astressin-2b and Nociceptive-Pain

Corticotropin-releasing factor (CRF) is involved in the regulation of pain sensitivity and can induce an analgesic effect in animals and humans. The periaqueductal gray matter (PAGM) of the midbrain is one of the key structures of the antinociceptive system. The aim of the study was to investigate the involvement of CRF receptor type 2 (CRF-R2 receptors), localized in the PAGM, in the analgesic effect caused by central or systemic CRF on somatic pain sensitivity in conscious rats. Somatic pain sensitivity was tested by a tail flick test (measuring tail flick latency induced by tail's thermal stimulation). The involvement of CRF-R2 receptors was studied by administering the selective antagonist astressin2-B into the PAGM. Both peripheral and central CRF administration caused an increase in tail flick latencies (analgesic effect). Administration of astressin2-B into the PAGM attenuated the analgesic effect induced by the central as well as systemic CRF administration. The results suggest that one of the mechanisms of the CRF-induced analgesic effect may be mediated by CRF-R2 receptors located in PAGM.

Topics: Analgesics; Animals; Behavior, Animal; Corticosterone; Corticotropin-Releasing Hormone; Male; Nociceptive Pain; Peptide Fragments; Peptides, Cyclic; Periaqueductal Gray; Rats; Rats, Sprague-Dawley; Receptors, Corticotropin-Releasing Hormone

Corticotropin-releasing factor (CRF) is involved in the regulation of pain sensitivity and can cause an analgesic effect in animals and humans. The aim of the study was to investigate the involvement of CRF1 and CRF2 receptors in CRF-induced analgesic effect (after intraperitoneal injection) on somatic pain sensitivity in conscious rats. Somatic pain sensitivity was tested by tail flick latency (tail flick test). The involvement of CRF1 and CRF2 receptors was studied by their selective antagonists NBI 27914 and astressin 2B, respectively. Systemic administration of CRF caused an increase in tail flick latency (analgesic effect). Pretreatment with NBI 27914 or astressin 2B eliminated CRF-induced analgesic effect. Besides, NBI 27914, but not astressin 2B, increased basal tail flick latency. The data obtained indicate that the analgesic effect can be mediated by both CRF1 and CRF2 receptors. CRF-1 receptor, in contrast to the CRF2 receptors, may be involved in the regulation of the basal level of pain sensitivity.

Topics: Analgesics; Aniline Compounds; Animals; Behavior, Animal; Consciousness; Corticotropin-Releasing Hormone; Gene Expression; Injections, Intraperitoneal; Male; Nociception; Nociceptive Pain; Peptide Fragments; Peptides, Cyclic; Pyrimidines; Rats; Rats, Sprague-Dawley; Receptors, Corticotropin-Releasing Hormone