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S Arrington

Publications and source records attributed to S Arrington.

4 recordsLinked to original sources
PubMed1999

A model program for the treatment of mentally ill offenders in the community.

There is a new and growing interest among community mental health providers and administrators in the area of correctional psychiatry. From a column in Psychiatric Times to committees and task forces in APA and the American Academy of Psychiatry and the Law, increased attention is being paid to the great need for the treatment of mentally ill offenders. In this article, we will introduce the reader to the magnitude of the correctional system and to the prevalence of mental illness in the correctional population. We will then describe several model programs designed to work with mentally disordered offenders, and outline a novel collaborative approach between a CMHC and a Probation Office designed to help mentally disordered offenders succeed in community treatment. Several barriers to treatment faced by this population will be identified, including double stigma, lack of family/social support, comorbidity, adjustment problems, and boundary issues. Case vignettes designed to illustrate key points will be included.

Adolescent↗
PubMed1996

RJR-2403: a nicotinic agonist with CNS selectivity I. In vitro characterization.

Increasing evidence for an involvement of nicotinic cholinergic systems in neurodegenerative disorders has stimulated the search for compounds with selectivity for CNS nicotinic ACh receptors (nAChRs). To this end, we have evaluated a number of nicotinic agonists for their ability to 1) bind to and up-regulate high-affinity nAChRs, 2) release [3H]-dopamine or induce 86Rb+ efflux in synaptosomes, 3) activate nAChRs in PC12 cells, 4) activate muscle-type nAChRs in human TE671/RD cells and 5) induce contraction of guinea pig ileum. Our results indicate that (E)-N-methyl-4-(3-pyridinyl)-3-butene-1-amine (RJR-2403) binds with high affinity to rat brain cortex (Ki = 26 +/- 3 nM). Functional studies show that RJR-2403 is comparable to nicotine in activating rat thalamic synaptosomes (EC50 = 732 +/- 155 nM and Emax = 91 +/- 8% for RJR-2403; EC50 = 591 +/- 120 nM and Emax = 100 +/- 25% for nicotine) but is one-tenth as potent in inducing dopamine release (EC50 = 938 +/- 172 nM and Emax = 82 +/- 5% for RJR-2403; EC50 = 100 +/- 25 nM and Emax = 100 +/- 13% for nicotine). At concentrations up to 1 mM, RJR-2403 does not significantly activate nAChRs in PC12 cells, muscle type nAChRs or muscarinic receptors. Dose-response curves for agonist-induced ileum contraction indicate that RJR-2403 is less than one-tenth as potent as nicotine with greatly reduced efficacy. RJR-2403 does not antagonize nicotine-stimulated muscle or ganglionic nAChR function (IC50 > 1 mM). Chronic exposure of M10 cells to RJR-2403 (10 microM) results in an up-regulation of high-affinity nAChRs phenomenologically similar to that seen with nicotine. These results suggest that RJR-2403 interacts with higher potency at CNS nAChR sub-types than at muscle, ganglionic or enteric nAChRs and has higher selectivity for CNS vs. muscle or ganglionic nAChRs than does nicotine.

Animals↗