TY - JOUR
T1 - Localization and activation of glutamate receptors in unmyelinated axons of rat glabrous skin
AU - Carlton, Susan M.
AU - Hargett, Gregory L.
AU - Coggeshall, Richard E.
N1 - Funding Information:
The authors would like to thank Brenda Kenworthy for secretarial assistance and Zhixia Ding for her expertise in performing the immunostaining and electron microscopy. Supported by NIH grants NS11255 and NS27910 to SMC and NS10161 to REC.
PY - 1995/9/1
Y1 - 1995/9/1
N2 - Immunohistochemical staining for the glutamate receptor subtypes N-methyl-d-aspartate (NMDA), kainate, and α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) results in a significant number of labeled unmyelinated axons in the glabrous skin of the rat hindpaw. Injection of glutamate into the rat hindpaw results in behavioral changes interpreted as mechanical allodynia and mechanical hyperalgesia. The anatomical findings provide a reasonable explanation for the action of the exogenous peripheral glutamate, namely that activation of these receptors leads to increased primary afferent activity in unmyelinated axons and thus to pain behaviors. AMPA receptors are frequently associated with small clear vesicles in the axoplasm of the unmyelinated axons, many of which have been previously shown to contain high concentrations of glutamate. This finding indicates that these might be autoreceptors and so glutamate itself might regulate certain types of peripheral impulse traffic. The presence of peripheral glutamate receptors associated with unmyelinated axons suggests the possibility that glutamate antagonists applied peripherally might prevent or attenuate some pain-related behaviors.
AB - Immunohistochemical staining for the glutamate receptor subtypes N-methyl-d-aspartate (NMDA), kainate, and α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) results in a significant number of labeled unmyelinated axons in the glabrous skin of the rat hindpaw. Injection of glutamate into the rat hindpaw results in behavioral changes interpreted as mechanical allodynia and mechanical hyperalgesia. The anatomical findings provide a reasonable explanation for the action of the exogenous peripheral glutamate, namely that activation of these receptors leads to increased primary afferent activity in unmyelinated axons and thus to pain behaviors. AMPA receptors are frequently associated with small clear vesicles in the axoplasm of the unmyelinated axons, many of which have been previously shown to contain high concentrations of glutamate. This finding indicates that these might be autoreceptors and so glutamate itself might regulate certain types of peripheral impulse traffic. The presence of peripheral glutamate receptors associated with unmyelinated axons suggests the possibility that glutamate antagonists applied peripherally might prevent or attenuate some pain-related behaviors.
KW - Kainate
KW - Mechanical allodynia
KW - Mechanical hyperalgesia
KW - N-Methyl-d-aspartate
KW - Non-N-methyl-d-aspartate
KW - α-Amino-3-hydroxy-5-methylisoxazole-4-propionic acid
UR - http://www.scopus.com/inward/record.url?scp=0029052635&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0029052635&partnerID=8YFLogxK
U2 - 10.1016/0304-3940(95)11889-5
DO - 10.1016/0304-3940(95)11889-5
M3 - Article
C2 - 8545047
AN - SCOPUS:0029052635
SN - 0304-3940
VL - 197
SP - 25
EP - 28
JO - Neuroscience Letters
JF - Neuroscience Letters
IS - 1
ER -