Acute effects of ethanol on spontaneous and auditory evoked electrical activity in cat brain

Changes in voltage‐operated calcium channels modify ethanol withdrawal hyperexcitability in mouse hippocampal slices

“…This syndrome is typified by the occurrence of phases of tremor, hyperreflexia and both tonic and clonic convulsions, indicating an increase in central nervous system (CNS) excitability in vivo. Electroencephalographic studies in rodents have demonstrated that this hyperexcitability is seen throughout the CNS (Perrin, Hockman, Kalant & Livingston, 1975), suggesting that epileptiform activity during ethanol withdrawal is caused by hyperexcitability in neurones throughout the brain. Work on specific brain regions, isolated from animals after chronic ethanol treatment, has demonstrated that the activity of neurones in discrete brain regions is altered during ethanol withdrawal, independently from other CNS structures.…”

Auditory brain stem potentials with alcohol

“…Ethyl alcohol is known to be associated with a decrease in the amplitudes of sensory evoked potentials, particularly those originating from association areas of the cortex (Schweigerdt et al 1965;Gross et al 1966;Himwich et al 1966;DiPerri et al 1968; Lewis et al 1969Lewis et al , 1970Soveri and Fruhstorfer 1969;Begleiter et al 1972;Himwich and Callison 1972;Salamy and Williams 1973;Kalant 1974;Perrin et al 1974;Grenell 1975;Rhodes et al 1975;Obitz etal. 1977;Kopell et al 1978).…”

The Pharmacology of Sedative/Hypnotics, Alcohol, and Anesthetics: Sites and Mechanisms of Action

“…Under such circumstances, tolerance is seen in man and animals in a few days, e.g., for behavioral and EEG effects in monkeys (HOGANS et al, 1961;STORY et al, 1961), operant behavior in rats (LESTER, 1961), motor behavior in dogs (MAYNERT and KLINGMAN, 1960) and in rats see also EBERT et al, 1964;CICERO et al, 1971;RATCLIFFE, 1969); the behavioral effects reportedly exhibit greater tolerance than the effects on the EEG (HOGANS et al, 1961). Acute tolerance has also been reported for EEG actions of ethanol in unanesthetized cats (PERRIN et al, 1974), motor reflexes (MAC-DONNELL and FESSOCK, 1972) and EEG in monkeys (STORY et al, 1961).…”

“…It is true that some of the conclusions of and NAKAI and DOMINO (1969) were based on low doses of ethanol relative to those of pentobarbital-yet had the ethanol dose been increased, it would have most likely altered the response via the reticular formation-but lowering the pentobarbital dose would not conceivably have resulted in a more selective action on the cortex. PERRIN et al (1974) interpreted their observations of a more rapid depression of the reticular formation evoked response during infusion of alcohol as indicating selective effects on the reticular system; depression of spontaneous frequency and amplitude occurred to lesser degrees in cerebral cortex, hypothalamus, and hippocampus, in that order. However, the figures and data presented fail to demonstrate convincingly a selective action on the reticular formation.…”

“…This phenomenon of acute tolerance has been repeatedly rediscovered and restudied (cf. e.g., ROSENBAUM, 1942;GOLDBERG, 1943;CASPERS and ABELE, 1956;MAYNERT and KLINGMAN, 1960;STORY et al, 1961;MACDoNNELL and FESSOCK, 1972;JONES and VEGA, 1972;HURST and BAGLEY, 1972;GREIZERSTEIN and SMITH, 1972GREIZERSTEIN, 1975;SUGAR-MAN et al, 1973;PERRIN et al, 1974PERRIN et al, , 1975, although it is not always evident (LOOMIS and WEST, 1958). Acute tolerance is readily demonstrated for both subjective effects of ethanol intoxication as well as psychomotor impairment; in fact, subjective phenomena appear to be sensitive indicators of ethanol action (EK-MAN et al, 1963;EKMAN, 1964;GOLDBERG, 1966;BROWN et al, 1975).…”