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Auditory evoked transient and sustained potentials in the human EGG: II. Effects of small doses of ethanol
Ps$riatr.r
Resenrch.
Q ElsevieriNorth-Holland
307
1, 307-3 12 (1979) Biomedical Press
Auditory Evoked Transient and Sustained Potentials in the Human EEG: II. Effects of Small Doses of Ethanol Ritta
Hari,
Mikko
Received September
Sams,
and Timo
5, 1979; accepted
Jglrvilehto
November
7, 1979.
Abstract. The effect of small doses of ethanol (0.4 g/kg) on auditory evoked transient and sustained potentials was studied. Tones of l-second duration were presented in trains of four stimuli (interstimulus interval = 1 second; intertrain interval = I minute). The electroencephalogram was recorded from derivation Cz-Al. Ethanol depressed the transient responses both at the first stimulus of the train and during repeated stimuli. The sustained potentials elicited by the first stimuli of the train were not affected by ethanol, whereas the sustained potentials elicited by repeated stimuli were larger in amplitude under the influence of ethanol than during control experiments. It is suggested that the decrease of the transient responses under the influence of ethanol is mainly due to depression of the reticular formation, whereas the increase of sustained potentials reflects ethanol-induced release of intracortical inhibition. Key Words. Ethanol,
evoked
potentials,
audition.
The results of Hari et al. (1979; this issue) showed that the relationship between auditory evoked transient and sustained potentials is complex and that the neural generators of these potentials are-at least partly-distinct. Indirect information on the underlying neural generators and their mutual relationships can be obtained by studying the responsiveness of evoked potentials to different types of experimental manipulations. The effects of ethanol on the spontaneous activity of the electroencephalogram (EEG) and on transient evoked potentials have been extensively studied (for a review, see Begleiter and Platz, 1972), but no information is available about the effects of ethanol on sustained potentials. In the present investigation, auditory evoked transient and sustained potentials were studied when the subject was under the influence of small doses of ethanol. The experiments described in Part I of this report (Hari et al., 1979) served as control conditions.
Methods The ethanol experiment was always carried out after the control experiment with the same subjects (Hari et al., 1979). The experimental situation and data processing were Preliminary reports of this study were presented at the Second European Neuroscience Meeting, Florence, 1978 (Hari et al.. 1978) and at the Fourth Biennial International Symposium on Biological Research in Alcoholism. Zurich. 1978 (Hari et al., in press). Ritta Hari, M.D., is Assistant Doctor, Department of Physiology, Mikko Sams, M.A., is Assistant, Department of Psychology, and Timo Jarvilehto, Ph.D., is Docent, Department of Psychology, University of Helsinki. (Reprint requests to Dr. Hari at Laboratory of Clinical Neurophysiology, Department of Neurology, University Central Hospital of Helsinki, Haartmaninkatu 4, 00290 Helsinki 29, Finland.)
308
identical to those in the control experiment except that 5 minutes after the end of the control experiment, the subject ingested 0.4 g/kg ethanol (diluted to 20% administration concentration by orange juice) during 5 minutes. The maximal blood ethanol concentration with this dose did not exceed 0.05%. The stimulation and EEG recording began 5 minutes after the end of the drinking and extended for 40 minutes. Each subject participated in two control and two ethanol experiments. The EEG recordings were both computer analyzed and visually inspected. If there was synchronized activity during the stimulus trains, its amplitude and frequency were measured. These measurements were used as controls for possible changes in the subject’s vigilance. In the statistical analysis of data, two-tailed t tests were used to test individual differences against zero. Results
During ethanol experiments the general configuration of the transient and sustained potentials was similar to that seen in control experiments (see Fig. 1). The expectation of the stimuli had a significant effect only on the amplitude of the P200 component of the transient response to the first stimulus of the train. Therefore, averaged values from the expecting and ignoring condition are used in our presentation of the differences between control and ethanol experiments. Fig. 1. Evoked potential ,
waveforms
control
ethanol WV +
I
stkll.
-
One subject’s averagea responses to the first stimulus of the stimulus train in control and ethanol experiment when the subject either expected or ignored the stimuli. Duration of the stimulus is 1 second. Number of summations = 17.
