Orofacial pain increases mRNA level for galanin in the trigeminal nucleus caudalis of the rat

Tokunaga, Atsushi; Senba, Emiko; Manabe, Yozo; Shida, Toru; Ueda, Yutaka; Tohyama, Masaya

doi:10.1016/0196-9781(92)90007-p

Cited by 16 publications

(11 citation statements)

References 34 publications

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“…It is worthwhile to point out that the enhancement of NPY mRNA appears as pronounced as that of dynorphin. The changes in peptide and in mRNA levels after inflammation were confined to the ipsilateral side, and therefore the noninjected side of spinal cord and DRG could be used as a control together with control rats, which is also consistent with many previous reports (Ruda et al, 1988;Noguchi et al, 1989; Dubner and Ruda, 1992;Tokunaga et al, 1992;Hanesch et al, 1993). Finally, the increase in the expression of c-Fos protein ulation and confirms several earlier studies (Hunt et al, 1987; in the ipsilateral laminae I, II, and V, where the majority of Presley et al, 1990;Noguchi et al, 1991;Hylden et al, 1992;Leah et al, 1992).…”

Section: Discussionsupporting

confidence: 75%

“…Accompanying these behavioral changes are alterations in the discharge properties ofafferent fibers and neurons in the CNS (Neugebauer and Schaible, 1990;Dubner and Ruda, 1992), as well as changes in levels of messenger molecules. Thus, it has been shown that peripheral inflammation induces upregulation of the synthesis of opioid peptides Noguchi et al, 1988;Ruda et al, 1988; see also Dubner and Ruda, 1992;Weihe et al, 1993), substance P (SP) (Noguchi et al, 1988) calcitonin gene-related peptide (CGRP) (Hanesch et al, 1993), glutamate (Sluka et al, 1992), NADPH-diaphorase (Solodkin et al, 1992), GABA (Castro-Lopes et al, 1992) and galanin (Tokunaga et al, 1992). Unilateral inflammation also evokes an increase in the dorsal horn expression of c-j& proto-oncogene (Hunt et al, 1987;Presley et al, 1990;Noguchi et al, 1991;Hylden et al, 1992;Leah et al, 1992).…”

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confidence: 99%

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Expression of neuropeptide Y and neuropeptide Y (Y1) receptor mRNA in rat spinal cord and dorsal root ganglia following peripheral tissue inflammation

et al. 1994

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By using in situ hybridization histochemistry and immunohistochemistry, neuropeptide Y (NPY) and NPY (Y1) receptor mRNA as well as NPY-like immunoreactivity were examined in the lumbar spinal cord (L4-L5) and in dorsal root ganglia (DRG, L5) in rats injected with complete Freund's adjuvant (CFA) into the hindpaw. A rapid and marked increase in NPY mRNA expression was observed in ipsilateral dorsal horn neurons 6 hr after inoculation as compared to the contralateral side. This was mainly found in the medial part of spinal lamina II. The peak level (88% increase) was reached at 3 d. In adjacent sections of the spinal cord, 96% and 33% increases were found in the number of dynorphin and enkephalin mRNA-positive neurons, respectively. Unilateral inflammation also induced a moderate increase in NPY-like immunoreactivity and the number of NPY-immunoreactive neurons in the medial part of the ipsilateral spinal dorsal horn. In addition, a marked elevation in the expression of c-Fos-like protein was observed in ipsilateral spinal neurons in laminae I, II, and V. However, no NPY mRNA-positive or NPY- immunoreactive neurons were found in the ipsilateral and contralateral DRGs in rats receiving CFA injection. Furthermore, a marked upregulation of NPY (Y1) receptor mRNA expression was detected in the ipsilateral spinal dorsal horn 1 d and 3 d after inoculation. These Y1 receptor mRNA-positive cells were mainly distributed in the medial laminae II and III. Numerous Y1 mRNA-positive, small neuron profiles were found bilaterally in the DRGs in CFA-treated rats. CFA evoked a 34% increase in the number of Y1 mRNA-positive neurons in ipsilateral DRGs as compared to contralateral DRGs. The distinct upregulation of NPY and NPY (Y1) receptor in response to peripheral inflammation suggests an involvement of NPY in the response to inflammation and in nociception.

