Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.17 (CaMKII)
 4,029 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The modulatory effect of substance P (SP) on strychnine-sensitive glycine (Gly) response was examined in neurons acutely dissociated from the rat sacral dorsal commissural nucleus (SDCN) using nystatin perforated patch recording configuration under voltage-clamp conditions. Application of SP potentiated 30 mumol/L Gly-activated chloride current (IGly) in a concentration-dependent manner over the range of 1 nmol/L to 1 mumol/L at a holding potential of -40 mV. SP neither changed the reversal potential of Gly response nor affected the affinity of Gly to its receptor. The SP potentiation effect could be blocked by spantide as well as a selective NK1 receptor antagonist, L-668, 169, but not by NK2 receptor antagonist, L-659, 877. The facilitatory action of SP on IGly could also be abolished by pretreatment with chelerythrine or KN-62 in different neurons, a finding suggesting that protein kinase C (PKC) or Ca2+/calmodulin-dependent protein kinase II (CaMK II) possibly contributes to an intracellular pathway of SP in the augmentation of IGly. The results imply that SP may suppress nociception in the spinal cord by potentiating Gly response.
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PMID:Modulation of glycine-activated chloride currents by substance P in rat sacral dorsal commissural neurons. 1149 62

Injection of capsaicin into the skin results in pain, primary heat and mechanical hyperalgesia, and secondary mechanical allodynia and hyperalgesia. Sensory receptors in the area of secondary mechanical allodynia and hyperalgesia are unaffected, and so the sensory changes must be due to central actions of the initial intense nociceptive discharge that follows the capsaicin injection. Central sensitization of the responses of spinothalamic tract neurons lasts several hours, but can be prevented by spinal cord administration of non-NMDA and NMDA glutamate receptor antagonists or NK1 substance P receptor antagonists. The long-lasting increase in excitability of spinothalamic tract cells depends on the activation of several second messenger cascades (PKC, PKA, and NO/PKG signal transduction pathways). The excitability change also depends on activation of calcium/calmodulin-dependent kinase II, which is consistent with the proposal that this central sensitization response is a form of long-term potentiation.
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PMID:Role of neurotransmitters in sensitization of pain responses. 1200 17