Topographic localization of calcitonin gene-related peptide in the rat brain: An immunohistochemical analysis

Kawai, Yoshinori; Takami, Kazumasa; Lee, Yasuhide; Shiosaka, Sadao; Emson, Piers C.; Hillyard, C. J.; MacIntyre, I.; Tohyama, Masaya; Shiotani, Yahe

doi:10.1016/0168-0102(85)90216-0

Cited by 23 publications

(50 citation statements)

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“…23 The presence of a high level of CGRP immunoreactivity has been demonstrated in the central amydaloid, caudate putamen, spinal trigeminal nucleus and tract, substantia gelatinosa, dorsal horn of spinal cord, hypothalamus, and medulla oblongata containing nucleus tractus solitarii in rats. 3 These findings suggest that CGRP might have a crucial role in the regulation of sensory, motor, and autonomic nerve functions. It has been reported that intracerebroventricular administration of CGRP produced a dose-dependent increase in blood pressure and heart rate in rats, which suggested that CGRP might act to modulate the noradrenergic sympathetic outflow in the brain.…”

Section: -2mentioning

confidence: 96%

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Calcitonin gene-related peptide in noradrenergic transmission in rat hypothalamus.

Tsuda¹,

Tsuda²,

Goldstein³

et al. 1992

Hypertension

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In the present study, we examined the regulatory mechanisms of calcitonin gene-related peptide on norepinephrine release in rat hypothalamus. Calcitonin gene-related peptide inhibited the stimulationevoked norepinephrine release from hypothalamic slices of Sprague-Dawley rats in a dose-dependent manner, although the peptide did not affect basal release of norepinephrine. The blockade of the o?2-adrenergic receptors by RX 781094 failed to modulate the inhibitory effects of calcitonin gene-related peptide on norepinephrine release. Pretreatment of slices with islet activating protein, a toxin that interferes with the coupling of the inhibitory receptors to adenylate cyclase, did not affect the suppression of norepinephrine release by calcitonin gene-related peptide. However, Bay K 8644, a dihydropyridinesensitive calcium channel agonist, significantly reversed the inhibitory effects of calcitonin gene-related peptide on norepinephrine release. These results show that calcitonin gene-related peptide might inhibit norepinephrine release in rat hypothalamus, partially mediated by interactions with dihydropyridinesensitive Ca 2+ channels but not by interactions with presynaptic « 2 -adrenergic receptors and inhibitory guanosine triphosphate binding proteins. In immunohistochemical studies, it has been shown that CGRP is widely distributed in both the central and peripheral nervous systems.23 The presence of a high level of CGRP immunoreactivity has been demonstrated in the central amydaloid, caudate putamen, spinal trigeminal nucleus and tract, substantia gelatinosa, dorsal horn of spinal cord, hypothalamus, and medulla oblongata containing nucleus tractus solitarii in rats.3 These findings suggest that CGRP might have a crucial role in the regulation of sensory, motor, and autonomic nerve functions. It has been reported that intracerebroventricular administration of CGRP produced a dose-dependent increase in blood pressure and

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Section: -2mentioning

confidence: 96%

“…Discussion In the present study, we investigated the effects of CGRP on fHJnorepinephrine release in the rat hypothalamus, a region in which both norepinephrine and CGRP are present in abundance. 3 The results show that CGRP inhibited stimulation-evoked […”

Section: Effects Of Calcitonin Gene-related Peptide In Combination Wimentioning

confidence: 99%

Calcitonin gene-related peptide in noradrenergic transmission in rat hypothalamus.

Tsuda¹,

Tsuda²,

Goldstein³

et al. 1992

Hypertension

View full text Add to dashboard Cite

show abstract

“…It is found in high concentration in neurons and fibers of sensory systems (Rosenfeld et al, 1983;Kawai et al, 1985;Skofitsch and Jacobowitz, 1985a;Kruger et al, 1988). It is also present in high concentrations in the AOS nuclei, but, surprisingly, is absent from the other primary visual nuclei (Ribak et al (1997).…”

Section: Calcitonin Gene-related Peptide (Cgrp) Neuropeptide Y (Npy)mentioning

confidence: 99%

The accessory optic system: basic organization with an update on connectivity, neurochemistry, and function

Giolli

Blanks

Lui

2006

Progress in Brain Research

143

123

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The accessory optic system (AOS) is formed by a series of terminal nuclei receiving direct visual information from the retina via one or more accessory optic tracts. In addition to the retinal input, derived from ganglion cells that characteristically have large receptive fields, are direction-selective, and have a preference for slow moving stimuli, there are now well-characterized afferent connections with a key pretectal nucleus (nucleus of the optic tract) and the ventral lateral geniculate nucleus. The efferent connections of the AOS are robust, targeting brainstem and other structures in support of visual-oculomotor events such as optokinetic nystagmus and visual-vestibular interaction. This chapter reviews the newer experimental findings while including older data concerning the structural and functional organization of the AOS. We then consider the ontogeny and phylogeny of the AOS and include a discussion of similarities and differences in the anatomical organization of the AOS in nonmammalian and mammalian species. This is followed by sections dealing with retinal and cerebral cortical afferents to the AOS nuclei, interneuronal connections of AOS neurons, and the efferents of the AOS nuclei. We conclude with a section on Functional Considerations dealing with the issues of the response properties of AOS neurons, lesion and metabolic studies, and the AOS and spatial cognition. The accessory optic system (AOS) is formed by a series of terminal nuclei receiving direct visual information from the retina via one or more accessory optic tracts. In addition to the retinal input, derived from ganglion cells that characteristically have large receptive fields, are direction-selective and have a preference for slow moving stimuli, there are now well characterized afferent connections with a key pretectal nucleus (nucleus of the optic tract) and the ventral lateral geniculate nucleus. The efferent connections of the AOS are robust, targeting brainstem and other structures in support of visual-oculomotor events such as optokinetic nystagmus and visual-vestibular interaction. The present chapter reviews the newer experimental findings while including older data concerning the structural and functional organization of the AOS. We then consider the ontogeny and phylogeny of the AOS and include a discussion of similarities and differences in the anatomical organization of the AOS in nonmammalian and mammalian species. This is followed by sections dealing with retinal and cerebral cortical afferents to the AOS nuclei, interneuronal connections of AOS neurons, and the efferents of the AOS nuclei. We conclude with a section on Functional Considerations dealing with the issues of the response properties of AOS neurons, lesion and metabolic studies, and the AOS and spatial cognition.

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“…In the CNS, CGRP is involved in modulating pain transmission [39]. Kawai et al [40] and Skofitsch and Jacobowitz [41] demonstrated the presence of CGRPpositive cell bodies in the preoptic area and hypothalamus, ventromedial thalamus, medial amygdala, hippocampus, superior colliculus, lateral lemniscus, and dentate gyrus and in Purkinje cells of the cerebellum [42]. The highest densities of neurons expressing the CGRP messenger RNA (mRNA) have been observed in all cranial nuclei with the exception of the dorsal motor nucleus of the vagus nerve (X) [33].…”

Section: Localizationmentioning

confidence: 99%

Targeting CGRP: A New Era for Migraine Treatment

Goldberg

Silberstein

2015

CNS Drugs

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Migraine is a highly prevalent headache disease that typically affects patients during their most productive years. Despite significant progress in understanding the underlying pathophysiology of this disorder, its treatment so far continues to depend on drugs that, in their majority, were not specifically designed for this purpose. The neuropeptide calcitonin gene-related peptide (CGRP) has been indicated as playing a critical role in the central and peripheral pathways leading to a migraine attack. It is not surprising that drugs designed to specifically block its action are gaining remarkable attention from researchers in the field with, at least so far, a safe risk profile. In this article, we highlight the evolution from older traditional treatments to the innovative CGRP target drugs that are revolutionizing the way to approach this debilitating neurological disease. We provide a brief introduction on pathophysiology of migraine and details on the characteristic, function, and localization of CGRP to then focus on CGRP receptor antagonists (CGRP-RAs) and CGRP monoclonal antibodies (CGRP mAbs). Key PointsThe neuropeptide calcitonin gene-related peptide (CGRP) has been indicated as playing a critical role in the central and peripheral pathways leading to a migraine attack.Targeting CGRP as a specific therapeutic tool for migraine may offer similar or even better efficacy than currently available treatments without the vasoconstrictive risk factors.Further studies are necessary to determine the exact role of CGRP receptor antagonists and CGRP monoclonal antibodies in migraine with aura, allodynia, and photophobia.

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Topographic localization of calcitonin gene-related peptide in the rat brain: An immunohistochemical analysis

Cited by 23 publications

References 0 publications

Calcitonin gene-related peptide in noradrenergic transmission in rat hypothalamus.

Calcitonin gene-related peptide in noradrenergic transmission in rat hypothalamus.

The accessory optic system: basic organization with an update on connectivity, neurochemistry, and function

Targeting CGRP: A New Era for Migraine Treatment

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