Inhibition of spinal nociceptive neurons by microinjections of somatostatin into the nucleus raphe magnus and the midbrain periaqueductal gray of the anesthetized cat

Helmchen, C.; Fu, Q.-G.; Sandkühler, Jürgen

doi:10.1016/0304-3940(95)11345-2

Cited by 33 publications

(14 citation statements)

References 17 publications

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“…The result in part contradicts with other reports that SOM is involved in mechanical or heat nociception (Kuraishi et al, 1985;Morton et al, 1989;Song et al, 2002). Nevertheless, it is in concordance with the previous reports that SOM has an inhibitory effect on dorsal horn neurons (Sandkühler et al, 1990;Helmchen et al, 1995;Taddese et al, 1995).…”

Section: Discussioncontrasting

confidence: 59%

“…First, SOM exhibits depressant actions on the excitability of neurons, particularly in the spinal cord (Murase et al, 1982;Taddese et al, 1995;Kim et al, 2002;Jiang et al, 2003). Second, SOM superfusion or systemic SOM in vivo inhibits the thermal responses of nociceptive spinal neurons (Sandkühler et al, 1990;Helmchen et al, 1995). Third, intrathecally applied SOM inhibits motor reflexes in response to noxious stimuli and reduces c-Fos expression and mechanical hyperalgesia in neuropathic pain model (Mollenholt et al, 1988;Tsai et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

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Effects of Somatostatin on the Responses of Rostrally Projecting Spinal Dorsal Horn Neurons to Noxious Stimuli in Cats

Jung

Lee

et al. 2008

Korean J Physiol Pharmacol

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Somatostatin (SOM) is a widely distributed peptide in the central nervous system and exerts a variety of hormonal and neural actions. Although SOM is assumed to play an important role in spinal nociceptive processing, its exact function remains unclear. In fact, earlier pharmacological studies have provided results that support either a facilitatory or inhibitory role for SOM in nociception. In the current study, the effects of SOM were investigated using anesthetized cats. Specifically, the responses of rostrally projecting spinal dorsal horn neurons (RPSDH neurons) to different kinds of noxious stimuli (i.e., heat, mechanical and cold stimuli) and to the Aδ -and C-fiber activation of the sciatic nerve were studied. Iontophoretically applied SOM suppressed the responses of RPSDH neurons to noxious heat and mechanical stimuli as well as to C-fiber activation. Conversely, it enhanced these responses to noxious cold stimulus and Aδ -fiber activation. In addition, SOM suppressed glutamate-evoked activities of RPSDH neurons. The effects of SOM were blocked by the SOM receptor antagonist cyclo-SOM. These findings suggest that SOM has a dual effect on the activities of RPSDH neurons; that is, facilitation and inhibition, depending on the modality of pain signaled through them and its action site.

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Section: Discussioncontrasting

confidence: 59%

Section: Introductionmentioning

confidence: 99%

Effects of Somatostatin on the Responses of Rostrally Projecting Spinal Dorsal Horn Neurons to Noxious Stimuli in Cats

Jung

Lee

et al. 2008

Korean J Physiol Pharmacol

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“…The changes in the SP-LI level in the hypothalamus on day 4 after CCI have been demonstrated for the first time in this study by using the Seltzer model. It has been suggested that the microinjection of SOM into the caudate putamen and PAG exerts an antinociceptive effect (Helmchen et al 1995). In the present study, the SOM-LI level in the PAG was significantly reduced after CCI and was slightly normalized by memantine treatment.…”

Section: Changes In the Levels Of Neuropeptides After Nerve Injury Anmentioning

confidence: 71%

Effect of Memantine on the Levels of Neuropeptides and Microglial Cells in the Brain Regions of Rats with Neuropathic Pain

et al. 2009

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Neuropathic pain induced by sciatic nerve injury not only causes peripheral dysfunctions but also affects the cortical and subcortical regions of the brain. It is still unknown whether neuropathic pain could relate to behavioral and neurochemical alterations in the central nervous system. This paper deals with the effect of peripheral neuropathic pain on mechanical allodynia, neuropeptide levels, neuropeptide-degrading enzyme activities, and microglial cells in the brain regions of rats by applying chronic constriction injury, a partial sciatic nerve injury. We examined the possible protection effect on the allodynia and changes in levels of neuropeptides and microglial activation in chronic constriction injury of the rat brain by memantine. On 4 days after chronic constriction injury, the induction of mechanical allodynia was suppressed by memantine treatment. Reductions in the substance P in the hypothalamus and somatostatin in the periaqueductal gray of chronic constriction injury rat brain were reversed by memantine. This suggests the role of these neuropeptides in pain information processing in the brain. Immunohistochemical experiments revealed that the expression of CD11b, a marker protein of microglia, was increased in the hypothalamus and periaqueductal gray in the chronic constriction injury rat brain as compared with the controls, and memantine treatment could suppress the activation of microglia, suggesting the involvement of microglia in pain mechanism. The present behavioral, biochemical, and immunohistochemical studies demonstrated that peripheral neuropathic pain affects the neuropeptide levels and microglial activation in the brain regions, and these events described above may play an important role in neuropathic pain pathogenesis.

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“…Experimental in vivo and in vitro evidence points to an inhibitory effect at the level of the spinal and trigeminal dorsal horns [56]. Further antinociceptive responses are elicited from the dorsal PAG, NRM, and caudate putamen [57,58], whereas intracerebroventricular administration of octreotide, an analog of somatostatin, reduces Fos expression in the TNC following noxious corneal stimulation in the rat [59]. Manipulation of the posterior hypothalamic somatostatin receptors modulates dural and facial trigeminal nociceptive transmission in the TNC.…”

Section: Other Hypothalamic Peptide Hormonesmentioning

confidence: 97%

Cluster headache, hypothalamus, and orexin

Holland

Goadsby²

2009

Current Science Inc

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Cluster headache (CH) is a highly disabling condition resulting in severe, recurrent unilateral bouts of pain and accompanying autonomic symptoms. This review describes some current views regarding the underlying pathophysiology covering the pain and cranial autonomic (parasympathetic) activation, and highlights the potential importance of the hypothalamus in CH. The hypothalamus is known to modulate many functions and has been shown to be involved in the pathophysiology of a variety of primary headaches, including CH. Hypothalamic structures are likely to underlie the circadian and circannual periodicity of attacks and contribute to the pain and autonomic disturbances. We discuss the hypothalamic involvement in CH and modulation of trigeminovascular processing and examine the emerging involvement of the hypothalamic orexinergic system as a possible key pathway in CH pathophysiology.

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Inhibition of spinal nociceptive neurons by microinjections of somatostatin into the nucleus raphe magnus and the midbrain periaqueductal gray of the anesthetized cat

Cited by 33 publications

References 17 publications

Effects of Somatostatin on the Responses of Rostrally Projecting Spinal Dorsal Horn Neurons to Noxious Stimuli in Cats

Effects of Somatostatin on the Responses of Rostrally Projecting Spinal Dorsal Horn Neurons to Noxious Stimuli in Cats

Effect of Memantine on the Levels of Neuropeptides and Microglial Cells in the Brain Regions of Rats with Neuropathic Pain

Cluster headache, hypothalamus, and orexin

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