309
Transient Responses to the Stimulus Onset (On Response). In all subjects the amplitude of the N120 component of the transient on response was smaller under the influence of ethanol than in the control experiment, both at the first stimulus of the train and during stimulus repetition. The mean decrease from the control to the ethanol session (Fig. 2) was 8.5 k 4.4 I.IV at the first stimulus (decrease of 28%from the control value, p < 0.001) and 2.0 * 1.2 PV during stimulus repetition (decrease of 19% from the control value, p < 0.001). The amplitude of the N 120 component of the averaged second to fourth response was, on the average, 41+ 12% of the amplitude of the first response. The rate of decrease did not differ from that in control experiments. The effect of ethanol on the amplitude of the P200 component was similar to that on N 120 so that ethanol depressed the amplitude of P200 both at the first stimulus of the train and during stimulus repetition in all subjects. The mean decrease of the amplitude of P200 was 6.7 k 2.3 r.lV at the first stimulus (decrease of 52% from the control value, p < 0.001) and 2.7 ? 1.6 I.~Vduring stimulus repetition (decrease of 36% from the control value, p < 0.001). Stimulus repetition did not result in any significant decrease of the amplitude of the P200 component. Fig. 3 shows the latencies of both the N 120 and P200 components in the control and ethanol conditions. At the first stimulus, there was no significant difference between the conditions, but during stimulus repetition the latencies were shorter under the influence of ethanol. The mean reduction of the latency of N 120 was 5 ms @ < 0.025) and that of P200 10 ms @ < 0.005). Transient Responses to the Stimulus Offset (Off Response). The peak-to-peak amplitude of the off response was, on the average, 1.6 + 1.4 WV smaller under the influence of ethanol than in the control experiment (decrease of 17% from the control value, p < 0.005). As was found in the control session, stimulus repetition did not result in any significant decrease of the amplitudes of the off responses. The latencies of both N120 and P200 components of the off response were shorter under the influence of ethanol than in the control session in all subjects. The mean reduction of the latencies was 17 ms for N 120 @ < 0.001) and 25 ms for P200 0, < 0.001). Sustained Potentials. At the first stimulus of the train, the amplitude of the sustained potential (SP) did not differ significantly from the mean amplitude obtained in control experiments. There were also no significant differences in the amplitudes measured at the end of the analysis period (see Methods of Part I; Hari et al., 1979) between ethanol and control experiments. During stimulus repetition, however, the SP amplitude was on the average I. 1 + 0.7 /IV larger under the influence of ethanol than in the control experiments (increase of 42% from the control value, p < 0.001). This SP increase under the influence of ethanol was seen in all but one subject. The SP amplitude of the averaged second-fourth response was 39 + 21% of that of the first response. This rate of SP decrease was slightly smaller than that observed in the control experiment @ < 0.05).
310 Fig. 2. EP amplitude
changes with ethanol
Pyi -30
1st RESPONSE
r
MEAN OF 2nd-4th
RESPONSES
q CXNTROL -20
q ETHANOL
:: A
- 10
7 Nl
0
P2’ -
+ 10 I
Mean amplitudes of the different components of theevoked potential complexat the first stimulus of the train (first response) and during stimulus repetition (mean of second-fourth response) in control and in ethanol experiment. All subjects pooled. The bars indicate the standard error of the mean. Nl = N120, P2 = P200, SP = sustained potential, OFF = off response N120-P200 peak-totrough.
Fig. 3. N120 and P200 latency changes with ethanol
100
NI
1.
2.
3.
’ stim. 4.
The mean peak latencies of the N120 and P200 components of the transient on response at consecutive stimuli of the train in control and ethanol experiment. All subjects pooled. The bars indicate the standard error of the mean.
