Glial and potassium responses to an afferent volley: suppression by enkephalin in the rat spinal cord in vitro

Tsuruhara, Hideaki; Takahashi, Tomoyuki

doi:10.1016/0304-3940(87)90417-4

Cited by 1 publication

(1 citation statement)

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“…OX 1 R are probably not on primary afferent terminals, excitatory interneuron, or projection neurons, which would increase nociceptive transmission when excited, a finding not in line with our observations (Figure 4). Based on our findings, OX 1 R are more likely to activate GABA, glycine or enkephalin containing neurons in the dorsal horn which are inhibitory in nature (Tsuruhara and Takahashi, 1987, Atsumi et al, 1993, Fleming and Todd, 1994, Jonas et al, 1998, Kerchner et al, 2001, Kodama and Kimura, 2002, Liu et al, 2002, Moore et al, 2002, Baba et al, 2003, Peever et al, 2003, Dergacheva et al, 2005, Ataka and Gu, 2006). Although there is no evidence for colocalization of OX 1 R on GABA, glycine, or enkephalin neurons to date, based on the antinociceptive role demonstrated in the present study, and the excitatory nature of orexin-A, it is likely that orexin-A neurons in the PH have an indirect inhibitory role on nociception in the dorsal horn by activating inhibitory interneurons, which then inhibit primary afferent terminals or projection neurons.…”

Section: Discussionmentioning

confidence: 65%

The role of spinal orexin-1 receptors in posterior hypothalamic modulation of neuropathic pain

Jeong

Holden

2009

Neuroscience

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The posterior hypothalamus (PH) is known to reduce nociceptive pain, but the effect of PH stimulation on neuropathic pain is not known. Because neurons containing the neurotransmitter orexin-A are located in the PH in some strains of rat and intrathecal injection of orexin-A produces antinociception in a neuropathic pain model, we hypothesized that orexin-A from neurons in the PH modifies nociception in the spinal cord dorsal horn. To test this hypothesis, the cholinergic agonist carbachol or normal saline was microinjected into the PH of lightly anesthetized female Sprague-Dawley rats with chronic constriction injury (CCI) and foot withdrawal latencies (FWL) were measured. Carbachol-induced PH stimulation produced dose dependent antinociception as shown by significantly increased FWL compared to saline controls. To investigate the role of orexin-A in PH-induced antinociception, the orexin-1 receptor antagonist SB334867 or dimethyl sulfoxide (DMSO) for control, was given intrathecally following carbachol-induced PH stimulation. SB334867 decreased FWL compared to DMSO controls. These data are suggestive that stimulating the PH produces antinociception in a neuropathic pain model and that the antinociceptive effect is mediated in part by orexin-1 receptors in the spinal cord dorsal horn.

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