Tags

Type your tag names separated by a space and hit enter

VR1 receptor activation induces glutamate release and postsynaptic firing in the paraventricular nucleus.
J Neurophysiol. 2004 Sep; 92(3):1807-16.JN

Abstract

Neurons in the paraventricular nucleus (PVN) are important in regulating autonomic function through projections to the brain stem and spinal cord. Although the vanilloid receptors (VR(1)) are present in the PVN, their physiological function is scarcely known. In this study, we determined the role of VR(1) receptors in the regulation of synaptic inputs and the excitability of spinally projecting PVN neurons. Whole cell patch-clamp recordings were performed on the PVN neurons labeled by a retrograde fluorescence tracer injected into the thoracic spinal cord of rats. Capsaicin significantly increased the frequency of glutamatergic miniature excitatory postsynaptic currents (mEPSCs) without changing the amplitude and decay time constant of mEPSCs. On the other hand, capsaicin had no effect on GABAergic miniature inhibitory postsynaptic currents (mIPSCs). The effect of capsaicin on mEPSCs was abolished by a specific VR(1) antagonist, iodo-resiniferatoxin (iodo-RTX), or ruthenium red. Importantly, iodo-RTX per se significantly reduced the amplitude of evoked EPSCs and the frequency of mEPSCs. Removal of extracellular Ca(2+), but not Cd(2+) treatment, also eliminated the effect of capsaicin on mEPSCs. Furthermore, capsaicin caused a large increase in the firing rate of PVN neurons, and such an effect was abolished in the presence of ionotropic glutamate receptor antagonists. Additionally, the double-immunofluorescence labeling revealed that all of the VR(1) immunoreactivity was colocalized with a presynaptic marker, synaptophysin, in the PVN. Thus this study provides the first evidence that activation of VR(1) receptors excites preautonomic PVN neurons through selective potentiation of glutamatergic synaptic inputs. Presynaptic VR(1) receptors and endogenous capsaicin-like substances in the PVN may represent a previously unidentified mechanism in hypothalamic regulation of the autonomic nervous system.

Authors+Show Affiliations

Department of Anesthesiology, H187, The Pennsylvania State University College of Medicine, 500 University Drive, Hershey, PA 17033-0850, USA.No affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15115794

Citation

Li, De-Pei, et al. "VR1 Receptor Activation Induces Glutamate Release and Postsynaptic Firing in the Paraventricular Nucleus." Journal of Neurophysiology, vol. 92, no. 3, 2004, pp. 1807-16.
Li DP, Chen SR, Pan HL. VR1 receptor activation induces glutamate release and postsynaptic firing in the paraventricular nucleus. J Neurophysiol. 2004;92(3):1807-16.
Li, D. P., Chen, S. R., & Pan, H. L. (2004). VR1 receptor activation induces glutamate release and postsynaptic firing in the paraventricular nucleus. Journal of Neurophysiology, 92(3), 1807-16.
Li DP, Chen SR, Pan HL. VR1 Receptor Activation Induces Glutamate Release and Postsynaptic Firing in the Paraventricular Nucleus. J Neurophysiol. 2004;92(3):1807-16. PubMed PMID: 15115794.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - VR1 receptor activation induces glutamate release and postsynaptic firing in the paraventricular nucleus. AU - Li,De-Pei, AU - Chen,Shao-Rui, AU - Pan,Hui-Lin, Y1 - 2004/04/28/ PY - 2004/4/30/pubmed PY - 2004/11/5/medline PY - 2004/4/30/entrez SP - 1807 EP - 16 JF - Journal of neurophysiology JO - J. Neurophysiol. VL - 92 IS - 3 N2 - Neurons in the paraventricular nucleus (PVN) are important in regulating autonomic function through projections to the brain stem and spinal cord. Although the vanilloid receptors (VR(1)) are present in the PVN, their physiological function is scarcely known. In this study, we determined the role of VR(1) receptors in the regulation of synaptic inputs and the excitability of spinally projecting PVN neurons. Whole cell patch-clamp recordings were performed on the PVN neurons labeled by a retrograde fluorescence tracer injected into the thoracic spinal cord of rats. Capsaicin significantly increased the frequency of glutamatergic miniature excitatory postsynaptic currents (mEPSCs) without changing the amplitude and decay time constant of mEPSCs. On the other hand, capsaicin had no effect on GABAergic miniature inhibitory postsynaptic currents (mIPSCs). The effect of capsaicin on mEPSCs was abolished by a specific VR(1) antagonist, iodo-resiniferatoxin (iodo-RTX), or ruthenium red. Importantly, iodo-RTX per se significantly reduced the amplitude of evoked EPSCs and the frequency of mEPSCs. Removal of extracellular Ca(2+), but not Cd(2+) treatment, also eliminated the effect of capsaicin on mEPSCs. Furthermore, capsaicin caused a large increase in the firing rate of PVN neurons, and such an effect was abolished in the presence of ionotropic glutamate receptor antagonists. Additionally, the double-immunofluorescence labeling revealed that all of the VR(1) immunoreactivity was colocalized with a presynaptic marker, synaptophysin, in the PVN. Thus this study provides the first evidence that activation of VR(1) receptors excites preautonomic PVN neurons through selective potentiation of glutamatergic synaptic inputs. Presynaptic VR(1) receptors and endogenous capsaicin-like substances in the PVN may represent a previously unidentified mechanism in hypothalamic regulation of the autonomic nervous system. SN - 0022-3077 UR - https://www.unboundmedicine.com/medline/citation/15115794/VR1_receptor_activation_induces_glutamate_release_and_postsynaptic_firing_in_the_paraventricular_nucleus_ L2 - http://www.physiology.org/doi/full/10.1152/jn.00171.2004?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -