Addiction Rehab: Amphetamine Paradoxically Augments Exocytotic Dopamine Release and Phasic Dopamine Signals.
Amphetamine paradoxically augments exocytotic dopamine release and phasic dopamine signals.
Filed under: Addiction Rehab
J Neurosci. 2013 Jan 9; 33(2): 452-63
Daberkow DP, Brown HD, Bunner KD, Kraniotis SA, Doellman MA, Ragozzino ME, Garris PA, Roitman MF
Drugs of abuse hijack brain-reward circuitry during the addiction process by augmenting action potential-dependent phasic dopamine release events associated with learning and goal-directed behavior. One prominent exception to this notion would appear to be amphetamine (AMPH) and related analogs, which are proposed instead to disrupt normal patterns of dopamine neurotransmission by depleting vesicular stores and promoting nonexocytotic dopamine efflux via reverse transport. This mechanism of AMPH action, though, is inconsistent with its therapeutic effects and addictive properties, which are thought to be reliant on phasic dopamine signaling. Here we used fast-scan cyclic voltammetry in freely moving rats to interrogate principal neurochemical responses to AMPH in the striatum and relate these changes to behavior. First, we showed that AMPH dose-dependently enhanced evoked dopamine responses to phasic-like current pulse trains for up to 2 h. Modeling the data revealed that AMPH inhibited dopamine uptake but also unexpectedly potentiated vesicular dopamine release. Second, we found that AMPH increased the amplitude, duration, and frequency of spontaneous dopamine transients, the naturally occurring, nonelectrically evoked, phasic increases in extracellular dopamine. Finally, using an operant sugar reward paradigm, we showed that low-dose AMPH augmented dopamine transients elicited by sugar-predictive cues. However, operant behavior failed at high-dose AMPH, which was due to phasic dopamine hyperactivity and the decoupling of dopamine transients from the reward predictive cue. These findings identify upregulation of exocytotic dopamine release as a key AMPH action in behaving animals and support a unified mechanism of abused drugs to activate phasic dopamine signaling.
HubMed – addiction
Electroconvulsive Therapy Teaching in Canada: Cause for Concern.
Filed under: Addiction Rehab
J ECT. 2013 Jan 8;
Patry S, Graf P, Delva NJ, Chan P, Enns M, Gilron I, Gosselin C, Jewell M, Lawson JS, Martin B, Milev R
AIM: The objective of this study was to present survey data on the teaching of electroconvulsive therapy (ECT) in health care centers across Canada. METHODS: Of 1273 centers identified, 175 were found to practice ECT. These centers were asked to complete a questionnaire, and 107 (61%) of them answered 5 questions dealing specifically with ECT teaching. These questions were as follows: RESULTS: Sixty percent of respondents had no ECT teaching program for psychiatry residents. Pedagogical methods varied, ranging from direct observation of ECT treatments to directed readings. Few centers required a minimum number of supervised treatments. No resident-administered ECT is performed without direct supervision. Interestingly, various groups of health care professionals were often invited to participate in ECT training. CONCLUSIONS: The situation regarding ECT teaching continues to be a cause for concern given the noted absence of organized, structured, and mandatory programs. No resident administering ECT, however, goes unsupervised, which is in keeping with good practice. Electroconvulsive therapy is taught in many different ways, and teaching is accessible to different groups of health care professionals. However, much remains to be done to standardize ECT teaching to render this therapy available to all those who need it and to overcome the stigma and bias associated with it.
HubMed – addiction
Pharmacological Strategies in the Prevention of Relapse After Electroconvulsive Therapy.
Filed under: Addiction Rehab
J ECT. 2013 Jan 8;
Prudic J, Haskett RF, McCall WV, Isenberg K, Cooper T, Rosenquist PB, Mulsant BH, Sackeim HA
OBJECTIVE: To determine whether starting antidepressant medication at the start of electroconvulsive therapy (ECT) reduces post-ECT relapse and to determine whether continuation pharmacotherapy with nortriptyline (NT) and lithium (Li) differs in efficacy or adverse effects from continuation pharmacotherapy with venlafaxine (VEN) and Li. METHODS: During an acute ECT phase, 319 patients were randomized to treatment with moderate dosage bilateral ECT or high-dosage right unilateral ECT. They were also randomized to concurrent treatment with placebo, NT, or VEN. Of 181 patients to meet post-ECT remission criteria, 122 (67.4%) participated in a second continuation pharmacotherapy phase. Patients earlier randomized to NT or VEN continued on the antidepressant, whereas patients earlier randomized to placebo were now randomized to NT or VEN. Lithium was added for all patients who were followed until relapse or 6 months. RESULTS: Starting an antidepressant medication at the beginning of the ECT course did not affect the rate or timing of relapse relative to starting pharmacotherapy after ECT completion. The combination of NT and Li did not differ from VEN and Li in any relapse or adverse effect measure. Older age was strongly associated with lower relapse risk, whereas the type of ECT administered in the acute phase and medication resistance were not predictive. Across sites, 50% of the patients relapsed, 33.6% continued in remission 6 months after ECT, and 16.4% dropped out. CONCLUSIONS: Starting an antidepressant medication during ECT does not affect relapse, and there are concerns about administering Li during an acute ECT course. Nortriptyline and VEN were equally effective in prolonging remission, although relapse rates after ECT are substantial despite intensive pharmacology. As opposed to the usual abrupt cessation of ECT, the impact of an ECT taper should be evaluated.
HubMed – addiction
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