Orphanin FQ (nociceptin) modulates responses of trigeminal neurons evoked by excitatory amino acids and somatosensory stimuli, and blocks the substance P-induced facilitation of N-methyl-d-aspartate-evoked responses

Neuroscience ◽  
1999 ◽  
Vol 93 (2) ◽  
pp. 703-712 ◽  
Author(s):  
X.-M. Wang ◽  
K.-M. Zhang ◽  
L.O. Long ◽  
S.S. Mokha
Keyword(s):  
Amino Acids ◽  
Substance P ◽  
Excitatory Amino Acids ◽  
Evoked Responses ◽  
Orphanin Fq ◽  
Trigeminal Neurons ◽  
Somatosensory Stimuli

Central sensitization following intradermal injection of capsaicin

1997 ◽  
Vol 20 (3) ◽  
pp. 471-471 ◽  
Author(s):  
William D. Willis
Keyword(s):  
Amino Acids ◽  
Substance P ◽  
Central Sensitization ◽  
Mechanical Allodynia ◽  
Excitatory Amino Acids ◽  
Intradermal Injection ◽  
Mechanical Hyperalgesia ◽  
Spinothalamic Tract ◽  
Nociceptive Neurons ◽  
Primary Hyperalgesia

Intradermal capsaicin in humans causes pain, primary hyperalgesia, and secondary mechanical hyperalgesia and allodynia. Parallel changes occur in the responses of primate spinothalamic tract cells and in rat behavior. Neurotransmitters that trigger secondary mechanical hyperalgesia and allodynia include excitatory amino acids and substance P. Secondary mechanical allodynia is actively maintained by central mechanisms. Our group has investigated mechanisms of central sensitization of nociceptive neurons by examining the responses to intradermal injection of capsaicin. These experiments are pertinent to issues raised by coderre & katz (sect. 2).

Nociceptin (orphanin FQ), an endogenous ligand for the QRL1 (opioid-receptor-like1) receptor; modulates responses of trigeminal neurons evoked by excitatory amino acids and somatosensory stimuli

1996 ◽  
Vol 76 (5) ◽  
pp. 3568-3572 ◽  
Author(s):  
X. M. Wang ◽  
K. M. Zhang ◽  
S. S. Mokha
Keyword(s):  
Inhibitory Effect ◽  
Trigeminal System ◽  
Evoked Responses ◽  
Trigeminal Nucleus ◽  
Orphanin Fq ◽  
Endogenous Ligand ◽  
Nociceptive Neurons ◽  
Inhibitory Modulation ◽  
Trigeminal Neurons

1. This is the first in vivo electrophysiological evidence demonstrating the effects of Phe-Gly-Gly-Phe-Thr-Gly-Ala-Arg-Lys-Ser-Ala-Arg-Lys-Leu-Ala-Asn-Gln (nociceptin or orphanin FQ), an endogenous ligand for the orphan ORL1 receptor, on nociceptive neurons in the CNS. The effects of nociceptin were tested on the responses of neurons recorded in the superficial and deeper dorsal horn of the medulla (trigeminal nucleus caudalis) in the rat. 2. Nociceptin applied microiontophoretically produced a predominantly long-lasting (5–30 min) inhibitory modulation of the N-methyl-D-aspartic acid (NMDA)-evoked responses of 24 of 31 nociceptive and 12 of 12 nonnociceptive neurons. Excitatory or biphasic effects of nociceptin were also observed in 6 of 43 neurons. Responses evoked by (+/-)-alpha-amino-3-hydroxy-5-methylisox-azole-4-propionic acid (AMPA) were reduced in eight of nine nociceptive and nonnociceptive neurons. 3. The inhibitory effect of nociceptin was not modality specific; responses to both noxious and nonnoxious stimuli were reduced. 4. Although naloxone applied iontophoretically blocked or reduced the peak inhibitory effect of [D-Ala2,N-Me-Phe4, Gly5-ol]-Enkephalin (DAMGO) or trans-(+/-)-3,4-dicholoro-N-methyl-N-(2-1-pyrrolidinyl-cyclo hexyl)-benzene acetamide (U50, 488H), it did not produce a significant alteration in the peak inhibitory effect of nociceptin. 5. Nociceptin administered intracerebroventricularly produced a long-lasting (20–35 min) reduction in the NMDA-evoked responses of three of three nociceptive neurons. 6. Nociceptin produces a predominantly antinociceptive action in the trigeminal system.

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