PMID- 15102917
OWN - NLM
STAT- MEDLINE
DCOM- 20040803
LR  - 20200225
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 24
IP  - 16
DP  - 2004 Apr 21
TI  - Corticotropin-releasing factor and Urocortin I modulate excitatory glutamatergic 
      synaptic transmission.
PG  - 4020-9
AB  - Corticotropin-releasing factor (CRF)-related peptides serve as hormones and 
      neuromodulators of the stress response and play a role in affective disorders. 
      These peptides are known to alter complex behaviors and neuronal properties, but 
      their receptor-mediated effects at CNS synapses are not well described. Here we 
      show that excitatory glutamatergic transmission is modulated by two endogenous 
      CRF-related peptide ligands, corticotropin-releasing factor [CRF rat/human (r/h)] 
      and Urocortin I (Ucn I), within the central nucleus of the amygdala (CeA) and the 
      lateral septum mediolateral nucleus (LSMLN). These limbic nuclei are reciprocally 
      innervated, are involved in stress and affective disorders, and have high 
      densities of the CRF receptors CRF1 and CRF2. Activation of these receptors 
      exerts diametrically opposed actions on glutamatergic transmission in these 
      nuclei. In the CeA, CRF(r/h) depressed excitatory glutamatergic transmission 
      through a CRF1-mediated postsynaptic action, whereas Ucn I facilitated synaptic 
      responses through presynaptic and postsynaptic CRF2-mediated mechanisms. 
      Conversely, in the LSMLN, CRF caused a CRF1-mediated facilitation of 
      glutamatergic transmission via postsynaptic mechanisms, whereas Ucn I depressed 
      EPSCs by postsynaptic and presynaptic CRF2-mediated actions. Furthermore, 
      antagonists of these receptors also affected glutamatergic neurotransmission, 
      indicating that endogenous ligands tonically modulated synoptic activity at these 
      synapses. These data show that CRF receptors in CeA and LSMLN synapses exert and 
      maintain a significant synaptic tone and thereby regulate excitatory 
      glutamatergic transmission. The results also suggest that CRF receptors may 
      provide novel targets in affective disorders and stress.
FAU - Liu, Jie
AU  - Liu J
AD  - Department of Pharmacology and Toxicology, University of Texas Medical Branch, 
      Galveston, Texas 77555-1031, USA.
FAU - Yu, Baojian
AU  - Yu B
FAU - Neugebauer, Volker
AU  - Neugebauer V
FAU - Grigoriadis, Dimitri E
AU  - Grigoriadis DE
FAU - Rivier, Jean
AU  - Rivier J
FAU - Vale, Wylie W
AU  - Vale WW
FAU - Shinnick-Gallagher, Patricia
AU  - Shinnick-Gallagher P
FAU - Gallagher, Joel P
AU  - Gallagher JP
LA  - eng
GR  - R01 DA011991/DA/NIDA NIH HHS/United States
GR  - R01 MH058327/MH/NIMH NIH HHS/United States
GR  - T32-A07287/PHS HHS/United States
GR  - DA 11991/DA/NIDA NIH HHS/United States
GR  - MH058327/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (CRF receptor type 2)
RN  - 0 (Ligands)
RN  - 0 (Receptors, Corticotropin-Releasing Hormone)
RN  - 0 (Urocortins)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - 5CLY6W2H1M (CRF receptor type 1)
RN  - 9015-71-8 (Corticotropin-Releasing Hormone)
SB  - IM
MH  - Amygdala/metabolism/physiology
MH  - Animals
MH  - Cell Membrane/drug effects/physiology
MH  - Corticotropin-Releasing Hormone/*metabolism/pharmacology
MH  - Excitatory Postsynaptic Potentials/drug effects/physiology
MH  - Glutamic Acid/*metabolism
MH  - Humans
MH  - In Vitro Techniques
MH  - Ligands
MH  - Limbic System/drug effects/*physiology
MH  - Male
MH  - Patch-Clamp Techniques
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Corticotropin-Releasing Hormone/metabolism
MH  - Septal Nuclei/metabolism/physiology
MH  - Synaptic Transmission/drug effects/*physiology
MH  - Urocortins
PMC - PMC6729414
EDAT- 2004/04/23 05:00
MHDA- 2004/08/04 05:00
PMCR- 2004/10/21
CRDT- 2004/04/23 05:00
PHST- 2004/04/23 05:00 [pubmed]
PHST- 2004/08/04 05:00 [medline]
PHST- 2004/04/23 05:00 [entrez]
PHST- 2004/10/21 00:00 [pmc-release]
AID - 24/16/4020 [pii]
AID - 10.1523/JNEUROSCI.5531-03.2004 [doi]
PST - ppublish
SO  - J Neurosci. 2004 Apr 21;24(16):4020-9. doi: 10.1523/JNEUROSCI.5531-03.2004.