PMID- 25195871
OWN - NLM
STAT- MEDLINE
DCOM- 20150723
LR  - 20141117
IS  - 1460-9568 (Electronic)
IS  - 0953-816X (Linking)
VI  - 40
IP  - 10
DP  - 2014 Nov
TI  - Altered synaptic transmission at olfactory and vomeronasal nerve terminals in 
      mice lacking N-type calcium channel Cav2.2.
PG  - 3422-35
LID - 10.1111/ejn.12713 [doi]
AB  - 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 (alpha1B) 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.
CI  - (c) 2014 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.
FAU - Weiss, Jan
AU  - Weiss J
AD  - Department of Physiology, University of Saarland School of Medicine, 
      Kirrbergerstrasse, Building 58, D-66421, Homburg, Germany.
FAU - Pyrski, Martina
AU  - Pyrski M
FAU - Weissgerber, Petra
AU  - Weissgerber P
FAU - Zufall, Frank
AU  - Zufall F
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140905
PL  - France
TA  - Eur J Neurosci
JT  - The European journal of neuroscience
JID - 8918110
RN  - 0 (Bsn protein, mouse)
RN  - 0 (Cacna1b protein, mouse)
RN  - 0 (Calcium Channel Blockers)
RN  - 0 (Calcium Channels, L-Type)
RN  - 0 (Calcium Channels, N-Type)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Olfactory Marker Protein)
RN  - 0 (Omp protein, mouse)
RN  - 0 (Slc17a6 protein, mouse)
RN  - 0 (Vesicular Glutamate Transport Protein 2)
RN  - EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
SB  - IM
MH  - Animals
MH  - Calcium Channel Blockers/pharmacology
MH  - Calcium Channels, L-Type/metabolism
MH  - Calcium Channels, N-Type/genetics/*metabolism
MH  - Excitatory Postsynaptic Potentials/drug effects/physiology
MH  - Female
MH  - Male
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - Mutation
MH  - Nerve Tissue Proteins/metabolism
MH  - Olfactory Bulb/drug effects/*physiology
MH  - Olfactory Marker Protein/metabolism
MH  - Olfactory Nerve/drug effects/physiology
MH  - Patch-Clamp Techniques
MH  - Presynaptic Terminals/drug effects/physiology
MH  - Synaptic Transmission/drug effects/*physiology
MH  - Tissue Culture Techniques
MH  - Tyrosine 3-Monooxygenase/metabolism
MH  - Vesicular Glutamate Transport Protein 2/metabolism
MH  - Vomeronasal Organ/drug effects/innervation/*physiology
OTO - NOTNLM
OT  - Cacna1b
OT  - aggression
OT  - channelopathy
OT  - olfactory plasticity
OT  - omega-conotoxin GVIA
EDAT- 2014/09/10 06:00
MHDA- 2015/07/24 06:00
CRDT- 2014/09/09 06:00
PHST- 2014/05/13 00:00 [received]
PHST- 2014/07/31 00:00 [revised]
PHST- 2014/08/04 00:00 [accepted]
PHST- 2014/09/09 06:00 [entrez]
PHST- 2014/09/10 06:00 [pubmed]
PHST- 2015/07/24 06:00 [medline]
AID - 10.1111/ejn.12713 [doi]
PST - ppublish
SO  - Eur J Neurosci. 2014 Nov;40(10):3422-35. doi: 10.1111/ejn.12713. Epub 2014 Sep 5.