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Acta Physiologica Congress

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Acta Physiologica 2012; Volume 204, Supplement 689
91st Annual Meeting of The German Physiological Society
3/22/2012-3/25/2012
Dresden, Germany


MINIATURE POSTSYNAPTIC CURRENTS RESULTING FROM CO-RELEASE OF GLYCINE AND GABA TO RESPIRATORY RHYTHMIC GLYCINERGIC NEURONS IN THE MOUSE PRE-BTZINGER COMPLEX IN SITU
Abstract number: P289

Rahman1 J., Latal2 T., Hirrlinger3 J., Hulsmann1 *S.

1Universittsmedizin Gttingen, Abteilung Neurophysiologie und Zellulre Biophysik, Gttingen, Germany
2Klinik und Poliklinik fr Ansthesiologie und Operative Intensivmedizin, Mnster, Germany
3Carl-Ludwig-Institute, Leipzig, Germany

The inhibitory neurotransmitters, glycine and GABA, use the same vesicular transporter VIAAT (also called VGAT) to enter the synaptic vesicles. Consequently, inhibitory postsynaptic currents have been recorded from different types of neurons in the brain that result from the co-release of GABA and glycine from the same single vesicle and subsequent simultaneous activation of GABA- and glycine receptors on the postsynaptic side. Since both GABAergic and glycinergic neurons play an important role for generation and modulation of the neuronal activity the respiratory network, we aimed to quantify the contribution of GABA/glycine co-release events to the synaptic input to respiratory neurons. Dual-events resulting from co-release were detected in every glycinergic neuron we recorded from in the pre-Bötzinger Complex in neonatal mice (P1-P9). These dual events were characterized and identified by their dual component decay resulting from the combination of a fast glycinergic and a slow GABAergic component. However, no reliable way to quantify dual synaptic events was found using different quantitative methods which are based on the comparison of the decay kinetics of individual mIPSCs. Nevertheless, our data suggest that glycinergic neurons in the pre-Bötzinger Complex receive inhibitory input from neurons co-releasing GABA and glycine.

To cite this abstract, please use the following information:
Acta Physiologica 2012; Volume 204, Supplement 689 :P289

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