311 Background Activity. In half of the recordings, occasional alpha activity was seen during the stimulus trains. In two recordings (of one subject) the frequency of alpha was 0.5 Hz and in one recording 1.0 Hz higher under the influence of ethanol. In three recordings a slowing of 0.5 Hz was seen. In all recordings where alpha activity was seen during ethanol experiments, it was seen in control experiments, too. Only slight unsystematic variations in the amount and amplitude of alpha activity from train to train were observed. Discussion The present results show that even small doses of ethanol have a marked influence on the evoked electrical activity of the brain. Ethanol depressed the transient responses both at the first stimulus of the train and during stimulus repetition. These findings are similar to those of earlier investigations of the effects of larger doses on transient auditory, visual and somatosensory responses elicited by short stimuli (Lewis et al., 1970; Perrin et al., 1974; Salamy and Williams, 1973). The slight shortening of the peak latencies of the components of the transient on and off responses under the influence of ethanol is probably due to the markedly decreased amplitudes of these potentials. The SPs recorded at the first stimulus of the train were not affected by ethanol. During stimulus repetition, however, amplitude of SP was significantly larger in the ethanol than in the control experiment. This opposite effect of ethanol on auditory evoked transient and sustained potentials elicited by repetitive stimuli further supports the hypothesis that there are different neural generators of these potentials (Picton et al., 1978). Drowsiness may contribute to some extent to the effects attributed to ethanol. Begleiter and Platz (1972), for example, stated that the amount of alpha activity increases and its frequency slows down under the influence of ethanol. These changes are further regarded as signs of decreased vigilance. In the present study, subjects were instructed to read a magazine during the control and during the ethanol experiment in order to maintain the activation level as stable as possible. Studies of the relationship between vigilance and auditory evoked transient responses (Fruhstorfer and Bergstrom, 1969) suggest that the decrease of the amplitude of the N120 component observed in the present study-if it were solely due to a decrease in vigilance-should have been accompanied by an EEG change from low voltage fast activity to continuous rhythmical alpha activity. However, such changes were never seen in the present recordings. Current evidence indicates that the central nervous system (CNS) effect ofethanol is mainly due to actions on neuronal membranes (Kalant, 1975). Ethanol hinders ionic conductances underlying neuronal synaptic and action potentials and thus results in decreased neuronal excitability (Faber and Klee, 1977). The CNS effect of ethanol is biphasic so that low blood ethanol levels are associated with a transient excitation at both a behavioral and an electrophysiological level while various signs of central depression become evident with higher blood ethanol levels (Pohorecky, 1977). The excitatory phase may be due more to suppression of inhibitory events than to excitatory effects (Person and Gunn, 1974; Hari, 1979). The present testing period (40 minutes) evidently includes both the excitatory phase and the beginning of the
312 depressing phase because small doses of ethanol were used and registration began soon after the end of the drinking. The effect of ethanol on different brain areas largely depends on the intrinsic organization of the neural networks concerned. If the principal site of action of small doses of ethanol is at the mesencephalic reticular formation (Perrin et al., 1974), then the decreased amplitude of the transient evoked potential under the influence of ethanol might be due to decreased extralemniscal afferent activity to the cortex. Sustained potentials may reflect more tonic intracortical events than the transient evoked potentials. Because of the numerous inhibitory connections in the cortex in comparison to the reticular formation, the ethanol-induced excitatory phase lasts longer at the cortical level than in the reticular formation (Hari, 1979). The increase in SP amplitude might therefore be due to the release of intracortical inhibition.
References Begleiter, H., and Platz, A. The effects of ethanol on the central nervous system in humans. Gross, M.M., ed. Advances in Experimental Medicine and Biology: Alcohol and Withdrawal-Experimental Studies. Plenum Press, New York (1972).
