TY - JOUR
T1 - Cholinergic modulation of neurons in the gustatory region of the nucleus of the solitary tract
AU - Uteshev, Victor V.
AU - Smith, David V.
N1 - Funding Information:
Supported in part by NIH grants DC00353 and DC000066 to D.V.S. Portions of these data were presented in poster form at the 27th annual meeting of the Association for Chemoreception Sciences, Sarasota, FL, April 2005, and at the 35th annual meeting of the Society for Neuroscience, November 2005. Thanks are due to Dr. Matthew Ennis for valuable comments on an earlier version of the manuscript.
PY - 2006/4/21
Y1 - 2006/4/21
N2 - The rostral portion of the nucleus of the solitary tract (rNST) is an obligatory relay for gustatory afferent input on its way to the forebrain. Previous studies have demonstrated excitation of rNTS neurons by glutamate and substance P and inhibition by γ-aminobutyric acid (GABA) and met-enkephalin (ENK). Despite the existence of cholinergic neurons and putative terminals within the rNTS, there are no data on the effects of acetylcholine (ACh) on rNTS processing. Here, we use patch-clamp recording of rNTS neurons in vitro to examine ACh-mediated responses and voltage-gated conductances in these cells. Results revealed (1) intrinsic voltage-gated inhibition via activation of voltage-gated potassium A-channels (IA), found almost exclusively in the medial rNTS, and hyperpolarization-activated potassium/sodium channels (Ih), found more frequently in the lateral rNST; and (2) ligand-gated inhibition via activation of muscarinic m2 ACh receptors (mAChRs) linked to inward rectifier potassium channels (Kir) evenly distributed throughout the rNTS, a mechanism dependent on cholinergic inputs. Muscarinic responses were blocked by AFDX-116, a selective m2 mAChR antagonist, and by BaCl2, an antagonist of Kir channels. In addition, many rNTS neurons exhibited excitation via α7 and non-α7 nicotinic AChRs. Non-α7 nAChRs, blocked by 10 μM mecamylamine, occurred more frequently in the lateral rNTS. In contrast, α7 nAChRs, blocked by 20 nM methyllcaconitine, were evenly distributed across the nucleus. As previously reported for voltage-activated conductances, none of these currents was related to neuronal morphology. These voltage- and ligand-dependent inhibitory mechanisms would be expected to contribute to the modulation of gustatory processing through the NST.
AB - The rostral portion of the nucleus of the solitary tract (rNST) is an obligatory relay for gustatory afferent input on its way to the forebrain. Previous studies have demonstrated excitation of rNTS neurons by glutamate and substance P and inhibition by γ-aminobutyric acid (GABA) and met-enkephalin (ENK). Despite the existence of cholinergic neurons and putative terminals within the rNTS, there are no data on the effects of acetylcholine (ACh) on rNTS processing. Here, we use patch-clamp recording of rNTS neurons in vitro to examine ACh-mediated responses and voltage-gated conductances in these cells. Results revealed (1) intrinsic voltage-gated inhibition via activation of voltage-gated potassium A-channels (IA), found almost exclusively in the medial rNTS, and hyperpolarization-activated potassium/sodium channels (Ih), found more frequently in the lateral rNST; and (2) ligand-gated inhibition via activation of muscarinic m2 ACh receptors (mAChRs) linked to inward rectifier potassium channels (Kir) evenly distributed throughout the rNTS, a mechanism dependent on cholinergic inputs. Muscarinic responses were blocked by AFDX-116, a selective m2 mAChR antagonist, and by BaCl2, an antagonist of Kir channels. In addition, many rNTS neurons exhibited excitation via α7 and non-α7 nicotinic AChRs. Non-α7 nAChRs, blocked by 10 μM mecamylamine, occurred more frequently in the lateral rNTS. In contrast, α7 nAChRs, blocked by 20 nM methyllcaconitine, were evenly distributed across the nucleus. As previously reported for voltage-activated conductances, none of these currents was related to neuronal morphology. These voltage- and ligand-dependent inhibitory mechanisms would be expected to contribute to the modulation of gustatory processing through the NST.
KW - Gustation
KW - I
KW - I
KW - Muscarinic
KW - NST
KW - Nicotinic
KW - Nucleus tractus solitarius
KW - Taste
UR - http://www.scopus.com/inward/record.url?scp=33746894194&partnerID=8YFLogxK
U2 - 10.1016/j.brainres.2006.02.023
DO - 10.1016/j.brainres.2006.02.023
M3 - Article
C2 - 16546141
AN - SCOPUS:33746894194
SN - 0006-8993
VL - 1084
SP - 38
EP - 53
JO - Brain Research
JF - Brain Research
IS - 1
ER -