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Inhibitory amino acid transmitters associated with axons in presynaptic apposition to cutaneous primary afferent axons in the cat spinal cord
Author(s) -
Sutherland Fiona I.,
Bannatyne B. Anne,
Kerr Robert,
Riddell John S.,
Maxwell David J.
Publication year - 2002
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.10374
Subject(s) - biology , postsynaptic potential , apposition , neuroscience , spinal cord , gabaergic , anatomy , horseradish peroxidase , axon , inhibitory postsynaptic potential , biochemistry , receptor , enzyme
The purpose of the present study was to characterize the transmitter content of structures in presynaptic apposition to the central terminals of cutaneous afferent fibers in the dorsal horn of the spinal cord. Axons in the Aαβ conduction velocity range were identified in adult cats, stained intra‐axonally with horseradish peroxidase, and prepared for combined light and electron microscopy. In total, we labeled two slowly adapting (Type 1) axons, two hair‐follicle afferents, and one rapidly adapting (Krause) afferent. Ninety‐nine labeled boutons were examined through complete series of serial sections. Approximately 80% of boutons originating from rapidly adapting and hair‐follicle afferents were postsynaptic to other axons, but only 50% of boutons from slowly adapting axons were associated with this type of arrangement. Postembedding immunogold reactions revealed that between 80% (for slowly adapting axons) and 100% (for rapidly adapting axons) of boutons presynaptic to primary afferents were immunoreactive for γ‐aminobutyric acid (GABA). The vast majority of these terminals (in excess of 80%) were also enriched with glycine. Therefore, presynaptic inhibition of these three functional classes of Aαβ cutaneous primary afferents is mediated principally by the subgroup of GABAergic interneuron that also contains glycine. J. Comp. Neurol. 452:154–162, 2002. © 2002 Wiley‐Liss, Inc.