Inflammation unmasks gabapentin's effect on A delta-fiber evoked excitatory postsynaptic currents in substantia gelatinosa neurons of rat spinal cord.

Abstract:

OBJECTIVE:To study the analgesic mechanism of gabapentin, an anticonvulsant, during antinociceptive clinical treatment. METHODS:Whole-cell voltage-clamp recordings were taken from adult rat spinal cord slices to investigate the effect of gabapentin on primary afferent A delta-fiber evoked excitatory postsynaptic currents (EPSCs) to substantia gelatinosa (SG) neurons in normal and inflamed (established by plantar injection of carrageenan) rats. RESULTS:Gabapentin (5 - 20 micro mol/L for 5 min) depressed dorsal root A delta fiber evoked polysynaptic, but not monosynaptic EPSCs to SG experiencing inflammation by about 25% (n = 10, P < 0.01). However, gabapentin did not depress the evoked polysynaptic or monosynaptic EPSCs in normal rats. Gabapentin failed to block a glutamate receptor subtype, N-methyl-D-aspartate (NMDA), -induced slow excitatory currents on SG neurons. CONCLUSIONS:Inflammation, at least in part, unmasks the gabapentin depression on nociception transmission in the dorsal horn, and this depression is not due to the blockade of postsynaptic NMDA receptor.

journal_name

Chin Med J (Engl)

journal_title

Chinese medical journal

authors

Liu Z,Xu R,Yang K

keywords:

subject

Has Abstract

pub_date

2003-06-01 00:00:00

pages

883-7

issue

6

eissn

0366-6999

issn

2542-5641

journal_volume

116

pub_type

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