Neuroscience
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There is experimental evidence indicating that, in humans, avoiding the concurrent activation of non-nociceptive A beta-fibers is a necessary condition for slower A delta-fiber nociceptive input to elicit reproducible event-related brain potentials (ERPs). Similarly, numerous studies have shown that for unmyelinated C-fiber nociceptive input to elicit ERPs, the concurrent activation of A delta-fibers must be avoided. As studies have shown that expectancy of the stimulus greatly conditions the magnitude of these evoked responses, it was hypothesized that the absence of cortical responses related to A delta- or C-fiber somatosensory input that is shortly preceded by A beta- or A delta-fiber somatosensory input could be explained by the fact that the first-arriving afferents render later-arriving afferents highly expected. ⋯ However, their amplitude was significantly reduced. Furthermore, the amplitude of A beta-fiber vertex potentials was similarly reduced by shortly-preceding A delta-fiber input. As expectancy of the stimulus could not account for this reduction, a new hypothesis was proposed, based on processes related to the perceptual fusion of multisensory inputs.
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Manipulation of glucocorticoid receptor signaling has been shown to alter the acquisition and expression of ethanol-induced locomotor sensitization in mice. It is unknown if other components of the hypothalamic-pituitary-adrenal (HPA)-axis modulate locomotor sensitization resulting from repeated ethanol administration. In the present investigation, we determined if pretreatment with an i.p. injection of CP-154,526, a selective corticotropin releasing factor (CRF) type-1 receptor antagonist, would block the acquisition and/or expression of ethanol-induced locomotor sensitization in male DBA/2J mice. ⋯ These data provide novel evidence that CRF1 receptor signaling modulates the expression of ethanol-induced locomotor sensitization, and add to a growing literature suggesting a role for neurochemicals and hormones associated with the HPA-axis in behavioral sensitization resulting from repeated exposure to drugs of abuse.
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The median preoptic nucleus (MnPO) has been implicated in the regulation of hydromineral balance and cardiovascular regulation. The MnPO also contains neurons that are active during sleep and in response to increasing homeostatic pressure for sleep. The potential role of these neurons in the regulation of arousal prompted an analysis of the efferent projections from the MnPO. ⋯ Few anterogradely labeled appositions were present juxtaposed to choline acetyltransferase-IR somata within the magnocellular preoptic area. The use of retrogradely transported neuroanatomical tracers placed within the prospective efferent terminal fields supported and confirmed findings from the anterograde tracer experiments. These anatomical findings support the hypothesis that MnPO neurons function to promote sleep by inhibition of orexinergic and monoaminergic arousal systems and disinhibition of sleep regulatory neurons in the ventrolateral preoptic area.
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Neuropathic alterations of sensory nerves involved in the mediation of neurogenic inflammation of the meninges may contribute to the increased incidence of headaches in diabetics. In the rat, activation of capsaicin-sensitive nociceptors, which express the transient receptor potential vanilloid type 1 (TRPV1) receptor, induces meningeal vasodilatation, a significant component of neurogenic inflammation, through the release of calcitonin gene-related peptide (CGRP). This study examines the effects of streptozotocin-induced diabetes on TRPV1 receptor-mediated neurogenic sensory vasodilatation, CGRP release and nerve fiber density in the rat dura mater. ⋯ Treatment of the diabetic rats with insulin restored both the vasodilatory response and the capsaicin-induced CGRP release toward control values. In conclusion, this study revealed a marked impairment of meningeal TRPV1-IR nerves in streptozotocin diabetic rats by showing reduced neurogenic sensory vasodilatation, decreased capsaicin-evoked CGRP release and reduction in the number of TRPV1-IR nerve fibers of the dura mater. The findings suggest that capsaicin-sensitive afferents may play an important role in meningeal nociceptor function and their dysfunction, e.g. due to a limited removal of inflammatory mediators and/or tissue metabolites from the meningeal tissue, may contribute to the enhanced incidence of headaches in diabetics.
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Repetition of visually common objects was examined in relation to prior intentional learning and memory status using a delayed match-to-sample task in humans. Both response time and two temporally separate event-related potential (ERP) components indexed repetition. ⋯ Our source localization results indicate that the late and posterior repetition effect in visual cortex is consistent with repetition suppression results reported in monkey physiology and human fMRI studies. Meanwhile, the early and anterior repetition effect, in temporal pole and frontal cortices, is modulated by explicit memory mechanisms.