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Regulation of neurokinin-1 receptor expression by GABA(B) receptor agonists.

Abstract：

:Activation of GABA(B) receptors produces analgesia in acute and chronic pain models. Data indicate that a possible mechanism for this effect is a GABA(B) receptor-induced blockade of neurokinin-1 (NK-1) receptor gene expression in the spinal cord. While much more potent GABA(B) receptor agonists (CGP 44532) have been developed, there is no information on their antinociceptive properties or their ability to influence NK-1 receptors. To address these issues, rats were treated with baclofen or CGP 44532 and tested for sedation, ataxia, and pain-related behaviors in a chronic pain model (formalin hindpaw injection). In a separate group of experiments the analgesic response to a single dose of CGP 44532 was tested prior, and subsequent to, its chronic administration. The results indicate that CGP 44532 is a substantially more potent analgesic than baclofen. In addition, after chronic administration baclofen was no longer capable of inducing analgesia or of inhibiting the increased expression of NK-1R mRNA and CGP 44532 was still fully effective in both regards. The results suggest that GABA(B) agonists could be clinically useful analgesics.

journal_name

Life Sci

journal_title

Life sciences

authors

Enna SJ,Harstad EB,McCarson KE

doi

10.1016/s0024-3205(98)00101-5

subject

Has Abstract

pub_date

1998-01-01 00:00:00

pages

1525-30

issue

17-18

eissn

0024-3205

issn

1879-0631

pii

S0024-3205(98)00101-5

journal_volume

62

pub_type

杂志文章

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