Neuroscience
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Comparative Study
Activation of lateral hypothalamic neurons stimulates brown adipose tissue thermogenesis.
The lateral hypothalamic area, containing orexin neurons, is involved in several aspects of autonomic regulation, including thermoregulation and energy expenditure. To determine if activation of lateral hypothalamic area neurons influences sympathetically-regulated thermogenesis in brown adipose tissue, we microinjected bicuculline (120 pmol, 60 nl, unilateral) into the lateral hypothalamic area in urethane/chloralose-anesthetized, artificially-ventilated rats. ⋯ Subsequent microinjections of glycine (30 nmol, 60 nl) to inhibit local neurons in raphe pallidus or in dorsomedial hypothalamus or of glutamate receptor antagonists into dorsomedial hypothalamus promptly reversed the increases in brown adipose tissue sympathetic nerve activity, brown adipose tissue temperature and heart rate evoked by disinhibition of neurons in lateral hypothalamic area. We conclude that neurons in the lateral hypothalamic area can influence brown adipose tissue sympathetic nerve activity, brown adipose tissue thermogenesis and heart rate through pathways that are dependent on the activation of neurons in dorsomedial hypothalamus and raphe pallidus.
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The corticospinal tract is widely used to study regeneration and is essential for voluntary movements in humans. In young rats, corticospinal axons on the uninjured side sprout and grow into the denervated side. Neurotrophin-3 (NT-3) induces such crossed collateral sprouting in adults. ⋯ NT-3 caused sprouting of local calcitonin gene-related peptide-positive fibers. These results suggest that NT-3 reduces collateral sprouting of spared corticospinal axons from within the denervated regions, possibly because of the injury environment or by increasing sprouting of local afferents. They identify an unexpected context-dependent outgrowth inhibitory effect of NT-3.
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Nerve injury resulting in chronic pain is associated with novel excitatory effects of norepinephrine on injured peripheral nerve terminals and their cell bodies, due to actions on alpha2-adrenoceptors. Paradoxically, alpha2-adrenoceptor agonists administered near peripheral terminals or their cell bodies results in analgesia, not pain. This study tested, using intracellular Ca2+ response to stimulation, the effects of alpha2-adrenoceptor agonists on injured sensory neurons and classified their neuronal phenotype. ⋯ Spinal nerve ligation resulted in a 4-10-fold increase in the percentage of clonidine inhibited cells which immunostained for calcitonin gene-related peptide. These data are consistent with the known inhibition of Ca2+ currents by alpha2-adrenoceptors and suggest that, at the level of intracellular Ca2+, the key determinant of neurotransmitter release, alpha2-adrenoceptors are inhibitory after nerve injury, not excitatory. There is a shift in phenotype of sensory neurons which are inhibited by clonidine after nerve injury, which may explain clonidine's increased potency in the treatment of neuropathic compared with acute pain.
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Comparative Study
Influence of feeding status on neuronal activity in the hypothalamus during lipopolysaccharide-induced anorexia in rats.
Fasting attenuates disease-associated anorexia, but the mechanisms underlying this effect are not well understood. In the present study, we investigated the extent to which a 48 h fast alters hypothalamic neuronal activity in response to the anorectic effects of lipopolysaccharide in rats. Male rats were fed ad libitum or fasted, and were injected with i.p. saline or lipopolysaccharide (250 microg/kg). ⋯ Lipopolysaccharide-induced circulating levels of interleukin-1 were similar across feeding status. Finally, fasting, but not lipopolysaccharide, affected circulating level of leptin and appetite-related neuropeptides expression in the arcuate nucleus. Together, our data show that fasting modulates lipopolysaccharide-induced anorexia and body weight loss in association with neural changes in specific hypothalamic nuclei.
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Comparative Study
Cortical processing of visceral and somatic stimulation: differentiating pain intensity from unpleasantness.
Visceral and somatic pain perception differs in several aspects: poor localization of visceral pain and the ability of visceral pain to be referred to somatic structures. The perception of pain intensity and affect in visceral and somatic pain syndromes is often different, with visceral pain reported as more unpleasant. To determine whether these behavioral differences are due to differences in the central processing of visceral and somatic pain, non-invasive imaging tools are required to examine the neural correlates of visceral and somatic events when the behavior has been isolated and matched for either unpleasantness or pain intensity. ⋯ Visceral stimuli induced deactivation of the perigenual cingulate bilaterally with a relatively greater activation of the right anterior insula-i.e. regions encoding affect. Somatic pain induced left dorso-lateral pre-frontal cortex and bilateral inferior parietal cortex activation i.e. regions encoding spatial orientation and assessing perceptual valence of the stimulus. We believe that the observed patterns of activation represent the differences in cortical process of interoceptive (visceral) and exteroceptive (somatic) stimuli when matched for unpleasantness.