PMID- 16508141
OWN - NLM
STAT- MEDLINE
DCOM- 20060517
LR  - 20190720
IS  - 0918-6158 (Print)
IS  - 0918-6158 (Linking)
VI  - 29
IP  - 3
DP  - 2006 Mar
TI  - Decreases in pheromonal responses at the accessory olfactory bulb of mice with a 
      deficiency of the alpha1B or beta3 subunits of voltage-dependent Ca2+-channels.
PG  - 437-42
AB  - Pheromones affect gonadal functions and sexual behaviors. Information in regard 
      to pheromones is received by the vomeronasal organ (VNO) and transmitted to the 
      accessory olfactory bulb (AOB). We investigated the physiological role of the 
      alpha1B and beta3 subunits of the N (neuronal)-type voltage-dependent Ca2+ 
      channel in the neurotransduction in the accessory olfactory (vomeronasal) system 
      using alpha1B-deficient mice and beta3-deficient mice. RT-PCR studies showed the 
      existence of beta1, beta2, beta3, beta4, alpha1A, alpha1B, and alpha1C subunits 
      of voltage-dependent Ca2+ channels in the mouse VNO. Immunohistochemical studies 
      showed that the alpha1A, alpha1B, and alpha1C subunits of voltage-dependent Ca2+ 
      channels exist in the sensory neurons and supporting cells of the mouse VNO. 
      Exposure of the VNO to urine samples excreted from male mice induced lower 
      Fos-immunoreactivity in the periglomerular (PG) cells of the AOBs in 
      alpha1B-deficient female mice than in those of wild mice. The density of 
      Fos-immunoreactive (Fos-ir) cells after exposure to female urine samples at the 
      periglomerular cell layer of alpha1B-deficient male mice was lower than that of 
      wild mice. Exposure of the VNO of beta3-deficient female mice to male urine 
      samples also induced low Fos-ir cells in the periglomerular cell layer of the 
      AOB. These data suggest the importance of the alpha1B and beta3 subunits of the 
      N-type voltage-dependent Ca2+ channel for the pheromone signal transduction 
      system.
FAU - Murakami, Manabu
AU  - Murakami M
AD  - Department of Pharmacology, Akita University School of Medicine, Japan.
FAU - Matsui, Hitosi
AU  - Matsui H
FAU - Shiraiwa, Takeshi
AU  - Shiraiwa T
FAU - Suzuki, Takashi
AU  - Suzuki T
FAU - Sasano, Hironobu
AU  - Sasano H
FAU - Takahashi, Eiki
AU  - Takahashi E
FAU - Kashiwayanagi, Makoto
AU  - Kashiwayanagi M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Japan
TA  - Biol Pharm Bull
JT  - Biological & pharmaceutical bulletin
JID - 9311984
RN  - 0 (Cacna1b protein, mouse)
RN  - 0 (Cacnb3 protein, mouse)
RN  - 0 (Calcium Channels)
RN  - 0 (Calcium Channels, N-Type)
RN  - 0 (Pheromones)
RN  - 0 (Proto-Oncogene Proteins c-fos)
RN  - 63231-63-0 (RNA)
SB  - IM
MH  - Animals
MH  - Calcium Channels/*genetics
MH  - Calcium Channels, N-Type/*genetics
MH  - Electrophysiology
MH  - Female
MH  - Immunohistochemistry
MH  - Male
MH  - Mice
MH  - Mice, Knockout
MH  - Olfactory Bulb/*drug effects
MH  - Pheromones/*pharmacology
MH  - Proto-Oncogene Proteins c-fos/urine
MH  - RNA/biosynthesis/genetics
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Signal Transduction/genetics
MH  - Vomeronasal Organ/physiology
EDAT- 2006/03/02 09:00
MHDA- 2006/05/18 09:00
CRDT- 2006/03/02 09:00
PHST- 2006/03/02 09:00 [pubmed]
PHST- 2006/05/18 09:00 [medline]
PHST- 2006/03/02 09:00 [entrez]
AID - JST.JSTAGE/bpb/29.437 [pii]
AID - 10.1248/bpb.29.437 [doi]
PST - ppublish
SO  - Biol Pharm Bull. 2006 Mar;29(3):437-42. doi: 10.1248/bpb.29.437.