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Anticonvulsant and anesthetic barbiturates

Different postsynaptic actions in cultured mammalian neurons

Laboratory of Developmental Neurobiology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, and the Department of Neurology, University of Virginia School of Medicine, Charlottesville, Virginia (Dr. Macdonald); and the Laboratory of Neurophysiology, National Institute of Neurological and Communicative Disorders and Stroke, Bethesda, Maryland (Dr. Barker).

Mammalian spinal cord neurons were grown in dissociated cell culture and used to study the effects of the anticonvulsant barbiturates phenobarbital and mephobarbital, and the anesthetic barbiturates pen-tobarbital, secobarbital, and 1,3-dimethyl-butylethyl barbituric acid on amino acid responses and neuronal membrane properties. All barbiturates augmented responses to GABA and diminished glutamate (GLU) responses, but the anesthetic barbiturates were more potent. The anesthetic barbiturates directly depressed excitability by increasing membrane conductance, an effect reversed by the GABA antagonists picrotoxin and penicillin. Anticonvulsant barbiturates, however, had only minimal GABA-mimetic inhibitory action at high doses. Modulation of synaptic events mediated by GABA and GLU might contribute to barbiturate anticonvulsant activity; and direct GABA-mimetic inhibition, combined with similar modulation of synaptic transmission, might underlie barbiturate anesthesia.

Dr. Macdonald's address is The University of Michigan, Department of Neurology, Neuroscience Laboratory Building, 1103 East Huron, Ann Arbor, MI 48109.

Presented in part at the annual meeting of the Society for Neuroscience, Anaheim, California, November 1977, and as the S. Weir Mitchell Award Paper at the thirtieth annual meeting of the American Academy of Neurology, Los Angeles, California, April 1978.

Accepted for publication August 16, 1978.

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