Effect of alprazolam on depression in panic disorder.
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Adolescent↗
Biomedical subjects
J A Melvin
Publications and source records attributed to J A Melvin.
Toxicity resulting from lithium augmentation of antidepressant treatment in elderly patients.
Lithium augmentation of antidepressant treatment is a commonly used strategy for treatment-resistant cases of depression. Two cases are described in which significant neurotoxicity developed in elderly patients despite therapeutic doses of antidepressant and lithium.
Aged↗
Pseudotetanus from illicit drug use.
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Adult↗
Neuroleptic malignant syndrome associated with basal ganglia hemorrhage.
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Aged↗
Mental illness and creativity.
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Achievement↗
Involvement of brain dopamine systems on neurotensin-induced protection against stress gastric lesions.
We have previously demonstrated that intracisternal (i.c.) administration of neurotensin (NT), a brain and gastrointestinal tridecapeptide, potently inhibits gastric ulcer formation induced by cold-restraint stress (CRS) in rats. This study evaluated the effect of i.c. NT (17.9 nmol) or vehicle (10 microliter of 0.9% NaCl) on the development of CRS-induced gastric ulcers and on dopamine (DA) concentrations and DA turnover (DOPAC/DA) in selected brain regions after 0, 1, 2 and 3 h of CRS. As anticipated, and in confirmation of previous findings, NT significantly reduced the incidence and severity of CRS gastric ulcers in a time-dependent manner. Neurotensin significantly decreased DA concentration and DA turnover in the striatum. In the nucleus accumbens, however, NT produced a decrease in DA concentration and a concomitant increase in DA turnover after 2 and 3 h of CRS. No significant effects of brain NT on DA concentration and DA turnover were observed in the hypothalamus or olfactory tubercles. These findings suggest that the anti-ulcer effect of brain NT may be mediated, at least in part, by a differential activation of the mesolimbic and nigrostriatal DA systems.
Animals↗
Role of brain neurotransmitters on neurotensin-induced gastric cytoprotection.
We have reported previously that intracisternal (IC) administration of neurotensin (NT) prevents stress-induced gastric ulcers in rats. This effect of NT appears to be mediated by the central nervous system because peripheral (IV) NT is totally ineffective. The present study sought to clarify the central mechanism of the cytoprotective effect of NT by utilizing pharmacological treatments which alter the function of brain neurotransmitter systems. Pretreatment with intracerebroventricular (ICV) administration of agonists and antagonists of acetylcholine (ACh), gamma-aminobutyric acid (GABA), and serotonin (5-HT) receptors or with an anti-opiate (naloxone) agent did not significantly alter NT-induced cytoprotection. However, pretreatment with ICV haloperidol, a dopamine (DA) receptor antagonist, totally blocked NT's cytoprotective effect. In addition, pretreatment with methylphenidate, a DA receptor agonist, produced cytoprotection similar to IC NT. These data indicate that NT-induced cytoprotection is not mediated by 5-HT, GABA, ACh (muscarinic) receptors, or endogenous opiate systems, but suggest interactions between brain DA systems and NT.
Animals↗