Neuroscience
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Entrainment of the circadian pacemaker in the suprachiasmatic nucleus is accomplished by two neural pathways, the retinohypothalamic and geniculohypothalamic tracts. The geniculohypothalamic tract, which originates from the intergeniculate leaflet and a portion of the ventral lateral geniculate nucleus, is composed of fibers immunoreactive to neuropeptide Y. To assess the processing of photic information by the geniculohypothalamic tract, neuropeptide Y immunoreactivity in the suprachiasmatic nucleus of rats kept under various external lighting conditions was determined by enzyme immunoassay of micropunched tissues. ⋯ This observation indicates that the photic pathway utilizing neuropeptide Y may be functional only when the endogenous circadian rhythm is synchronized to external light and dark cycles. Administration of an excitatory amino acid antagonist (MK-801) blocked the increase of neuropeptide Y by light, while an agonist (N-methyl-D-aspartate) induced similar facilitatory effects to that of light on the neuropeptide Y level in the rat suprachiasmatic nucleus. These results suggest that the geniculohypothalamic tract processes photic information so as to facilitate distinction of the transition between light and darkness that occurs either at subjective dawn or dusk.
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Intracellular recordings from neurons in the dorsal root ganglion and dorsal horn, in an in vitro spinal cord-dorsal root ganglion preparation, were used to investigate the role of large and small afferent fibers in the sensory synaptic transmission of the superficial dorsal horn. Raising the extracellular potassium concentration from 3.1 to 25-50 mM in the dorsal root ganglion compartment evoked a large amplitude depolarization and blocked action potentials in the large neurons of dorsal root ganglion, and it synaptically excited dorsal horn neurons. Excitatory postsynaptic potentials that were evoked by electrical stimulation of large myelinated fibers, but not those evoked by activation of small unmyelinated fibers, were blocked by the potassium treatment of the dorsal root. ⋯ During the period of capsaicin desensitization, synaptic activation of dorsal horn neurons by application of high potassium to the dorsal root ganglion and electrical stimulation of slow fibers was blocked. The opioid receptor agonist (D-Ala2, D-Leu5)-enkephalinamide (1 microM), applied to the spinal cord slice, abolished the dorsal horn neuron excitation evoked by electrical or chemical activation of slow primary afferent fibers. These findings indicate that high concentrations of K+ applied to the dorsal root ganglia selectively activate a primary afferent input to the dorsal horn, which is capsaicin sensitive and tetrodotoxin resistant.
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gamma-Hydroxybutyric acid is a naturally occurring compound which induces bilaterally synchronous spike and wave discharges in rats. The gamma-hydroxybutyric acid model of absence seizures simulates clinical absence seizures behaviorally as well as electrographically. The present study was undertaken in order to establish the role of the high-affinity gamma-hydroxybutyric acid binding sites in the generation of gamma-hydroxybutyric acid-induced spike and wave discharges. ⋯ The CA3 field or dorsal hippocampus possesses the highest density of [3H]gamma-hydroxybutyric acid binding sites of all brain regions. However, no significant change in [3H]gamma-hydroxybutyric acid binding was observed in this region nor was the CA3 field involved in the generation of spike and wave discharges during gamma-hydroxybutyric acid-induced absence-like seizures. These findings confirm that gamma-hydroxybutyric acid-induced absence-like seizures originate from thalamocortical pathways and that the onset of gamma-hydroxybutyric acid-induced spike and wave discharges is directly related to the regulation of gamma-hydroxybutyric acid binding sites in those regions which constitute the involved thalamocortical loop.
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The rostral ventral medulla has been shown to consist of three distinct subregions: the midline or raphé region, the lateral paragigantocellular-gigantocellular region and the rostro-ventrolateral reticular nucleus. All three regions have been shown to contribute to central vaso-regulation and to project towards sympathetic preganglionic neurons of the thoracic spinal cord. Therefore it is of particular interest to describe the interconnections between the three regions and to see if local afferents reach cells which have been implicated in the regulation of descending inputs. ⋯ The results of the present light microscopic tract-tracing study revealed a different pattern of the intramedullary projection of the lateral paragigantocellular-gigantocellular region and the rostroventrolateral reticular nucleus. These data are in support of the proposed parcellation of the two cytoarchitectonically different areas of the rostral ventrolateral medulla into two functionally distinct subdivisions. Furthermore, the direct anatomical connection revealed in the present study between cells of the rostral ventrolateral and ventromedial medulla oblongata indicates the possibility that vasoregulatory effects of some cells of the rostral ventrolateral medulla oblongata might be executed via direct projections onto serotonin-immunoreactive cells of the medullary raphé nuclei.
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The kynurenine pathway metabolites quinolinic acid and kynurenic acid have been hypothetically linked to the occurrence of seizure phenomena. The present immunohistochemical study reports the activation of astrocytes containing three enzymes responsible for the metabolism of quinolinic acid and kynurenic acid in a rat model of chronic epilepsy. Rats received 90 min of patterned electrical stimulation through a bipolar electrode stereotaxically positioned in one hippocampus. ⋯ In the hippocampus, the number of immunoreactive glial cells increased in parallel to the hypertrophic responses. In addition, pronounced increases in immunoreactivities, associated with hypertrophied astrocytes, occurred around lesioned sites in the thalamus and piriform cortex. These findings indicate that kynurenine metabolites derived from glial cells may play a role in chronic epileptogenesis.