Thirty-Minute Psychiatric Management Visits in Academic Medical Centers: Framing and Exploring Distinct Clinical-Educational Social Processes.

ABSTRACT: To address high clinical demand and manage workflow, some university-based practice settings are tending to replace traditional hour-long outpatient appointments with 30-minute psychiatric management visits, which must comply with multiple regulatory requirements for documentation and billing. This care model can significantly shape the culture of psychiatric treatment and education. Based on the limited published literature on this topic and pooled experiences of faculty, residents, and administrators, this article offers observations and raises questions concerning 1) clinical, educational and administrative benefits, limitations, and challenges for conducting 30-minute psychiatric visits in training contexts; 2) how administrative impositions affecting resident and faculty time and attention impact clinical encounters; 3) how various teaching settings manage regulatory requirements differently; and 4) considerations for education needs and opportunities, research gaps, and policy implications. Quality of care and education could be improved by judicious overhaul of administrative requirements to minimize burdens offering little clinical or educational value.

Density of α4ß2* nAChR on the surface of neurons is modulated by chronic antagonist exposure.

The expression of high-affinity α4ß2* nicotinic acetylcholine receptors (nAChR) increases following chronic exposure to nicotinic agonists. While, nAChR antagonists can also produce upregulation, these changes are often less pronounced than achieved with agonists. It is unknown if nAChR agonists and antagonists induce receptor upregulation by the same mechanisms. In this study, primary neuronal cultures prepared from cerebral cortex, hippocampus, diencephalon, and midbrain/hindbrain of C57BL/6J mouse embryos were treated chronically with nicotine (agonist), mecamylamine (noncompetitive antagonist) or dihydro-ß-erythroidine (competitive antagonist) or the combination of nicotine with each antagonist. The distribution of intracellular and surface [(125)I]epibatidine-binding sites were subsequently measured. Treatment with 1 µmol/L nicotine upregulated intracellular and cell surface [(125)I]epibatidine binding after 96 h. Chronic dihydro-ß-erythroidine (10 µmol/L) treatment also increased [(125)I]epibatidine binding on the cell surface; however, mecamylamine was ineffective in upregulating receptors by itself. The combination of 1 µmol/L nicotine plus 10 µmol/L mecamylamine elicited a significantly higher upregulation than that achieved by treatment with nicotine alone due to an increase of [(125)I]epibatidine binding on the cell surface. This synergistic effect of mecamylamine and nicotine was found in neuronal cultures from all four brain regions. Chronic treatment with nicotine concentrations as low as 10 nmol/L produced upregulation of [(125)I]epibatidine binding. However, the effect of mecamylamine was observed only after coincubation with nicotine concentrations equal to or greater than 100 nmol/L. Vesicular trafficking was required for both nicotine and nicotine plus mecamylamine-induced upregulation. Results presented here support the idea of multiple mechanisms for nAChR upregulation.

Regulation of the distribution and function of [(125)I]epibatidine binding sites by chronic nicotine in mouse embryonic neuronal cultures.

Chronic nicotine produces up-regulation of α4ß2* nicotinic acetylcholine receptors (nAChRs) (* denotes that an additional subunit may be part of the receptor). However, the extent of up-regulation to persistent ligand exposure varies across brain regions. The aim of this work was to study the cellular distribution and function of nAChRs after chronic nicotine treatment in primary cultures of mouse brain neurons. Initially, high-affinity [(125)I]epibatidine binding to cell membrane homogenates from primary neuronal cultures obtained from diencephalon and hippocampus of C57BL/6J mouse embryos (embryonic days 16-18) was measured. An increase in α4ß2*-nAChR binding sites was observed in hippocampus, but not in diencephalon, after 24 h of treatment with 1 µM nicotine. However, a nicotine dose-dependent up-regulation of approximately 3.5- and 0.4-fold in hippocampus and diencephalon, respectively, was found after 96 h of nicotine treatment. A significant fraction of total [(125)I]epibatidine binding sites in both hippocampus (45%) and diencephalon (65%) was located on the cell surface. Chronic nicotine (96 h) up-regulated both intracellular and surface binding in both brain regions without changing the proportion of those binding sites compared with control neurons. The increase in surface binding was not accompanied by an increase in nicotine-stimulated Ca(2+) influx, suggesting persistent desensitization or inactivation of receptors at the plasma membrane occurred. Given the differences observed between hippocampus and diencephalon neurons exposed to nicotine, multiple mechanisms may play a role in the regulation of nAChR expression and function.