PMID- 19474170
OWN - NLM
STAT- MEDLINE
DCOM- 20090924
LR  - 20220309
IS  - 0022-3077 (Print)
IS  - 1522-1598 (Electronic)
IS  - 0022-3077 (Linking)
VI  - 102
IP  - 2
DP  - 2009 Aug
TI  - Excitatory actions of noradrenaline and metabotropic glutamate receptor 
      activation in granule cells of the accessory olfactory bulb.
PG  - 1103-14
LID - 10.1152/jn.91093.2008 [doi]
AB  - Modulation of dendrodendritic synapses by the noradrenergic system in the 
      accessory olfactory bulb (AOB) plays a key role in the formation of memory in 
      olfactory-mediated behaviors. We have recently shown that noradrenaline (NA) 
      inhibits mitral cells by increasing gamma-aminobutyric acid inhibitory input onto 
      mitral cells in the AOB, suggesting an excitatory action of NA on granule cells 
      (GCs). Here, we show that NA (10 microM) elicits a long-lasting depolarization of 
      GCs. This effect is mediated by activation of alpha(1)-adrenergic receptors as 
      the depolarization is mimicked by phenylephrine (PE, 30 microM) and completely 
      blocked by the alpha(1)-adrenergic receptor antagonist prazosin (300 nM). In 
      addition to this depolarization, application of NA induced the appearance of a 
      slow afterdepolarization (sADP) following a stimulus-elicited train of action 
      potentials. Similarly, the group I metabotropic glutamate receptor (mGluR1) 
      agonist DHPG (10-30 microM) also produced a depolarization of GCs and the 
      appearance of a stimulus-induced sADP. The ionic and voltage dependence and 
      sensitivity to blockers of the sADP suggest that it is mediated by the 
      nonselective cationic conductance I(CAN). Thus the excitatory action resulting 
      from the activation of these receptors could be mediated by a common transduction 
      target. Surprisingly, the excitatory effect of PE on GCs was completely blocked 
      by the mGluR1 antagonist LY367385 (100 microM). Conversely, the effect of DHPG 
      was not antagonized by the alpha(1)-adrenergic receptor antagonist prazosin (300 
      nM). These results suggest that most of the noradrenergic effect on GCs in the 
      AOB is mediated by potentiation of a basal activity of mGluR1s.
FAU - Smith, Richard S
AU  - Smith RS
AD  - Department of Biology, University of Maryland, College Park, Maryland 20742, USA.
FAU - Weitz, Christopher J
AU  - Weitz CJ
FAU - Araneda, Ricardo C
AU  - Araneda RC
LA  - eng
GR  - Howard Hughes Medical Institute/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090527
PL  - United States
TA  - J Neurophysiol
JT  - Journal of neurophysiology
JID - 0375404
RN  - 0 (Adrenergic alpha-1 Receptor Agonists)
RN  - 0 (Adrenergic alpha-1 Receptor Antagonists)
RN  - 0 (Adrenergic alpha-Agonists)
RN  - 0 (Adrenergic alpha-Antagonists)
RN  - 0 (Benzoates)
RN  - 0 (Excitatory Amino Acid Agonists)
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (Receptors, Adrenergic, alpha-1)
RN  - 0 (Receptors, Metabotropic Glutamate)
RN  - 0 (Resorcinols)
RN  - 0 (metabotropic glutamate receptor type 1)
RN  - 146669-29-6 (alpha-methyl-4-carboxyphenylglycine)
RN  - 1WS297W6MV (Phenylephrine)
RN  - 5YR2N37E6D (3,5-dihydroxyphenylglycine)
RN  - TE7660XO1C (Glycine)
RN  - X4W3ENH1CV (Norepinephrine)
RN  - XM03YJ541D (Prazosin)
SB  - IM
MH  - Action Potentials/drug effects/physiology
MH  - Adrenergic alpha-1 Receptor Agonists
MH  - Adrenergic alpha-1 Receptor Antagonists
MH  - Adrenergic alpha-Agonists/pharmacology
MH  - Adrenergic alpha-Antagonists/pharmacology
MH  - Animals
MH  - Benzoates/pharmacology
MH  - Excitatory Amino Acid Agonists/pharmacology
MH  - Excitatory Amino Acid Antagonists/pharmacology
MH  - Female
MH  - Glycine/analogs & derivatives/pharmacology
MH  - In Vitro Techniques
MH  - Male
MH  - Membrane Potentials/drug effects/physiology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Neurons/drug effects/*physiology
MH  - Norepinephrine/*metabolism
MH  - Olfactory Bulb/drug effects/*physiology
MH  - Phenylephrine/pharmacology
MH  - Prazosin/pharmacology
MH  - Receptors, Adrenergic, alpha-1/*metabolism
MH  - Receptors, Metabotropic Glutamate/agonists/antagonists & inhibitors/*metabolism
MH  - Resorcinols/pharmacology
PMC - PMC2724365
EDAT- 2009/05/29 09:00
MHDA- 2009/09/25 06:00
PMCR- 2010/08/01
CRDT- 2009/05/29 09:00
PHST- 2009/05/29 09:00 [entrez]
PHST- 2009/05/29 09:00 [pubmed]
PHST- 2009/09/25 06:00 [medline]
PHST- 2010/08/01 00:00 [pmc-release]
AID - 91093.2008 [pii]
AID - J91093-8 [pii]
AID - 10.1152/jn.91093.2008 [doi]
PST - ppublish
SO  - J Neurophysiol. 2009 Aug;102(2):1103-14. doi: 10.1152/jn.91093.2008. Epub 2009 
      May 27.