cgp-36742 and Pain

cgp-36742 has been researched along with Pain* in 2 studies

Reviews

1 review(s) available for cgp-36742 and Pain

ArticleYear
GABAB receptor: a site of therapeutic benefit.
    Current opinion in pharmacology, 2006, Volume: 6, Issue:1

    Although the presence of functional GABAB receptors in mammalian brain has been known for more than 20 years, there is still only one therapeutic agent in use, baclofen, which mediates its effects directly via this receptor. However, activation of this receptor can produce numerous effects that might be amenable to drug development. Evidence from preclinical studies also suggests that antagonism of the GABAB receptor produces beneficial clinical effects.

    Topics: Animals; Baclofen; Brain; Clinical Trials as Topic; Cognition; Drug Evaluation, Preclinical; Epilepsy, Absence; GABA Agonists; GABA Antagonists; Humans; Muscle Spasticity; Organophosphorus Compounds; Pain; Receptors, GABA-B; Substance-Related Disorders

2006

Other Studies

1 other study(ies) available for cgp-36742 and Pain

ArticleYear
Nerve growth factor- and neurotrophin-3-induced changes in nociceptive threshold and the release of substance P from the rat isolated spinal cord.
    The Journal of neuroscience : the official journal of the Society for Neuroscience, 1997, Nov-01, Volume: 17, Issue:21

    Acute superfusion of nerve growth factor (NGF; 1-100 ng/ml) through a naive rat spinal cord preparation did not alter basal or electrically evoked release of substance P-like immunoreactivity (SP-LI). In contrast, neurotrophin-3 (NT-3; 1-100 ng/ml), although not modifying SP-LI basal outflow, dose-dependently inhibited the electrically evoked, but not capsaicin (10 nM)-induced, release of the peptide. This NT-3 (10 ng/ml)-induced inhibition persisted even in the presence of 100 ng/ml NGF in the perfusion fluid and was still significant when the evoked release of SP-LI was enhanced by a prolonged in vivo treatment with NGF. Co-superfusion with naloxone (0.1 microM), but not CGP 36742 (100 microM), a GABAB antagonist, prevented NT-3 (10 ng/ml) inhibition of SP-LI release. Basal and electrically evoked release of SP-LI from the rat spinal cord in vitro was not modified 24 hr after single systemic injection of either NGF (1 mg/kg) or NT-3 (10 mg/kg). At these time intervals from administration, NGF had induced thermal and mechanical hyperalgesia in the rat hindpaw, and NT-3 had induced mechanical, but not thermal, hypoalgesia. NT-3 administered six times over a 2 week period (at 1 mg/kg) did not alter thermal threshold but significantly reduced electrically evoked release of SP-LI from the spinal cord. An identical treatment regimen with 1 mg/kg NGF induced a significant increase in evoked release of SP-LI. However, this was not associated with a significant hyperalgesia. Although finding that NGF-induced hyperalgesia does not clearly correlate with changes in the release of SP-LI in the spinal cord, this study shows that NT-3 is an inhibitor of SP-LI release and suggests that this mechanism may be responsible for NT-3-induced antinociception.

    Topics: Analgesics; Animals; Capsaicin; Dose-Response Relationship, Drug; Drug Interactions; Evoked Potentials; GABA Antagonists; GABA-B Receptor Antagonists; Hot Temperature; Hyperalgesia; Hypesthesia; Injections, Subcutaneous; Male; Naloxone; Narcotic Antagonists; Nerve Growth Factors; Neurotrophin 3; Organophosphorus Compounds; Pain; Pain Threshold; Perfusion; Pressure; Rats; Rats, Wistar; Secretory Rate; Single-Blind Method; Spinal Cord; Substance P

1997