In: Intoxication
Faber, D.S., and Klee, M.R. Actions of ethanol on neuronal membrane properties and synaptic transmission. In: Blum, K., ed. Alcohol and Opiates. Neurochemical and Behavioral Mechanisms. Academic Press, New York (1977). Fruhstorfer, H., and Bergstrijm, R.M. Human vigilance and auditory evoked responses. Electroencephalography and Clinical Neurophysiology, 27, 346 (1969). Hari, R. Biphasic effect of ethanol on behavioral and electrophysiological parameters can be explained by functional organization of neural networks. TIT Journal of Life Sciences: Tower International Technomedical Institute. 9, 15 (1979). Hari, R., Sams, M., and JPrvilehto, T. Opposite effects of ethanol on auditory evoked transient and sustained potentials. Neuroscience Letters, Suppl. 1, S5 (1978). Hari, R., Sams, M., and JPrvilehto, T. Auditory evoked transient and sustained potentials. 1. Effects of expectation of stimuli. Psychiatry Research, 1, 297 (1979). Hari, R., Sams, M., and Jlrvilehto, T. Effects of small ethanol doses on the auditory evoked transient and sustained potentials in the human EEG. In: Begleiter, H., ed. Biological Effects of Alcohol. Plenum Press, New York (in press). Kalant, H. Direct effects of ethanol on the nervous system. Federation Proceedings, 34, 1930 (1975). Lewis, E.G., Dustman, R.E., and Beck, E.C. The effects of alcohol on visual and somatosensory evoked responses. Electroencephalography and Clinical Neurophysiolog_v, 28, 202 ( 1970). Perrin, R.G., Hockman, C.H., Kalant, H., and Livingston, K.E. Acute effects of ethanol on spontaneous and auditory evoked electrical activity in cat brain. Electroencephalography and Clinical Neurophysiology. 36, 19 (1974). Person, R.J., and Gunn, C.G. Effects of ethanol on recruiting, augmenting and reticular activation response thresholds. Quarter[v Journal of Studies on Alcohol, 35, 987 (I 974). Picton, T.W., Woods, D.L., and Proulx, G.B. Human auditory sustained potentials: 1. The nature of the response. Electroencephalography and Clinical Neuroph_vsiology, 45, 186 (1978). Pohorecky, L.A. Biphasic action of ethanol. Biobehavioral Review, 1, 231 (1977). Salamy, A., and Williams, H.L. The effects of alcohol on sensory evoked and spontaneous cerebral potentials in man. Electroencephalography and Clinical Neurophysiology. 35, 3 (1973). This study was supported
by the Finnish
Foundation
for Alcohol
Studies.
Resenrch.
Q ElsevieriNorth-Holland
307
1, 307-3 12 (1979) Biomedical Press
Auditory Evoked Transient and Sustained Potentials in the Human EEG: II. Effects of Small Doses of Ethanol Ritta
Hari,
Mikko
Received September
Sams,
and Timo
5, 1979; accepted
Jglrvilehto
November
7, 1979.
Abstract. The effect of small doses of ethanol (0.4 g/kg) on auditory evoked transient and sustained potentials was studied. Tones of l-second duration were presented in trains of four stimuli (interstimulus interval = 1 second; intertrain interval = I minute). The electroencephalogram was recorded from derivation Cz-Al. Ethanol depressed the transient responses both at the first stimulus of the train and during repeated stimuli. The sustained potentials elicited by the first stimuli of the train were not affected by ethanol, whereas the sustained potentials elicited by repeated stimuli were larger in amplitude under the influence of ethanol than during control experiments. It is suggested that the decrease of the transient responses under the influence of ethanol is mainly due to depression of the reticular formation, whereas the increase of sustained potentials reflects ethanol-induced release of intracortical inhibition. Key Words. Ethanol,
evoked
potentials,
audition.
The results of Hari et al. (1979; this issue) showed that the relationship between auditory evoked transient and sustained potentials is complex and that the neural generators of these potentials are-at least partly-distinct. Indirect information on the underlying neural generators and their mutual relationships can be obtained by studying the responsiveness of evoked potentials to different types of experimental manipulations. The effects of ethanol on the spontaneous activity of the electroencephalogram (EEG) and on transient evoked potentials have been extensively studied (for a review, see Begleiter and Platz, 1972), but no information is available about the effects of ethanol on sustained potentials. In the present investigation, auditory evoked transient and sustained potentials were studied when the subject was under the influence of small doses of ethanol. The experiments described in Part I of this report (Hari et al., 1979) served as control conditions.
Methods The ethanol experiment was always carried out after the control experiment with the same subjects (Hari et al., 1979). The experimental situation and data processing were Preliminary reports of this study were presented at the Second European Neuroscience Meeting, Florence, 1978 (Hari et al.. 1978) and at the Fourth Biennial International Symposium on Biological Research in Alcoholism. Zurich. 1978 (Hari et al., in press). Ritta Hari, M.D., is Assistant Doctor, Department of Physiology, Mikko Sams, M.A., is Assistant, Department of Psychology, and Timo Jarvilehto, Ph.D., is Docent, Department of Psychology, University of Helsinki. (Reprint requests to Dr. Hari at Laboratory of Clinical Neurophysiology, Department of Neurology, University Central Hospital of Helsinki, Haartmaninkatu 4, 00290 Helsinki 29, Finland.)
