Capsaicin-induced effects on c-fos expression and NADPH-diaphorase activity in the feline spinal cord

Pilyavskii, A. I.; Maznychenko, A. V.; Maisky, Vladimir A.; Kostyukov, A. I.; Hellström, Fredrik; Windhorst, U.

doi:10.1016/j.ejphar.2005.08.006

Cited by 20 publications

(18 citation statements)

References 46 publications

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“…The laminar distribution of fatigue-evoked c-fos expression in the cervical segments in the study is consistent with sites of location of the spinal neurons activated by nociceptive signals in the lumbar segments after fatiguing stimulation of hindlimb muscles in rat (Pilyavskii et al 2001). The rostrocaudal extent of c-fos expression to the lumbar segments of the spinal cord after stimulation of the neck muscle nociceptors by capsaicin was recently shown in cats (Pilyavskii et al 2005). Previously, it has been reported that the majority of neurons located in superWcial layers and in the neck of the dorsal horn could be implicated into the spino-parabrachio-amygdaloid pathway providing the nociceptive information from skin, muscles, joints and viscera to the amygdala (Bernard et al 1996;Jasmin et al 1997).…”

Section: Discussionsupporting

confidence: 70%

“…Cervical and lumbar segments and forebrains were cut into coronal frozen sections (40 m thick). Fos-immunoreactive (Fos-ir) nuclei of neurons were detected in the various layers of the spinal cord and amygdaloid subnuclei according to the standard avidin-biotin-peroxidase technique (Hsu et al 1981;Pilyavskii et al 2005) using a rabbit polyclonal antibody directed against c-Fos protein (1:2000, Oncogene Note a gradual decline in muscle tension followed by each session of stimulation. At the last (30th) period the tension of trapezius and splenius muscle was reduced to 35 and 30% of the initial values, respectively.…”

Section: Fos Immunohistochemistrymentioning

confidence: 99%

“…The post-fatiguing changes in CNS are presumably initiated predominantly by fatigue-induced inXow of the nociceptive signals from the high-threshold muscle aVerents (Darques and Jammes 1997) including capsaicin-sensitive peripheral terminals of group IV (Kaufman et al 1982). Stimulation of vanilloid receptors (TRPV1) in neck muscles induces deWned patterns of nociceptive signals in the cervical and lumbar spinal cord, thus displaying c-fos expression along the cervico-lumbar direction (Pilyavskii et al 2005). TRPV1 expressing neurons were also observed in all cortical areas and in amygdaloid complex (Mezey et al 2000).…”

Section: Introductionmentioning

confidence: 99%

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Coupling of c-fos expression in the spinal cord and amygdala induced by dorsal neck muscles fatigue

Maznychenko

Pilyavskii

Kostyukov

et al. 2007

Histochem Cell Biol

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c-fos gene expression in the cervical spinal cord and amygdala was examined in anaesthetized rats following muscle fatigue caused by intermittent high-rate (100 s(-1)) electrical stimulation of the dorsal neck muscles (m. trapezius and m. splenius). Fatigue-related increases in c-fos expression were observed on the stimulated muscle side in the cervical C2-C4 (layers 1, 3-5, 7 and 10) spinal segments, bilaterally in the lumbar L4-L6 (layer 1) segments and in contralateral central (Ce), medial (Me), and basomedial (BM) amygdaloid nuclei. A scarce number of staining cells were found within lateral and basolateral nuclei. The rostro-caudal extent of c-fos expression in the spinal cord supports functional coupling of the cervical and lumbar regions during the neck muscle fatigue development. The distinct c-fos expression in the Ce and Me amygdaloid nuclei suggests that they may contribute to mediating the neck muscle fatigue-related nociception, autonomic and behavioural responses.

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Section: Discussionsupporting

confidence: 70%

Section: Fos Immunohistochemistrymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Coupling of c-fos expression in the spinal cord and amygdala induced by dorsal neck muscles fatigue

Maznychenko

Pilyavskii

Kostyukov

et al. 2007

Histochem Cell Biol

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“…In other words, changes were opposite to those evoked by injections of hypertonic NaCl solution into the biceps, i.e., into the muscle directly involved (as an effector) in the reflex. Afferents of the neck muscles have no monosynaptic connections with motoneurons of the flexors and extensors of the elbow joint, but these afferents form numerous ascending and descending polysynaptic projections reaching, in particular, spinal motor centers in the brachial enlargement [22][23][24]. It can be supposed that suppression of the biceps/triceps stretch reflexes was mediated by activation of the above inhibitory descending intersegmental projections.…”

Section: Discussionmentioning

confidence: 99%

Effects of Local and Remote Muscle Pain on Stretch ReflexActivities in the Elbow Joint Flexors and Extensors of Unanesthetized Cats

