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Corticotropin-releasing factor and Urocortin I modulate excitatory glutamatergic synaptic transmission.
J Neurosci 2004; 24(16):4020-9JN

Abstract

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.

Authors+Show Affiliations

Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston, Texas 77555-1031, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15102917

Citation

Liu, Jie, et al. "Corticotropin-releasing Factor and Urocortin I Modulate Excitatory Glutamatergic Synaptic Transmission." The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, vol. 24, no. 16, 2004, pp. 4020-9.
Liu J, Yu B, Neugebauer V, et al. Corticotropin-releasing factor and Urocortin I modulate excitatory glutamatergic synaptic transmission. J Neurosci. 2004;24(16):4020-9.
Liu, J., Yu, B., Neugebauer, V., Grigoriadis, D. E., Rivier, J., Vale, W. W., ... Gallagher, J. P. (2004). Corticotropin-releasing factor and Urocortin I modulate excitatory glutamatergic synaptic transmission. The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, 24(16), pp. 4020-9.
Liu J, et al. Corticotropin-releasing Factor and Urocortin I Modulate Excitatory Glutamatergic Synaptic Transmission. J Neurosci. 2004 Apr 21;24(16):4020-9. PubMed PMID: 15102917.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Corticotropin-releasing factor and Urocortin I modulate excitatory glutamatergic synaptic transmission. AU - Liu,Jie, AU - Yu,Baojian, AU - Neugebauer,Volker, AU - Grigoriadis,Dimitri E, AU - Rivier,Jean, AU - Vale,Wylie W, AU - Shinnick-Gallagher,Patricia, AU - Gallagher,Joel P, PY - 2004/4/23/pubmed PY - 2004/8/4/medline PY - 2004/4/23/entrez SP - 4020 EP - 9 JF - The Journal of neuroscience : the official journal of the Society for Neuroscience JO - J. Neurosci. VL - 24 IS - 16 N2 - 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. SN - 1529-2401 UR - https://www.unboundmedicine.com/medline/citation/15102917/Corticotropin_releasing_factor_and_Urocortin_I_modulate_excitatory_glutamatergic_synaptic_transmission_ L2 - http://www.jneurosci.org/cgi/pmidlookup?view=long&pmid=15102917 DB - PRIME DP - Unbound Medicine ER -