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This Article Full Text Full Text (PDF) All Versions of this Article: 102/5/2846    most recent 00168.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Swartz, J. B. Articles by Weinreich, D. PubMed PubMed Citation Articles by Swartz, J. B. Articles by Weinreich, D.

RESEARCH-ARTICLE

Influence of Vagotomy on Monosynaptic Transmission at Second-Order Nucleus Tractus Solitarius Synapses

¹Program in Neuroscience and ²Department of Pharmacology and Experimental Therapeutics, University of Maryland, School of Medicine, Baltimore, Maryland

Submitted 25 February 2009; accepted in final form 28 August 2009

ABSTRACT

Manipulations of vagal activity are used to treat medical pathologies, but the underlying CNS changes caused by these treatments are not well understood. Furthermore, heart and lung transplant as well as treatments for many gastrointestinal disorders result in section of the vagus nerve (vagotomy). Following unilateral vagotomy under isoflurane anesthesia of Sprague-Dawley rats, electrophysiological properties were recorded with whole cell patch techniques in horizontal brain stem slices. Vagotomy significantly reduced the median amplitude of evoked excitatory postsynaptic currents (evEPSCs; –121; n = 43) in the nucleus tractus solitarius (NTS) when compared with controls (–157 pA; n = 66; P < 0.05) but had no significant effect on the passive properties or on the average amplitude or frequency of miniature EPSCs. The degree of synaptic failure exhibited during a 50-Hz train of stimuli was used to define two separate classes of synapses: "low failure" and "high failure" (HF); failure rates <5 and 5%, respectively. HF synapses had significantly smaller median evEPSCs (–88 vs. –184 pA; P < 0.05). After vagotomy, the percentage of HF synapses nearly doubled to 56% (n = 24/43) when compared with controls (30%; n = 20/66). Additionally, the overall percentage of failures after the second to fifth stimuli significantly increased by at least twofold. These results suggest that vagotomy causes a decrease in synaptic efficacy by both increasing the overall percentage of synaptic failures and shifting the population of NTS synapses toward more HF transmission. In addition, the alterations due to vagotomy are likely to be presynaptic in nature.