Tal'nov

2009

Neurophysiology

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In experiments on unanesthetized cats, we compared the effects of experimentally induced pain in the m. biceps brachii or in the neck muscles on EMG activity of the flexors and extensors of the elbow joint (mm. biceps et triceps brachii, respectively) evoked by a passive extension-flexion of the above joint. Muscle pain was induced by injections of 0.5 ml of a hypertonic (7%) NaCl solution into the above-mentioned muscles. In the case of pain in the biceps, i.e., in the muscle directly involved in realization of the reflex, we observed an increase in the amplitude and significant shortening of the latency of EMG responses of this muscle. The amplitude of a short-latency (supposedly monosynaptic) component of the biceps reflex (М1 response) increased by 65%, while an increment of the latter (supposedly polysynaptic) М2 component was 117%. When pain was induced in anatomically remote neck muscles, the stretch reflex in the biceps was considerably suppressed. The maximum amplitudes of the М1 and М2 components decreased by 25 and 30%, respectively, but the latencies of these components decreased significantly, similarly to what was observed in the case of induction of experimental pain in the biceps. Under both conditions of experimental pain, changes in the parameters of EMG responses of the forearm extensor (m. triceps brachii) demonstrated similarity with those of the biceps responses. The maximum effect of pain induction was observed within the first 5 min after injections of the hypertonic solution; full recovery of the stretch reflex parameters was observed on the 20th to 30th min. We conclude that the effects of pain induction on the reflex under study are not generalized. They depend on the site of such induction with respect to the muscle where the stretch reflex is elicited. Unidirectional effects of both types of pain on the antagonist muscles allow us to suppose that modulation of the reflex reactions upon pain induction is mediated by influences from the supraspinal CNS structures. Induction of pain in the biceps increased the amplitude of EMG manifestations of the stretch reflex, while such induction in the neck muscles decreased such responses; nonetheless, in both cases the latency of the reflexes decreased. This fact allows us to believe that the sensitivity of muscle spindles increased under both conditions of the pain influence.

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“…CB1 activation seemed to lead to NO production in several neuronal culture lines and in brain slices (49). Hence, TRPV1 activation in cat dorsal neck muscles increased NADPH-diaphorase activity in the cervical and lumbar spine, thus indicating that activation of peripheral TRPV1 receptors is involved in central plasticity (50). Recently, it was also reported that CB1 activation in N18TG2 neuroblastoma cells resulted in translocation of the ß1 subunit of soluble guanylyl cyclase to the membrane (51).…”

Section: Cross-talk Between Endocannabinoids and Nitric Oxidementioning

confidence: 99%

Unconventional neurotransmitters, neurodegeneration and neuroprotection

Leonelli

Torrão

Britto

2009

Braz J Med Biol Res

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Neurotransmitters are also involved in functions other than conventional signal transfer between nerve cells, such as development, plasticity, neurodegeneration, and neuroprotection. For example, there is a considerable amount of data indicating developmental roles for the glutamatergic, cholinergic, dopaminergic, GABA-ergic, and ATP/adenosine systems. In this review, we discuss the existing literature on these "new" functions of neurotransmitters in relation to some unconventional neurotransmitters, such as the endocannabinoids and nitric oxide. Data indicating both transcriptional and post-transcriptional modulation of endocannabinoid and nitrinergic systems after neural lesions are discussed in relation to the non-conventional roles of these neurotransmitters. Knowledge of the roles of neurotransmitters in brain functions other than information transfer is critical for a more complete understanding of the functional organization of the brain and to provide more opportunities for the development of therapeutical tools aimed at minimizing neuronal death. The endocannabinoid system Endocannabinoids are defined as endogenous ligands of the cannabinoid receptors CB1 and CB2 (1). The basal levels of endocannabinoids are similar in different areas of the brain, including the brainstem, striatum, hippocampus, neocortex, diencephalon, and cerebellum. However, provocative data indicate that there is no direct correlation between the concentration of the endocannabinoids and the expression of the CB1 receptor, which suggests that endocannabinoids could also be involved in other neurotransmitter systems. Actually, it is also known that these compounds can directly modulate several other receptors, such as the serotonergic 5-HT 2 and 5-HT 3 receptors, the glutamatergic N-methyl-D-aspartate (NMDA) receptor, and the transient receptor potential vanilloid type 1 (TRPV1) (2).The first endocannabinoid to be isolated was N-arachidonoylethanolamine, or anandamide, an amide of arachidonic acid with ethanolamine. In 1995, 2-arachidonoylglycerol (2-AG) was discovered, an ester of arachidonic acid with glycerol, which is the most abundant cannabinoid ligand in the central nervous system. Since then, several other lipids, all derived from arachidonic acid, have been shown to modulate the cannabinoid receptors, such as 2-arachidonoylglycerol ether (noladin ether), O-arachidonoylethanolamine (virodhamina), and N-arachidonoyldopamine (3).Both anandamide and 2-AG are synthesized on demand under neuronal stimulation. Anandamide is produced by the enzymes N-acyl-phosphatidylethanolaminehydrolyzing-phospholipase D and is degraded by fatty acid amide hydrolase. 2-AG is synthesized by diacylglycerol

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Capsaicin-induced effects on c-fos expression and NADPH-diaphorase activity in the feline spinal cord

Cited by 20 publications

References 46 publications

Coupling of c-fos expression in the spinal cord and amygdala induced by dorsal neck muscles fatigue

Coupling of c-fos expression in the spinal cord and amygdala induced by dorsal neck muscles fatigue

Effects of Local and Remote Muscle Pain on Stretch ReflexActivities in the Elbow Joint Flexors and Extensors of Unanesthetized Cats

Unconventional neurotransmitters, neurodegeneration and neuroprotection

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