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Section: Discussionsupporting

confidence: 75%

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confidence: 99%

Expression of neuropeptide Y and neuropeptide Y (Y1) receptor mRNA in rat spinal cord and dorsal root ganglia following peripheral tissue inflammation

et al. 1994

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“…However, in this model, galanin peptide levels have been shown to decrease in spinal cord by 28 days (Qinyang et al, 2004). Galanin is released into the spinal cord of rats with ankle inflammation (Hope et al, 1994;Garry et al, 2005), and inflammatory orofacial pain increases galanin in the trigeminal nucleus caudalis (Tokunaga et al, 1992). The peptide is also present in neurons innervating the Achilles tendon in a rupture model (Ackermann et al, 2003).…”

Section: Galanin Family Peptides and Receptorsmentioning

confidence: 99%

“…126 2011, 2012), chronic constriction nerve injury (Nahin et al, 1994), orofacial pain (Tokunaga et al, 1992), exercise (Legakis et al, 2000), electroconvulsive stimulation (Christiansen, 2011), and herpes simplex virus infection (Henken and Martin, 1992).…”

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confidence: 99%

Physiology, Signaling, and Pharmacology of Galanin Peptides and Receptors: Three Decades of Emerging Diversity

et al. 2014

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“…The studies have primarily used immunocytochemical methods or the application of chemicals having an agonist or antagonist action on an endogenous neurochemical. For example, the presence of these neurochemicals, or of cell receptors for them, has been documented in the VBSNC (especially the subnucleus caudalis) and spinal dorsal horn or in the central sites from which inhibitory influences on nociceptive transmission can be elicited, and application of these neurochemicals or their agonists to different components of the VBSNC can suppress the activity of nociceptive neurons or nociceptive behavior (Tokunaga et al, 1992;Salter et al, 1993;Grudt et al, 1995;Travagli, 1996; and see Gobel et al, 1982;Dubner and Bennett, 1983;Sessle, 1987Sessle, , 1996Johnson et al, 1991). The descending modulatory inputs to the VBSNC may exert their inhibitory effects on nociceptive transmission by the release of certain of these neurochemicals from their endings within the VBSNC (e.g., release of enkephalin or 5-HT from their terminals within the subnucleus caudalis).…”

Section: Associated Neurochemical Mechanismsmentioning

confidence: 99%

Acute and Chronic Craniofacial Pain: Brainstem Mechanisms of Nociceptive Transmission and Neuroplasticity, and Their Clinical Correlates

Sessle

2000

Critical Reviews in Oral Biology & Medicine

614

541

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This paper reviews the recent advances in knowledge of brainstem mechanisms related to craniofacial pain. It also draws attention to their clinical implications, and concludes with a brief overview and suggestions for future research directions. It first describes the general organizational features of the trigeminal brainstem sensory nuclear complex (VBSNC), including its input and output properties and intrinsic characteristics that are commensurate with its strategic role as the major brainstem relay of many types of somatosensory information derived from the face and mouth. The VBSNC plays a crucial role in craniofacial nociceptive transmission, as evidenced by clinical, behavioral, morphological, and electrophysiological data that have been especially derived from studies of the relay of cutaneous nociceptive afferent inputs through the subnucleus caudalis of the VBSNC. The recent literature, however, indicates that some fundamental differences exist in the processing of cutaneous vs. other craniofacial nociceptive inputs to the VBSNC, and that rostral components of the VBSNC may also play important roles in some of these processes. Modulatory mechanisms are also highlighted, including the neurochemical substrate by which nociceptive transmission in the VBSNC can be modulated. In addition, the long-term consequences of peripheral injury and inflammation and, in particular, the neuroplastic changes that can be induced in the VBSNC are emphasized in view of the likely role that central sensitization, as well as peripheral sensitization, can play in acute and chronic pain. The recent findings also provide new insights into craniofacial pain behavior and are particularly relevant to many approaches currently in use for the management of pain and to the development of new diagnostic and therapeutic procedures aimed at manipulating peripheral inputs and central processes underlying nociceptive transmission and its control within the VBSNC.

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Orofacial pain increases mRNA level for galanin in the trigeminal nucleus caudalis of the rat

Cited by 16 publications

References 34 publications

Expression of neuropeptide Y and neuropeptide Y (Y1) receptor mRNA in rat spinal cord and dorsal root ganglia following peripheral tissue inflammation

Expression of neuropeptide Y and neuropeptide Y (Y1) receptor mRNA in rat spinal cord and dorsal root ganglia following peripheral tissue inflammation

Physiology, Signaling, and Pharmacology of Galanin Peptides and Receptors: Three Decades of Emerging Diversity

Acute and Chronic Craniofacial Pain: Brainstem Mechanisms of Nociceptive Transmission and Neuroplasticity, and Their Clinical Correlates

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