The effects of chemical or surgical deafferentation on [ 3H]-acetylcholine release from rat spinal cord

Cholinergic modulation of nociceptive transmission through both nicotinic and muscarinic receptors in the spinal cord represents an important mechanism in pain signaling. However, what neuronal elements release acetylcholine and how release might change in response to deafferentation are unclear. Th...

Full description

Saved in:

Bibliographic Details
Published in:	Neuroscience Vol. 135; no. 4; pp. 1269 - 1276
Main Authors:	Dussor, G.O., Jones, D.J., Hulsebosch, C.E., Edell, T.A., Flores, C.M.
Format:	Journal Article
Language:	English
Published:	Oxford Elsevier Ltd 2005 Elsevier
Subjects:	Acetylcholine - pharmacology Acetylcholine - secretion Afferent Pathways - injuries Afferent Pathways - metabolism Afferent Pathways - surgery Animals Biological and medical sciences capsaicin Capsaicin - pharmacology choline choline acetyltransferase Cholinergic Agents - pharmacology Enzyme Inhibitors - pharmacology Fundamental and applied biological sciences. Psychology Hemicholinium 3 - pharmacology Ligation Male neuropathic Organ Culture Techniques pain Pain - metabolism Pain - physiopathology Rats Rats, Sprague-Dawley Rhizotomy Spinal Cord - drug effects Spinal Cord - metabolism Spinal Nerves - drug effects Spinal Nerves - injuries Spinal Nerves - surgery Vertebrates: nervous system and sense organs neuropathic BrACh HC-3 choline pain choline acetyltransferase ACh capsaicin ChAT DRG DRX [ 3H]-ACh Acyltransferases Spinal cord Rat Enzyme Capsaicin Transferases Rodentia Central nervous system Choline O-acetyltransferase Vertebrata Mammalia Pain Animal Surgery Neurotransmitter Acetylcholine Deafferentation Release
Online Access:	Get full text
Tags:	Add Tag No Tags, Be the first to tag this record!

Description
Summary:	Cholinergic modulation of nociceptive transmission through both nicotinic and muscarinic receptors in the spinal cord represents an important mechanism in pain signaling. However, what neuronal elements release acetylcholine and how release might change in response to deafferentation are unclear. The present studies demonstrated Ca ++- and K +-dependent release of [ 3H]-acetylcholine from slices of regional areas of rat spinal cord. That [ 3H]-acetylcholine was synthesized from [ 3H]-choline was demonstrated by the lack of [ 3H]-acetylcholine release following incubation with either the choline uptake inhibitor hemicholinium or the choline acetyltransferase inhibitor bromoacetylcholine. Rats treated neonatally with capsaicin or with spinal nerve ligation as adults showed a significantly decreased K +-stimulated release of [ 3H]-acetylcholine from dorsal horn but not ventral horn lumbar spinal cord slices. In rats subjected to dorsal rhizotomy, while basal release from lumbar dorsal spinal cord slices was reduced, K +-stimulated [ 3H]-acetylcholine release, while decreased, was not significantly different compared with controls. The data presented here show that there are regional differences in the release of acetylcholine from spinal cord and that this release can be modulated by chemical or surgical deafferentation. These results also indicate that the source of acetylcholine in the dorsal cord originates mainly from resident somata and their collaterals, interneurons and/or descending terminals, with only very minor contributions coming from primary afferents. The present data help to further elucidate the role of acetylcholine in spinal signaling, particularly with respect to the effects of nerve injury and nociceptive neurotransmission.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0306-4522 1873-7544
DOI:	10.1016/j.neuroscience.2005.07.019