ABSTRACT
Neuropsychiatric and neuropsychological evaluations were performed in a pilot study of adolescents with DSM-III-R disruptive behavior disorders, including conduct disorder (CD) and attention-deficit hyperactivity disorder (ADHD). The following comparisons were made: 1) CD comorbid with ADHD vs. CD only; 2) all subjects with ADHD vs. all non-ADHD; and 3) all subjects with CD vs. all non-CD. The CD + ADHD group had increased left-sided soft signs compared with the CD group. CD + ADHD subjects significantly underperformed CD subjects on several executive functioning measures, with no differences on Verbal IQ subtests. Results are discrepant with previous findings of deficient verbal functioning in delinquent populations. However, findings may not be generalizable because of sampling limitations.
Subject(s)
Attention Deficit Disorder with Hyperactivity/diagnosis , Attention Deficit Disorder with Hyperactivity/psychology , Child Behavior Disorders/diagnosis , Child Behavior Disorders/psychology , Adolescent , Adolescent Behavior/psychology , Child , Female , Humans , Male , Neurologic Examination , Neuropsychological Tests , Psychiatric Status Rating Scales , Psychology, Adolescent , Psychology, ChildABSTRACT
The effect of chronic systemic treatment (once a day for 2-3 weeks) with different antidepressant drugs (desipramine, mianserin, fluvoxamine 15 mg/kg per day i.p. or s.c.) on the behavioral responses elicited by intra-accumbens injection of graded doses (1-10,000 ng) of apomorphine and two doses (10 and 100 ng) of melatonin was investigated in rats. Treatment with antidepressant drugs consistently facilitated apomorphine-induced hypermotility, but differentially influenced apomorphine-induced hypomotility. The drugs completely antagonized melatonin-induced behavioral changes (hypomotility and increased duration of sniffing). The data suggest that chronic treatment with antidepressant drugs results in postsynaptic dopamine receptor supersensitivity in the nucleus accumbens, a terminal area of the mesolimbic dopaminergic system. It is postulated that the development of supersensitivity may be mediated by the inhibition of melatonin-induced effects observed after acute and chronic treatment with these antidepressants. The present findings may be relevant for the mode of therapeutic action of antidepressant drugs.
Subject(s)
Antidepressive Agents/pharmacology , Dopamine/physiology , Melatonin/physiology , Nucleus Accumbens/physiology , Animals , Apomorphine/pharmacology , Behavior, Animal/drug effects , Desipramine/pharmacology , Dose-Response Relationship, Drug , Fluvoxamine/pharmacology , Male , Melatonin/pharmacology , Mianserin/pharmacology , Neurotransmitter Uptake Inhibitors/pharmacology , Nucleus Accumbens/drug effects , Rats , Rats, Wistar , Receptors, Dopamine/drug effects , Receptors, Dopamine/physiology , Sensitivity and SpecificityABSTRACT
Propranolol binding to human alpha 1-acid glycoprotein (AAG) delipidated by two methods is described. Commercial AAG (99% pure) was either precipitated by ethanol-acetone and then washed by ether, or it was precipitated by ethanol. Binding capacity was quantified by the product n x Ka where n denotes the number of binding sites and Ka the association constant (M-1). Propranolol binding to nondelipidated AAG (n x Ka = 0.113 +/- 0.013 microM-1) was clearly increased after precipitation by ethanol-acetone (n x Ka = 0.386 +/- 0.109 microM-1) or precipitation by ethanol (n x Ka = 0.312 +/- 0.096 microM-1). Binding capacity potentiation cannot be due to modification of AAG microheterogeneity forms, as two-dimensional gel electrophoresis pattern of AAG in presence of concanavalin A was not altered after both methods. Recombination of precipitated AAGs with supernatant dry residue resulted in the abrogation of observed potentiation. Moreover, addition of a polar lipid, linoleic acid, (from 30 to 300 microM) strongly inhibited propranolol binding. These results indicated that glycoprotein precipitation by ethanol provided a simple method to further study binding inhibitors associated with isolated AAG.
