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Biomedical subjects

W R Adey

Publications and source records attributed to W R Adey.

154 records · Page 9Linked to original sources

Periventricular cerebral impedance after intraventricular injection of calcium.

Injection of small volumes of calcium solution into the lateral ventricle of the cat wa followed by large electrical-impedance changes in gray matter bounding the ventricle, including the caudate nucleus and hippocampus. These changes lasted more than 24 hours and were accompanied by epileptiform electroencephalographic activity. Biweekly injections led to status epilepticus. Injections of similar amounts of magnesium ions were without comparable effects. Possible interactions between calcium ions and intercellular macromolecular material are discussed as a basis for certain impedance shifts in cerebral tissue.

Animals↗

Effects of gravity on the functions of the central nervous system.

The sensitivity of the mammalian central nervous system to gravitational influences involves both direct and indirect factors. Gradual loss of cerebral circulation with increasing acceleration beyond 5 G has been shown to evoke changes in patterns of brain electrical activity, with epileptiform discharges triggered primarily in the hippocampal system of the temporal lobe, and spreading into other brain systems. The relationship of these structures to judgment and discriminative functions is discussed. Complete loss of cerebral circulation is associated with electrical silence in the brain. The possible effects of weightlessness on intracranial fluid distribution are reviewed. Tests of vibrational stimuli in the monkey have disclosed "driving" of electrical brain rhythms at the shaking frequency, particularly in the range from 11 to 15 cycles per second. These effects are unrelated to photic stimulation, and are abolished by anesthesia or death. Tests of discriminative capability at frequencies producing maximum driving have shown increased response latencies and increased errors. The neurophysiological basis for adaptive phenomena in recurrent vestibular stimulation has been found to reside partly in the vestibular nuclei of the medulla, and not to require integrity of connections with higher vestibular centers. The potentiation of responsiveness to vestibular stimulation in the weightless state has been shown to have a basis in the exaggerated responsiveness of medullary vestibular centers following loss of proprioceptive influxes from the spinal cord. The possible contribution of weightlessness to anomalous psychophysiological functions is reviewed. This area presents a major challenge in experimental design, and may require evaluation of such phenomena as distortion of the body image, modified sleep patterns and changes in optimal sleep-work cycles.

Acceleration↗

Induction of delayed synchronized bursts in hippocampal slices by weak sine-wave stimulation; role of the NMDA receptor.

Weak (20-50 microA) sine-wave stimulation at 60 Hz (SWS) of either the mossy fibers or the Schaffer collaterals promoted epileptiform synchronized bursts in the CA2/3 area of rat hippocampal slices in the absence of epileptogenic agents. Following brief SWSs (2-10 sec every 5 min), delayed synchronized bursts (DSBs) were triggered by weak test pulses in either pathway and transmitted to CA1. The long (2-10 sec) refractory periods which followed synchronized bursts in CA2/3 limited their rate of occurrence. Furthermore, SWS decreased the activity for several minutes in slices that exhibited frequent bursts. DSBs were reversibly blocked by perfusion with the N-methyl-D-aspartate (NMDA) specific antagonist DL-2-amino-5-phosphono-valeric acid (APV). The involvement of NMDA receptors was further suggested by the facilitation of CA2/3 synchronized bursts in medium with NMDA (5 microM) or lacking magnesium, and by iontophoresis of NMDA in the CA2/3 stratum radiatum. The findings that SWS-induced DSBs persisted for hours in undisturbed slices, and that bursts abolished by APV reappeared during washout in control solution, suggest long-term changes in the CA2/3 synaptic region.

2-Amino-5-phosphonovalerate↗