipramine indicated that an up-regulation of factors inhibiting cyclic GMP formation takes place. 4. Most probably it is the D2 dopamine receptor which undergoes functional up-regulation, resulting from the enhancement of its biosynthesis.

tofranil 300 mg 2016-04-24

The solute carrier family 41 (SLC41) encompasses three members A1, A2, and A3. Based on their distant homology to the bacterial Mg²⁺ channel MgtE, all have been linked to Mg²⁺ transport. There is only very limited knowledge on the molecular biology and exact functions of SLC41A2 and SLC41A3. SLC41A1 is ubiquitously expressed and data on its functional and molecular properties, regulation, complex-forming ability, and spectrum of binding partners are available. SLC41A1 was recently identified as being the Na⁺/ Zantac Reviews Mg²⁺ exchanger (NME)-a predominant Mg²⁺ efflux system. Mg²⁺-dependent and hormonal regulation of NME activity is now known to depend on the intracellular N terminus of SLC41A1 that is involved in Mg²⁺ sensing and contains phosphorylation sites for protein kinase (PK) A and PKC. Data showing a link between SLC41A1 and human disorders such as Parkinson's disease, nephronophthisis (induced by the null mutation c.698G>T in renal SLC41A1), and preeclampsia make the protein a candidate therapeutic target.

tofranil pm generic 2016-08-27

Many male narcoleptic patients complain of erectile dysfunction related to chemotherapy, and some find it so distressing that they fail to continue treatments. This is a potentially dangerous situation. We studied the erectile capabilities of 28 narcoleptic men who had complaints of erectile dysfunction with our objective sleep laboratory measurement of nocturnal penile tumescence (NPT) for diagnostic workup. We found that while short REM latency, a classic indicator of narcolepsy, was present in all patients, NPT, which is associated with REM sleep, did not coincide with the short REM latencies in about half the patients. This may be partially due to the fact that first-cycle REM is often not accompanied by NPT episodes (even in the control population). We also found that, in a few cases, the patients' subjective beliefs about their erectile capacity tended to underestimate our measurements. The patients receiving drug treatment already had some vasculogenic or neurogenic genital impairment, which probably made them more vulnerable to the effects of the drugs. Patients who had none Norvasc Dosing of these complications showed similar erectile impairment under the influence of medication. Additionally, we found unique manifestations of the disease in three drug-free patients; one had cataplectic attacks upon arousal, and two had unexplained erectile impairment.

tofranil drug category 2016-05-14

The delayed onset of therapeutic response to antidepressants remains a major problem in the treatment of depression. Among the strategies to accelerate response to treatment, the early addition of thyroid hormone to antidepressants has been suggested as a viable method. The authors performed a meta-analysis Sinemet Usual Dosage of the literature on the use of thyroid hormone supplementation to accelerate the treatment of depression to determine whether there is sufficient evidence to support the clinical efficacy of this strategy.

tofranil 75 mg 2017-05-17

N-isopropyl p-iodoamphetamine (IMP) demonstrates a high affinity for lung and brain during the first pass following intravenous injection. Its high brain affinity has been used to advantage for cerebral perfusion imaging, but the effects of drugs on IMP distribution could affect its utility. In this study, we determined the effects of the tricyclic antidepressant imipramine and the MAO inhibitors deprenyl and phenelzine on the biodistribution of IMP. We first determined the effect of loading dose and anesthesia on the biodistribution of IMP. In rats, biodistribution was not dependent on loading dose between 0.1 and 1.1 mg/kg. Anesthesia with thiopental and chloral hydrate depressed lung and brain IMP uptake. In rats, preloading doses of imipramine depressed lung uptake but did not result in increased brain IMP Propecia Buy uptake; postloading doses of imipramine did not release IMP from the lung. In rabbits, simultaneous or postloading doses of imipramine resulted in release of IMP from the lung with an increase in brain activity. Both mixed A and B MAO inhibitors (phenelzine) and B selective MAO inhibitors (deprenyl) did not affect IMP distribution in rats. Based on the action of imipramine on IMP uptake and clearance in the lung, we postulate that IMP uptake and metabolism within the lung is related to the mixed function oxidase (MFO) system. As the lung is rich in the MFO system in humans, we would also predict from this study that IMP distribution in patients under antidepressant therapy would not be affected by either tricyclic or MAO inhibitor agents apart from the effect of these drugs on cerebral perfusion.

tofranil generic name 2015-08-10

In order to assess the effects of inverse benzodiazepine agonists and antagonists on brain function, computerized EEG (CEEG) analysis was performed in rats following the i.p. administration of SR 95195 (7-phenyl-3-methyl-1,2,4 triazolo-[4,3-b]pyridazine) and CGS 8216 (2-phenylpyrazolo-[4,3c]-quinoline-3-[5H]-one) two benzodiazepine receptor inverse agonists (BRIAGs) and of flumazepil (Ro 15-1788), a benzodiazepine receptor antagonist (BRANT). The EEG effects of SR 95195 (3, 10, 30 and 60 mg/kg), CGS 8216 (10 and 30 mg/kg) and flumazepil (3, 10, 30 and 60 mg/kg) were compared to those of the psychostimulant drugs DL-amphetamine (0.1, 0.3 and 1 mg/kg), and caffeine (10 and 30 mg/kg) and those of aniracetam (100 and 300 mg/kg), a nootropic pyrrolidone derivative. The CEEG profiles of SR 95195, CGS 8216 and flumazepil were mainly characterized by a power increase in the 20-32 Hz frequency range and by a power reduction in the 8-16 Hz range. These effects were quite similar to those of the psychostimulants DL-amphetamine and caffeine as well as to those of the nootropic aniracetam. Other psychotropic drugs with CNS-depressant properties, namely diazepam (10 mg/kg p.o.), pentobarbital (30 mg/kg p.o.), chlorpromazine (10 mg/kg i.p.) and imipramine (10 mg/kg i.p.) induced quite different EEG power modifications. These Nexium Recommended Dosage results show that BRIAGs and BRANTs possess a marked intrinsic activity at the central level and suggest that this activity is CNS-activating in nature.