NDLI: Altered synaptic transmission at olfactory and vomeronasal nerve terminals in mice lacking N-type calcium channel Cav2.2.

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Altered synaptic transmission at olfactory and vomeronasal nerve terminals in mice lacking N-type calcium channel Cav2.2.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Weiss, Jan Pyrski, Martina Weissgerber, Petra Zufall, Frank
Description	Country affiliation: Germany Author Affiliation: Weiss J ( Department of Physiology, University of Saarland School of Medicine, Kirrbergerstrasse, Building 58, D-66421, Homburg, Germany.)
Abstract	We investigated the role of voltage-activated calcium (Cav) channels for synaptic transmission at mouse olfactory and vomeronasal nerve terminals at the first synapse of the main and accessory olfactory pathways, respectively. We provided evidence for a central role of the N-type Cav channel subunit Cav2.2 in presynaptic transmitter release at these synapses. Striking Cav2.2 immunoreactivity was localised to the glomerular neuropil of the main olfactory bulb (MOB) and accessory olfactory bulb (AOB), and co-localised with presynaptic molecules such as bassoon. Voltage-clamp recordings of sensory nerve-evoked, excitatory postsynaptic currents (EPSCs) in mitral/tufted (M/T) and superficial tufted cells of the MOB and mitral cells of the AOB, in combination with established subtype-specific Cav channel toxins, indicated a predominant role of N-type channels in transmitter release at these synapses, whereas L-type, P/Q-type, and R-type channels had either no or only relatively minor contributions. In Cacna1b mutant mice lacking the Cav2.2 ( 1B) subunit of N-type channels, olfactory nerve-evoked M/T cell EPSCs were not reduced but became blocker-resistant, thus indicating a major reorganisation and compensation of Cav channel subunits as a result of the Cav2.2 deletion at this synapse. Cav2.2-deficient mice also revealed that Cav2.2 was critically required for paired-pulse depression of olfactory nerve-evoked EPSCs in M/T cells of the MOB, and they demonstrated an essential requirement for Cav2.2 in vomeronasal nerve-evoked EPSCs of AOB mitral cells. Thus, Cacna1b loss-of-function mutations are unlikely to cause general anosmia but Cacna1b emerges as a strong candidate in the search for mutations causing altered olfactory perception, such as changes in general olfactory sensitivity and altered social responses to chemostimuli.
File Format	HTM / HTML
ISSN	0953816X
Issue Number	10
Volume Number	40
e-ISSN	14609568
Journal	European Journal of Neuroscience
Language	English
Publisher	Wiley-Blackwell
Publisher Date	2014-11-01
Publisher Place	France
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Neuroscience Calcium Channels, N-type Metabolism Olfactory Bulb Physiology Synaptic Transmission Vomeronasal Organ Animals Calcium Channel Blockers Pharmacology Calcium Channels, L-type Genetics Excitatory Postsynaptic Potentials Drug Effects Female Male Mice, Inbred C57bl Mice, Transgenic Mutation Nerve Tissue Proteins Olfactory Marker Protein Olfactory Nerve Patch-clamp Techniques Presynaptic Terminals Tissue Culture Techniques Tyrosine 3-monooxygenase Vesicular Glutamate Transport Protein 2 Innervation Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Neuroscience

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