Diazepam suppression of evoked after-discharges in rat lateral geniculate nucleus and visual cortex.
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Biomedical subjects
Publications and source records attributed to E Eidelberg.
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Monkeys, previously trained to discriminate between "warm" and "cool" stimuli to the skin, were used to test whether the interruption of certain pathways in the spinal cord causes permanet deficits in thermoesthesia. Lesions of the spinothalamic, spinocervical and dorsal funiculi pathways failed to interrupt temperature discrimination, as did also hemisection of the cord. It appears that there is a large safety factor for the conduction of the sensory afferent data singling skin temperature.
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Compression injury of the spinal cord of cats produced increased outflux of potassium from the damaged site. Conduction by large axons in sensory pathways of the spinal cord was blocked partially by bathing the cord in solutions containing potassium concentrations of the order of 50-100 mEq/liter. It is suggested that block by increased K+ concentration in the extracellular space could interfere with long tract function immediately after cord injury before the onset of gross structural changes, and that increased extracellular potassium may be a link in the mechanisms producing thses later changes.
We have studied the interactions between morphine and a dopamine-blocking agent (haloperidol) and a dopamine precursor, L-3,4-dihydroxyphenylalanine (L-dopa). We found that haloperidol potentiated morphine-induced analgesia and enhanced morphine tolerance. Morphine-tolerant mice exhibited enhanced sensitivity to the locomotor excitatory actions of L-dopa. We propose that morphine exerts some of its central nervous actions by first interfering with dopamine-mediated synaptic transmission and then initiating compensatory changes that superficially resemble denervation supersensitivity. These compensatory changes may underlie the excitatory actions of morphine.
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Injection of small quantities of morphine into the cerebral ventricular system of awake, relatively unrestrained, monkeys depressed or abolished operant food-reinforced lever pressing. After repeated injections progressively higher doses of morphine were needed to depress responding. Also, dependence could be demonstrated in these animals by precipitating specific abstinence signs with an antagonist.
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