Brain research
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The suprachiasmatic nucleus (SCN) of the hypothalamus contains the primary circadian pacemaker in both diurnal and nocturnal mammals. The lower subparaventricular zone (LSPV) immediately dorsal to the SCN may also play an important role in the regulation of circadian rhythms. The SCN contains a multitude of oscillator cells that generate circadian rhythms through transcriptional/translational feedback loops involving a set of clock genes including per1 and per2. ⋯ Rhythmic expression of PER1 and PER2 was also seen in the LSPV providing support for the hypothesis that this region might participate in circadian time keeping in the diurnal grass rat. In addition, rhythms were seen lateral to the LSPV and the SCN. Results of this study are discussed in light of similarities and differences in the circadian time-keeping systems of day- and night-active animals.
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Comparative Study
Transhemispheric depolarizations persist in the intracerebral hemorrhage swine brain following corpus callosal transection.
Spontaneous episodes of spreading depression (SD) originating in multiple sources adjacent to a focal intracerebral hemorrhage (ICH) propagate into brain regions away from the lesion site soon after injury onset. Although these transient depolarizations have not been established in the opposite hemisphere of the swine ICH model, we have reported a diminishing of sensory responsiveness in this homotopic brain region following induction of a unilateral hemorrhage lesion. This study examined whether transient depolarizations exist in this distant brain region contralateral to the ICH site. ⋯ These transient depolarizations also persisted throughout 11-h recording period indicating that the corpus callosal transection did not hinder these remote propagating waves of depolarization. The presence of SD in the SI cortices of both hemispheres in all experimental groups of this study suggests that a focal mechanical or hemorrhagic injury increases the susceptibility of distant ipsilateral and contralateral brain regions to depolarizing perturbations. The mechanism for these transient depolarizations in the contralateral hemisphere apparently does not involve transhemispheric propagation along corpus callosal fibers.
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It has been demonstrated that spinal microglial activation is involved in formalin-induced pain and that minocycline, an inhibitor of microglial activation, attenuate behavioral hypersensitivity in neuropathic pain models. We investigated whether minocycline could have any anti-nociceptive effect on inflammatory pain, after intraperitonial administration of minocycline, 1 h before formalin (5%, 50 microl) injection into the plantar surface of rat hindpaw. Minocycline (15, 30, and 45 mg/kg) significantly decreased formalin-induced nociceptive behavior during phase II, but not during phase I. ⋯ Analysis with OX-42 antibody revealed the inhibitory effect of minocycline on microglial activation 3 days after formalin injection. These results demonstrate the anti-nociceptive effect of minocycline on formalin-induced inflammatory pain. In addition to the well-known inhibitory action of minocycline on microglial activation, the anti-edematous action in peripheral tissue, as well as the inhibition of synaptic transmission in SG neurons, is likely to be associated with the anti-nociceptive effect of minocycline.
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Norepinephrine, acting via beta-adrenoceptors, enhances the perforant path-evoked potential in dentate gyrus. Using systemic idazoxan to increase norepinephrine, and paired perforant path pulses to probe early inhibition, previous investigators reported that idazoxan increased initial spike amplitude and increased somatic feedback inhibition. Here, feedback inhibition was re-examined in idazoxan-treated (5 mg/kg) rats under urethane anesthesia. ⋯ Decreased EPSP slope ratios with similar paired pulse intervals have been reported in novel environments. Since exposure to novel environments activates locus coeruleus neurons, norepinephrine may mediate the change in EPSP slope inhibition reported in awake rats. In summary, these results are consistent with the hypothesis that idazoxan potentiates granule cell responses to perforant path input in the dentate gyrus via increases in norepinephrine that lead to beta-adrenoceptor activation, and, further, that idazoxan reduces paired pulse feedback spike facilitation and enhances EPSP slope, but not spike, feedback inhibition.
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The phosphorylated Extracellular Signal-regulated Kinase (pERK) and Fos expression and masticatory muscle activity were analyzed in rats with capsaicin-induced acute inflammation of the tooth pulp in order to clarify the role of the spinal trigeminal nucleus and upper cervical spinal cord in tooth pulp pain. Digastric and masseteric muscle activities were significantly increased following capsaicin injection into the molar tooth pulp but not after vehicle treatment. The pERK-like immunoreactive (LI) neurons were observed in the subnuclei interpolaris-caudalis transition (Vi/Vc) zone, the paratrigeminal nucleus (Pa5) and the superficial laminae of the caudal Vc/C2 zone. ⋯ After capsaicin application into the upper molar tooth pulp, no pERK-LI cells were observed in the ventral part of the Vi/Vc zone, whereas many Fos protein-LI cells were expressed in this region. The difference in the distribution pattern of pERK- and Fos protein-LI cells in the Vi/Vc zone suggests their differential temporal expression profiles after capsaicin. The present findings suggest that tooth-pulp-driven neurons in the spinal trigeminal nucleus are involved in tooth pulp pain through activation of the intracellular signal transduction pathway that involves earlier ERK phosphorylation and subsequent Fos expression.