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The distribution of the beta 1 (beta 1) and beta 2 (beta 2) subtypes of the beta-adrenergic receptor was examined in rat and nondiseased control human tissue. The distribution of the beta 1 and beta 2 receptors was also examined in schizophrenic cases, with additional studies in schizophrenic suicide and nonschizophrenic suicide cases. Scatchard analysis of the binding of [125I]iodopindolol (IPIN) to cortical membranes showed a similar Kd in human (177 pM) and rat (161 pM), but a lower maximum binding site (Bmax) in the human tissue (18.7 fmol/mg protein and 55.6 fmol/mg protein). For the autoradiographic studies [125I]IPIN was used to visualize both subtypes (total) or was displaced with the selective beta 1-receptor antagonist ICI-89,406 to visualize beta 2 sites, or with the selective beta 2-receptor antagonist ICI-118,551 to visualize beta 1 sites. Important differences in the regional distribution of the two subtypes of the beta-adrenergic receptors were noted between rat and human. In the nucleus accumbens and ventral putamen (ventral striatum), a patchy distribution of beta 1 receptors was observed that was not evident in the rat. These patches were aligned with markers of the matrix compartment of the striatum. The schizophrenic cases showed significant increases in the labeling of the beta 1-receptor patches with [125I]IPIN. In contrast to the frontal cortex of the nondisease controls, the parietal and temporal cortex showed a high ratio of beta 1 to beta 2 receptors and a highly laminar organization of the subtypes. [125I]IPIN binding to beta 1 receptors was highest in the external laminae with the reverse gradient for the beta 2 subtype. The medial temporal cortex displayed an alteration in the ratio of the 2 subtypes of the beta-adrenergic receptor, with the parahippocampus and hippocampus of the human, in contrast to the rat brain, predominantly expressing the beta 2 receptor. Moreover, there were consistently higher densities of beta 2 receptors in the hippocampus of the right hemisphere than the left hemisphere of the nondisease controls. There was not a left and right hemispheric asymmetry of beta 2 receptors in the hippocampus of elderly schizophrenics or in young schizophrenics who committed suicide. The asymmetry was evident in nonschizophrenic suicides, suggesting that the lack of asymmetry in the hippocampus of schizophrenics is evident early in the disease process. Thus limbic structures show alterations in the patterning of beta 1 and beta 2 receptors in the schizophrenic cases.
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The higher increase of the metabolites as compared with the parent compounds can be explained by a paroxetine-induced inhibition of the liver enzyme cytochrome P4502D6, which catalyses the second step of the TCA metabolism, i.e. the hydroxylation of the metabolites. Blood levels should be meticulously monitored, if TCAs are combined with paroxetine.
The effect of various drugs on the extracellular concentration of dopamine in two terminal dopaminergic areas, the nucleus accumbens septi (a limbic area) and the dorsal caudate nucleus (a subcortical motor area), was studied in freely moving rats by using brain dialysis. Drugs abused by humans (e.g., opiates, ethanol, nicotine, amphetamine, and cocaine) increased extracellular dopamine concentrations in both areas, but especially in the accumbens, and elicited hypermotility at low doses. On the other hand, drugs with aversive properties (e.g., agonists of kappa opioid receptors, U-50,488, tifluadom, and bremazocine) reduced dopamine release in the accumbens and in the caudate and elicited hypomotility. Haloperidol, a neuroleptic drug, increased extracellular dopamine concentrations, but this effect was not preferential for the accumbens and was associated with hypomotility and sedation. Drugs not abused by humans [e.g., imipramine (an antidepressant), atropine (an antimuscarinic drug), and diphenhydramine (an antihistamine)] failed to modify synaptic dopamine concentrations. These results provide biochemical evidence for the hypothesis that stimulation of dopamine transmission in the limbic system might be a fundamental property of drugs that are abused.
There is an increasing body of evidence suggesting that GABA plays an important role in the therapeutic effects of antidepressant/antipanic drugs. Phenelzine and imipramine are efficacious in the treatment of depression and panic disorder and phenelzine has been reported to elevate GABA levels while imipramine enhances GABA release in rat brains. In the present study, using a multiprobe quantitative solution hybridization assay, we measured the steady-state levels of mRNAs that encode glutamic acid decarboxylase (GAD67 and GAD65), the GABA transporter GAT-1 and GABA transaminase (GABA-T) in rat cortex after treatment with constant infusion (via osmotic minipumps) of phenelzine or imipramine for a short-term (3 days) or long-term (21 days) period. We found that none of the treatments gave rise to significant changes in the steady-state levels of mRNAs encoding GAD67, GAD65 or GABA-T at any time point. The steady-state levels of GAT-1 mRNA were increased significantly (23%) after long-term, but not by short-term, treatment with phenelzine. Imipramine treatment, short- or long-term, did not alter the steady-state levels of GAT-1 mRNA. These results suggest that the GABA enhancing effects of phenelzine or imipramine in rat cortex do not affect the steady-state levels of mRNAs that encode GAD67, GAD65 and GABA-T. Further, the previously observed increases in GABA levels or GABA release induced by these drugs are probably not a consequence of changes in the expression of these genes.
