Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The paroxysmal (px) chick is a mutant White Leghorn (Gallus domesticus) which appears normal at hatching and during the subsequent week. By ca. 8 days posthatching, various symptoms develop, of which the most obvious are depressed food intake (anorexia) and audiogenic seizures. Histological evidence suggests that central auditory and vestibular nuclei and fiber tracts begin to degenerate prior to seizure onset. This degeneration, which affects central and peripheral components of both systems, becomes increasingly severe over time although auditory stimulation continues to elicit seizures. Characterization and analysis of peripheral and brainstem auditory response to auditory stimuli indicated that major response differences between px and normal chicks exist in peaks reflecting brainstem activity (P3A, P3B, P4A, P5A). In 5 of 8 px chicks, these later response peaks were either grossly abnormal in terms of amplitude and latency (including amplitude input/output functions) or often entirely absent. Early peaks (P1A and P2A), however, in px waveforms were normal in morphology and amplitude, indicating normal function of peripheral auditory structures. Although lower body temperature of px chicks may account for some of the longer latencies observed, other abnormalities (e.g. absence of peaks) could not be produced in normal birds by induced hypothermia.
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PMID:Peripheral and brainstem auditory function in paroxysmal (px) White Leghorn chicks. 356 41

The present study examined the effects of Dizocilpine (MK-801; a noncompetitive N-methyl-D-aspartate receptor antagonist) on flash-evoked potentials recorded from both the visual cortex (VC) and superior colliculus (SC) of chronically implanted hooded rats. The potentials were recorded at 5, 20, and 35 min following i.p. injections of saline, and of 0.1, 0.3, and 1.0 mg/kg MK-801 on separate days. The amplitude of VC component P1 was unaltered following drug treatment. N1 was increased in amplitude by the 0.1-, 0.3-, and 1.0-mg/kg doses, while two other negative peaks in the VC emerged, beginning with the 0.1-mg/kg dose, to complicate the waveform. One negative peak developed between N1 and P2, while the other effectively split peak P2 (forming P2A and P2B). P2A was depressed at all doses, while P2B was depressed at 0.1 mg/kg but augmented at the 1.0-mg/kg dose. N2 was elevated by the 0.3- and 1.0-mg/kg doses, while P3 was increased in amplitude by all doses. N3 was transiently enhanced by the 0.3-mg/kg dose. SC amplitudes were less affected, with P3 and N4 reduced in amplitude by the 0.3- and 1.0-mg/ kg doses. The latencies of most components in both structures were decreased, often with all doses, but generally at the later recording times. A second experiment demonstrated significant MK-801-induced hyperthermia at all of the above doses, although a higher dose of 3.0 mg/kg MK-801 caused hypothermia. The reduction in component latencies may, therefore, result at least in part from a drug-induced hyperthermia. A third experiment demonstrated MK-801-induced changes in locomotor activity in rats in an open field. The effects were both dose and time dependent. The 0.3-mg/kg dose of MK-801 produced significant increases in the number of line crossings from 20-60 min in comparison to the saline condition. Increases in the number of line crossings with the 1.0-mg/kg dose peaked at 15 min, and then gradually declined. It is unlikely, however, that these changes in movement can account for the effects of MK-801 on evoked potentials. In conclusion, the results show that blockade of the ion channel associated with the NMDA receptor produces profound changes in the activity of the neural pathways that are reflected in the middle components of the flash-evoked potential recorded from the VC.
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PMID:Effects of dizocilpine (MK-801) on flash-evoked potentials, body temperature, and locomotor activity of hooded rats. 1008 Feb 51