We have previously reported that supraspinally and spinally located CCK receptors are involved in antagonizing supraspinally administered opioid-induced antinociception. Cold water swimming stress (CWSS) produces antinociception and opioid receptors are involved in CWSS-induced antinociception. The present study was designed to determine if supraspinal and spinal CCK receptors were involved in modulating the CWSS-induced antinociception. Antinociception was assessed by the tail-flick test. CWSS caused a profound inhibition of the tail-flick response. Various doses of CCK injected intracerebroventricularly (i.c.v.) or intrathecally (i.t.) alone did not show any antinociceptive effect. The i.c.v. or i.t. pretreatment with CCK (0.05-0.5 ng) dose dependently attenuated the CWSS-induced inhibition of the tail-flick response. In addition, i.c.v. pretreatment with lorglumide (0.1-10 pg) but not PD135,158 (1-100 pg) dose dependently reversed CCK's inhibition of the tail-flick response induced by CWSS. However, both lorglumide and PD-135,158 injected i.t. reversed the antagonism of CCK against the inhibition of the tail-flick response induced by CWSS in a dose-dependent manner. Our results suggest that, at the supraspinal level, CCK(A) but not CCK(B) receptors may be involved in antagonizing the CWSS-induced antinociception. In the spinal cord both CCK(A) and CCK(B) receptors appear to be involved in antagonizing the CWSS-induced antinociception.
ASJC Scopus subject areas
- Endocrine and Autonomic Systems
- Cellular and Molecular Neuroscience