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Although serotonin receptor and cytoarchitectonic alterations are reported in prefrontal cortex (PFC) in suicide and depression, no study has considered binding relative to neuron density. Therefore, we measured neuron density and serotonin transporter (SERT), 5-HT1A and 5-HT2A binding in matched suicides and controls. Suicides and normal controls (n=15 matched pairs) were psychiatrically characterized. Neuron density and binding were determined in dorsal [Brodmann area (BA) 9] and ventral (BA 47) PFC by stereology and quantitative autoradiography in near-adjacent sections. Binding index was defined as the ratio of receptor binding to neuron density. Suicides had lower neuron density in the gyrus of both areas. The binding index was lower for SERT in BA 47 but not in BA9; the 5-HT1A binding index was higher in BA 9 but not in BA 47, while the 5-HT2A binding index was not different between groups. SERT binding was lower in suicides in BA 47 but not BA 9, while 5-HT1A binding was higher in BA 9 but not BA 47. SERT binding negatively correlated with 5-HT1A binding in BA 47 in suicides. Neuron density decreased with age. The 5-HT1A binding index was higher in females than males. We found lower neuron density and lower SERT binding index in both PFC regions in suicides. More 5-HT1A binding with less SERT binding and the negative correlation in depressed suicides suggests post-synaptic receptor up-regulation, and it is independent of the difference in neuron density. Thus, abnormalities in both cortical neurons and in their serotonergic innervation are present in suicides and future studies will need to determine whether cortical changes reflect the trophic effect of altered serotonin innervation.
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Using 7% or greater weight change as the measure of clinical significance, 4.3% of SSRI-treated patients had lost weight at any point in the acute phase versus 1.7% of those treated with nefazodone (p = .017). However, at any point during the long-term phase, significantly more SSRI-treated patients than nefazodone-treated patients showed a significant increase in body weight (17.9% vs. 8.3%; p = .003). At any point in the acute phase, significantly more imipramine-treated patients than nefazodone-treated patients had a 7% or greater increase in body weight (4.9% vs. 0.9%; p = .027), and for the long-term phase the comparison yielded 24.5% versus 9.5%. The difference during the long-term phase was statistically significant in women (p = .017), but not in men (p = .078) due to the small numbers of men in each group.
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We have used a human SCLC cell line and fetal hamster pulmonary neuroendocrine cells with in vitro kinase activation assays and western blots to assess the levels of expression and activation of Raf-1, MAPK and c-myc to address this issue.
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Imipramine serum protein binding was measured by equilibrium dialysis in healthy subjects (88 women and 57 men; age 21 to 79 yr) who were relatively evenly distributed according to age, sex, smoking habits, and oral contraceptive use. Average free fraction was 10.9 +/- 1.4%. Interindividual variation in degree of binding was less than 100%, the free fraction varying from 8% to 14.7%. Women age 30 to 39 yr had significantly lower binding than all other female age groups and lower binding than men age 30 to 39 yr. Oral contraceptive use and smoking habits did not correlate to degree of binding. Serum concentrations of 12 proteins were measured in subjects with the highest binding (n = 17) and lower binding (n = 18). The concentration of orosomucoid, complement C3c, and apolipoprotein B was higher in the high-binding group than in the low-binding group. Since covariation among concentrations of these three proteins was modest, the data indicate a separate significance of the three proteins. The binding of 3H-imipramine did not correlate with the albumin concentration.
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The effects of chronic clomipramine, imipramine and clorgyline on 5-HT1C receptors were studied in discrete brain regions, in male Wistar rats, using [3H]mesulergine to label the receptor binding sites. Clorgyline treatment significantly reduced [3H]mesulergine binding (Bmax values) in both the hypothalamus and striatum compared to saline-treated animals. There were no differences in the maximum number of [3H]mesulergine binding sites following clorgyline in the hippocampus, frontal cortex or brainstem. Neither clomipramine or imipramine treatment resulted in any significant changes in 5-HT1C receptor number in the brain regions examined here. Furthermore, the Kd values (receptor affinity) for [3H]mesulergine binding were not significantly different comparing treatment groups to control animals. The significant changes in discrete brain regions following chlorgyline treatment suggest that 5-HT1C receptors may be involved in the clinical efficacy for the treatment of depression and other neuropsychiatric disorders.
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Dietary supplement use has increased during the past decade. Epidemiologic studies suggest that patients turn to dietary supplements because of a reluctance to take prescription medications or a lack of satisfaction with the results. They often perceive dietary supplements to be a safer or more natural alternative. Patients with mental health conditions, including depression, anxiety, and sleep disorders, are among those who use dietary supplements. St. John's Wort is used to treat depression. Clinical studies comparing dietary supplements with low-dose antidepressants (maprotiline, amitriptyline, or imipramine at 75 mg/day) or high-dose antidepressants (imipramine at 150 mg/day) find no significant difference between treatments. Kava kava is used to treat anxiety. Clinical trials demonstrate it to be superior to placebo, and roughly equivalent to oxazepam 15 mg/day or bromazepam 9 mg/day. Agents discussed for use in sleep disorders include melatonin, valerian, 5-hydroxytryptamine, catnip, chamomile, gotu kola, hops, L-tryptophan, lavender, passionflower, skullcap, and valerian. Familiarity with the evidence for use and the possible resulting risks can help health professionals to guide patient decisions regarding use of dietary supplements.
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Despite the high prevalence and significant morbidity associated with posttraumatic stress disorder (PTSD) in children and adolescents, there are limited and conflicting data to guide psychopharmacologic interventions. With these considerations in mind, we sought to summarize the current evidence for psychopharmacologic interventions in youth with PTSD.