“…Immunohistochemical, autoradiographic and neurochemical studies show that there is a dense concentration of GABA terminals (Miyata & Otsuka, 1975;Barber et al, 1978;Hunt et al, 1981), GABA receptors (Price et al, 1984;Young & Kuhar, 1980), enkephalin-immunoreactive terminals (Hokfelt et al, 1977;Hunt et al, 1981) and opiate receptors (Atweh & Kuhar, 1977) in superficial layers of the dorsal horn. Probably both GABA and enkephalins act as inhibitory neurotransmitters of spinal interneurones in this region.…”
The saphenous nerve-evoked slow v.r.p. was depressed by [Met5] enkephalin (0.1-1 EM), dynorphin (1-13X0.2 gM) and morphine (1-2 pM), and these effects were reversed by naloxone (1 pM).6 Two endogenous peptides, galanin (1-2 pM) and somatostatin (1-2.5 pM), inhibited the slow v.r.p. evoked by saphenous nerve stimulation, whereas another endogenous peptide, calcitonin generelated peptide (0.1-0.5 pM), potentiated the slow v.r.p. The slow v.r.p. was also inhibited by yaminobutyric acid (GABA, 20pM) and muscimol (0.2 pM), and their effects were antagonized by bicuculline (1 pM). 7 The present results suggest that substance P and neurokinin A are involved in the saphenous nerve-evoked C-fibre response in the spinal cord of the newborn rat.
“…Immunohistochemical, autoradiographic and neurochemical studies show that there is a dense concentration of GABA terminals (Miyata & Otsuka, 1975;Barber et al, 1978;Hunt et al, 1981), GABA receptors (Price et al, 1984;Young & Kuhar, 1980), enkephalin-immunoreactive terminals (Hokfelt et al, 1977;Hunt et al, 1981) and opiate receptors (Atweh & Kuhar, 1977) in superficial layers of the dorsal horn. Probably both GABA and enkephalins act as inhibitory neurotransmitters of spinal interneurones in this region.…”
The saphenous nerve-evoked slow v.r.p. was depressed by [Met5] enkephalin (0.1-1 EM), dynorphin (1-13X0.2 gM) and morphine (1-2 pM), and these effects were reversed by naloxone (1 pM).6 Two endogenous peptides, galanin (1-2 pM) and somatostatin (1-2.5 pM), inhibited the slow v.r.p. evoked by saphenous nerve stimulation, whereas another endogenous peptide, calcitonin generelated peptide (0.1-0.5 pM), potentiated the slow v.r.p. The slow v.r.p. was also inhibited by yaminobutyric acid (GABA, 20pM) and muscimol (0.2 pM), and their effects were antagonized by bicuculline (1 pM). 7 The present results suggest that substance P and neurokinin A are involved in the saphenous nerve-evoked C-fibre response in the spinal cord of the newborn rat.
“…In support of a physiological counterpart to these effects of exogenous NT, high concentrations of NTimmunoreactive cell bodies and axon terminals have been detected in the superficial layers of the dorsal horn of the spinal cord (Uhl et al, 1979;Gibson et al, 1981;Hunt et al, 1981;Ninkovic et al, 1981;Seybold and Elde, 1982;Yaksh et al, 1982;Reinecke et al, 1983;Difiglia et al, 1984;Urban and Smith, 1993).…”
Intrathecal administration of the neuropeptide neurotensin (NT) was shown previously to exert antinociceptive effects in a variety of acute spinal pain paradigms including hotplate, tail-flick, and writhing tests. In the present study, we sought to determine whether some of these antinociceptive effects might be elicited via stimulation of low-affinity NTS2 receptors. We first established, using immunoblotting and immunohistochemical techniques, that NTS2 receptors were extensively associated with putative spinal nociceptive pathways, both at the level of the dorsal root ganglia and of the superficial layers of the dorsal horn of the spinal cord. We then examined the effects of intrathecal administration of NT or selective NTS2 agonists on acute thermal pain. Both NT and NTS2 agonists, levocabastine and Boc-Arg-Arg-Pro-Tyr⌿(CH 2 NH)Ile-Leu-OH (JMV-431), induced dose-dependent antinociceptive responses in the tail-flick test. The effects of levocabastine and of JMV-431 were unaffected by coadministration of the NTS1-specific antagonist 2-[(1-(7-chloro-4-quinolinyl)-5-(2,6-dimethoxy-phenyl)pyrazol-3-yl)carboxylamino]tricyclo)3.3.1.1.
3.7)-decan-2-carboxylic acid (SR48692), confirming that they were NTS2 mediated. In contrast, the antinociceptive effects of NT were partly abolished by coadministration of SR48692, indicating that NTS1 and NTS2 receptors were both involved. These results suggest that NTS2 receptors play a role in the regulation of spinal nociceptive inputs and that selective NTS2 agonists may offer new avenues for the treatment of acute pain.
“…It acts as a neuromodulator that inhibits neuronal activity or modulates neurotransmitter release (Beitz et al, 1983;Patel, 1999). This peptide exists in organs processing nociceptive information, such as small dorsal root ganglion (DRG) cells (Rang et al, 1994;Helyes et al, 2000;Carlton et al, 2001), substantia gelatinosa neurons of the spinal dorsal horn (Hunt et al, 1981), intrinsic interneurones or relay neurons of the superficial dorsal horn (Lu and Ho, 1992;Mather and Ho, 1992), and midbrain periaqueductal gray that projects to the medullary nucleus raphe magnus (Beitz et al, 1983;Millhorn et al, 1987). However, the physiological function of SOM in the spinal nociceptive processing has not yet been fully elucidated.…”
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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