Tags

Type your tag names separated by a space and hit enter

Regulation of synaptic inputs to paraventricular-spinal output neurons by alpha2 adrenergic receptors.
J Neurophysiol 2005; 93(1):393-402JN

Abstract

Neurons in the paraventricular nucleus (PVN) that project to the brain stem and spinal cord are important for autonomic regulation. The excitability of preautonomic PVN neurons is controlled by the noradrenergic input from the brain stem. In this study, we determined the role of alpha(2) adrenergic receptors in the regulation of excitatory and inhibitory synaptic inputs to spinally projecting PVN neurons. Excitatory and inhibitory postsynaptic currents (EPSCs and IPSCs) were recorded using whole cell voltage-clamp techniques on PVN neurons labeled by a retrograde fluorescence tracer injected into the thoracic spinal cord of rats. Bath application of 5-20 muM clonidine, an alpha(2) receptor agonist, significantly reduced the amplitude of evoked GABAergic IPSCs in a dose-dependent manner. Also, 10 microM clonidine significantly decreased the frequency (from 2.68 +/- 0.41 to 1.22 +/- 0.40 Hz) but not the amplitude of miniature IPSCs (mIPSCs), and this effect was blocked by the alpha(2) receptor antagonist yohimbine. Furthermore, clonidine increased the paired-pulse ratio of evoked IPSCs from 1.25 +/- 0.05 to 1.61 +/- 0.08 (P < 0.05). On the other hand, clonidine had little effect on evoked glutamatergic EPSCs, mEPSCs, and the paired-pulse ratio of evoked EPSCs in most labeled cells examined. Additionally, immunofluorescence labeling revealed that the alpha(2A) receptor and GABA immunoreactivities were co-localized in close apposition to labeled PVN neurons. Collectively, these data suggest that stimulation of alpha(2) adrenergic receptors primarily attenuates GABAergic inputs to PVN output neurons to the spinal cord. The presynaptic alpha(2) receptors function as heteroreceptors to modulate synaptic GABA release and contribute to the hypothalamic regulation of sympathetic outflow.

Authors+Show Affiliations

Department of Anesthesiology, H187, Pennsylvania State University College of Medicine, 500 University Dr., Hershey, PA 17033-0850, USA. hpan@psu.eduNo affiliation info availableNo 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

15356178

Citation

Li, De-Pei, et al. "Regulation of Synaptic Inputs to Paraventricular-spinal Output Neurons By Alpha2 Adrenergic Receptors." Journal of Neurophysiology, vol. 93, no. 1, 2005, pp. 393-402.
Li DP, Atnip LM, Chen SR, et al. Regulation of synaptic inputs to paraventricular-spinal output neurons by alpha2 adrenergic receptors. J Neurophysiol. 2005;93(1):393-402.
Li, D. P., Atnip, L. M., Chen, S. R., & Pan, H. L. (2005). Regulation of synaptic inputs to paraventricular-spinal output neurons by alpha2 adrenergic receptors. Journal of Neurophysiology, 93(1), pp. 393-402.
Li DP, et al. Regulation of Synaptic Inputs to Paraventricular-spinal Output Neurons By Alpha2 Adrenergic Receptors. J Neurophysiol. 2005;93(1):393-402. PubMed PMID: 15356178.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Regulation of synaptic inputs to paraventricular-spinal output neurons by alpha2 adrenergic receptors. AU - Li,De-Pei, AU - Atnip,Lindsay M, AU - Chen,Shao-Rui, AU - Pan,Hui-Lin, Y1 - 2004/09/08/ PY - 2004/9/10/pubmed PY - 2005/3/1/medline PY - 2004/9/10/entrez SP - 393 EP - 402 JF - Journal of neurophysiology JO - J. Neurophysiol. VL - 93 IS - 1 N2 - Neurons in the paraventricular nucleus (PVN) that project to the brain stem and spinal cord are important for autonomic regulation. The excitability of preautonomic PVN neurons is controlled by the noradrenergic input from the brain stem. In this study, we determined the role of alpha(2) adrenergic receptors in the regulation of excitatory and inhibitory synaptic inputs to spinally projecting PVN neurons. Excitatory and inhibitory postsynaptic currents (EPSCs and IPSCs) were recorded using whole cell voltage-clamp techniques on PVN neurons labeled by a retrograde fluorescence tracer injected into the thoracic spinal cord of rats. Bath application of 5-20 muM clonidine, an alpha(2) receptor agonist, significantly reduced the amplitude of evoked GABAergic IPSCs in a dose-dependent manner. Also, 10 microM clonidine significantly decreased the frequency (from 2.68 +/- 0.41 to 1.22 +/- 0.40 Hz) but not the amplitude of miniature IPSCs (mIPSCs), and this effect was blocked by the alpha(2) receptor antagonist yohimbine. Furthermore, clonidine increased the paired-pulse ratio of evoked IPSCs from 1.25 +/- 0.05 to 1.61 +/- 0.08 (P < 0.05). On the other hand, clonidine had little effect on evoked glutamatergic EPSCs, mEPSCs, and the paired-pulse ratio of evoked EPSCs in most labeled cells examined. Additionally, immunofluorescence labeling revealed that the alpha(2A) receptor and GABA immunoreactivities were co-localized in close apposition to labeled PVN neurons. Collectively, these data suggest that stimulation of alpha(2) adrenergic receptors primarily attenuates GABAergic inputs to PVN output neurons to the spinal cord. The presynaptic alpha(2) receptors function as heteroreceptors to modulate synaptic GABA release and contribute to the hypothalamic regulation of sympathetic outflow. SN - 0022-3077 UR - https://www.unboundmedicine.com/medline/citation/15356178/Regulation_of_synaptic_inputs_to_paraventricular_spinal_output_neurons_by_alpha2_adrenergic_receptors_ L2 - http://www.physiology.org/doi/full/10.1152/jn.00564.2004?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -