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Capsaicin desensitization induces atrophy of brown adipose tissue in rats.
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Interscapular brown adipose tissue (BAT) of capsaicin-desensitized (Cap-Des) rats is atrophied, having a lower wet weight, a reduced total protein content, and as little as 10% of the normal content of uncoupling protein (UCP). Because the mitochondrial concentration of UCP, relative to other
Capsaicin treatment induces selective sensory degeneration and increased sympathetic innervation in the rat ureter.
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Quantitative immunohistochemistry was used to study the innervation of the ureter in adult rats pretreated with capsaicin as neonates (50 mg/kg) or as adults (100-150 mg/kg, 10-22 days prior to being killed) using antibodies against protein gene-product 9.5, neuron-specific enolase, substance P,
Rapid but transient atrophy of brown adipose tissue in capsaicin-desensitized rats.
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Our previous studies showed atrophy of brown adipose tissue (BAT) in capsaicin-desensitized rats during the period 11-28 days after injections [Cui et al., Am. J. Physiol. 259 (Regulatory Integrative Comp. Physiol. 28): R324-R332, 1990]. The objective of the present studies was to assess the
Prior optic nerve transection reduces capsaicin-induced degeneration in rat subcortical visual structures.
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Capsaicin is a neurotoxin capable of causing degeneration in specific sites throughout the neuraxis, including the suprachiasmatic nucleus (SCh), the ventrolateral geniculate nucleus (VLG), the intergeniculate leaflet (IGL), and the olivary and medial pretectal nuclei (OPT and MPT). In this
Changes in features of degenerating primary sensory neurons with time after capsaicin treatment.
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Capsaicin (50 mg/kg) was injected into new born mice and 5 and 12 h, and 1, 2, 3, and 5 days later, their lumbar dorsal root ganglia (DRG) with the nerve roots were fixed by immersion. The morphological changes which ensued with time after treatment were examined by light and electron microscopy.
Degeneration of capsaicin sensitive sensory nerves enhances myocardial injury in acute myocardial infarction in rats.
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BACKGROUND
Evidence indicated an involvement of afferent nerves in the pathology of acute myocardial infarction. This study was undertaken to clarify the role and mechanisms by which the sensory afferent degeneration exacerbates the myocardial injury in acute myocardial infarction in
Selective degeneration of chemosensitive primary sensory neurones induced by capsaicin: glial changes.
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Capsaicin treatment of newborn rats results in the degeneration of primary sensory neurones involved in the mediation of chemogenic pain. In the present study glial changes following the pharmacologically-induced degeneration of unmyelinated primary afferent fibres terminating in Rexed's laminae I
Physiological and pathological characterization of capsaicin-induced reversible nerve degeneration and hyperalgesia.
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The study aimed to investigate the physiology, psychophysics, pathology and their relationship in reversible nociceptive nerve degeneration, and the physiology of acute hyperalgesia.
We enrolled 15 normal subjects to investigate intraepidermal nerve fibre (IENF) density, contact heat-evoked
Capsaicin-induced neuronal degeneration: silver impregnation of cell bodies, axons, and terminals in the central nervous system of the adult rat.
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Capsaicin is a neurotoxic substance valued in neurobiological research because of its ability to selectively damage small unmyelinated primary sensory neurons. Previous work has indicated that systemic capsaicin administration causes permanent neuronal degeneration in neonatal rats, but evidence
Degeneration of axons in the ureteric and duodenal nerve plexuses of the adult rat following in vivo treatment with capsaicin.
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The fine structure of the ureteric and duodenal nerve plexuses was studied in specimens taken from adult rats 24 h after subcutaneous injection of 50 mg/kg capsaicin and in specimens taken from rats injected with the vehicle used to emulsify the capsaicin. In specimens from capsaicin-treated rats,
Intracisternal capsaicin: selective degeneration of chemosensitive primary sensory afferents in the adult rat.
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The present study reports that intracisternal administration of capsaicin induces the selective degeneration of chemosensitive primary sensory afferents and results in a practically complete abolition of chemical pain sensitivity in the adult rat. This treatment, however, failed to affect neurogenic
Transganglionic degeneration of capsaicin-sensitive C-fiber primary afferent terminals.
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Local treatment of rat peripheral nerves with capsaicin induces permanent impairment of afferent C-fiber functions and changes in the response properties of spinal dorsal horn neurons. In this study a new experimental approach, the "capsaicin gap" technique, has been utilized in an attempt to
Capsaicin-induced neuronal degeneration in the brain and retina of preweanling rats.
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Capsaicin is a neurotoxin known for its ability to cause degeneration of small unmyelinated primary sensory neurons in both spinal and cranial nerves. Although lower motor neurons do not degenerate following capsaicin treatment, the extent to which capsaicin may damage neurons in the brain has not
Age-related changes in capsaicin-induced degeneration in rat brain.
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Previous results indicate that the pattern of capsaicin-induced degeneration in the rat central nervous system is age-related. Experiments utilizing capsaicin's selective neurodegenerative effects to study the function of central neural circuits will therefore require a detailed understanding of
Degeneration of infrared receptor terminals of snakes caused by capsaicin.
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Capsaicin, the main pungent ingredient in hot peppers (genus Capsicum), caused degeneration of the infrared receptor terminals in infrared sensitive snakes, Trimeresurus flavoviridis, when it was applied perineurally to a branch of the trigeminal nerve. The degeneration of the terminals was found 6
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