Jacob N. Young

Block of (Na+,K+)ATPase with ouabain induces spreading depression-like depolarization in hippocampal slices

We used ouabain (100 microM) to block Na+,K(+)ATPase of in vitro rat hippocampal slices. This treatment was sufficient to cause the sudden depolarization that is the hallmark of both spreading depression (SD) and of the SD-like anoxic depolarization (AD). This depolarization was accompanied by a large and sudden increase in [K](o), also reminiscent of that observed during both SD and AD. Ouabain-induced SD did not require a complete inactivation of Na+,K(+)ATPase, as it occurred when the enzyme was still capable of providing recovery of both V(o) and [K](o). The data indicate that functional inactivation of Na+,K(+)ATPase per se initiates events that lead to an SD-like AD. This ouabain-induced depolarization was not affected by block of synaptic transmission, instead it was abolished by hyperosmolarity of the extracellular space. The possible relevance of these findings to the pathophysiology of AD is discussed.

Ion channel involvement in hypoxia-induced spreading depression in hippocampal slices

Rat hippocampal tissue slices were made hypoxic in control medium and in medium containing the ion channel blockers tetraethylammonium (TEA), 4-aminopyridine (4-AP), or tetrodotoxin (TTX). Postsynaptic evoked potentials, extracellular DC potential Vec, and in some experiments extracellular potassium concentration [K+]o were monitored in stratum pyramidale of the CA1 region. TEA (10 mM) decreased the latency of hypoxia-induced spreading depression (SD), and reduced the amplitudes of the changes in Vec and [K+]o. 4-AP (50 microM) also decreased the latency of SD but had no effect on the Vec shift. In most slices, TTX (1 microM) increased SD latency but had no effect on the Vec shift. In some slices, TTX blocked the occurrence of SD.

Solitary eosinophilic granuloma invading the clivus of an adult: case report.

A 41-year-old white man with facial pain and diplopia was found to have an invasive lesion of the clivus. The final pathological diagnosis was eosinophilic granuloma. The patients symptoms resolved completely after transsphenoidal resection of the lesion. The pathological and radiological diagnosis and the treatment of solitary eosinophilic granulomas are discussed.

Calcium, magnesium, and long-term recovery from hypoxia in hippocampal tissue slices

Ortho- and antidromic responses recovered and remained robust for 5 h in slices exposed to transient hypoxia in low calcium, while responses remained depressed in slices made hypoxic in normal calcium. Elevating magnesium in addition to reducing calcium did not improve recovery compared to reducing calcium alone. Spreading depression-like hypoxic depolarization occurred earlier in low calcium than in control fluid. We conclude that loss of function was triggered by calcium uptake by neurons and not by cell swelling, and that activation of NMDA receptors probably played no part.

Deafferentation syndrome in the rat: effects of sex, age, and lesion type.

A deafferentation syndrome can be produced in Sprague-Dawley rats following dorsal root sections. The behavior may be objective evidence of dysesthesias, thus serving as an experimental model to study chronic dysesthesias caused by deafferentation in humans. This article examines the effects of sex, age, and lesion type on the expression of the deafferentation syndrome in Sprague-Dawley rats. No significant differences were found in the expression of the deafferentation syndrome with respect to age and weight in male rats within the ranges studied. Sex and lesion type did alter the expression of the syndrome.

The expression of a deafferentation syndrome in the Sprague-Dawley rat : effects of frontoparietal cortical lesions

&NA; Forelimb sensorimotor (SMI) cortical lesions in the rat have been found to suppress a deafferentation syndrome which follows C5‐T2 ganglionectomy/avulsion whether the cortical lesions were made prior to, or several days after, the dorsal root lesions. None of the 6 rats with only frontoparietal lesions developed a deafferentation syndrome. These results may be influenced by the presence of a sensorimotor amalgam in the parietal cortex of the rat.