308
identical to those in the control experiment except that 5 minutes after the end of the control experiment, the subject ingested 0.4 g/kg ethanol (diluted to 20% administration concentration by orange juice) during 5 minutes. The maximal blood ethanol concentration with this dose did not exceed 0.05%. The stimulation and EEG recording began 5 minutes after the end of the drinking and extended for 40 minutes. Each subject participated in two control and two ethanol experiments. The EEG recordings were both computer analyzed and visually inspected. If there was synchronized activity during the stimulus trains, its amplitude and frequency were measured. These measurements were used as controls for possible changes in the subject’s vigilance. In the statistical analysis of data, two-tailed t tests were used to test individual differences against zero. Results
During ethanol experiments the general configuration of the transient and sustained potentials was similar to that seen in control experiments (see Fig. 1). The expectation of the stimuli had a significant effect only on the amplitude of the P200 component of the transient response to the first stimulus of the train. Therefore, averaged values from the expecting and ignoring condition are used in our presentation of the differences between control and ethanol experiments. Fig. 1. Evoked potential ,
waveforms
control
ethanol WV +
I
stkll.
-
One subject’s averagea responses to the first stimulus of the stimulus train in control and ethanol experiment when the subject either expected or ignored the stimuli. Duration of the stimulus is 1 second. Number of summations = 17.
309
Transient Responses to the Stimulus Onset (On Response). In all subjects the amplitude of the N120 component of the transient on response was smaller under the influence of ethanol than in the control experiment, both at the first stimulus of the train and during stimulus repetition. The mean decrease from the control to the ethanol session (Fig. 2) was 8.5 k 4.4 I.IV at the first stimulus (decrease of 28%from the control value, p < 0.001) and 2.0 * 1.2 PV during stimulus repetition (decrease of 19% from the control value, p < 0.001). The amplitude of the N 120 component of the averaged second to fourth response was, on the average, 41+ 12% of the amplitude of the first response. The rate of decrease did not differ from that in control experiments. The effect of ethanol on the amplitude of the P200 component was similar to that on N 120 so that ethanol depressed the amplitude of P200 both at the first stimulus of the train and during stimulus repetition in all subjects. The mean decrease of the amplitude of P200 was 6.7 k 2.3 r.lV at the first stimulus (decrease of 52% from the control value, p < 0.001) and 2.7 ? 1.6 I.~Vduring stimulus repetition (decrease of 36% from the control value, p < 0.001). Stimulus repetition did not result in any significant decrease of the amplitude of the P200 component. Fig. 3 shows the latencies of both the N 120 and P200 components in the control and ethanol conditions. At the first stimulus, there was no significant difference between the conditions, but during stimulus repetition the latencies were shorter under the influence of ethanol. The mean reduction of the latency of N 120 was 5 ms @ < 0.025) and that of P200 10 ms @ < 0.005). Transient Responses to the Stimulus Offset (Off Response). The peak-to-peak amplitude of the off response was, on the average, 1.6 + 1.4 WV smaller under the influence of ethanol than in the control experiment (decrease of 17% from the control value, p < 0.005). As was found in the control session, stimulus repetition did not result in any significant decrease of the amplitudes of the off responses. The latencies of both N120 and P200 components of the off response were shorter under the influence of ethanol than in the control session in all subjects. The mean reduction of the latencies was 17 ms for N 120 @ < 0.001) and 25 ms for P200 0, < 0.001). Sustained Potentials. At the first stimulus of the train, the amplitude of the sustained potential (SP) did not differ significantly from the mean amplitude obtained in control experiments. There were also no significant differences in the amplitudes measured at the end of the analysis period (see Methods of Part I; Hari et al., 1979) between ethanol and control experiments. During stimulus repetition, however, the SP amplitude was on the average I. 1 + 0.7 /IV larger under the influence of ethanol than in the control experiments (increase of 42% from the control value, p < 0.001). This SP increase under the influence of ethanol was seen in all but one subject. The SP amplitude of the averaged second-fourth response was 39 + 21% of that of the first response. This rate of SP decrease was slightly smaller than that observed in the control experiment @ < 0.05).
310 Fig. 2. EP amplitude
changes with ethanol
Pyi -30
1st RESPONSE
r
MEAN OF 2nd-4th
RESPONSES
q CXNTROL -20
q ETHANOL
:: A
- 10
7 Nl
0
P2’ -
+ 10 I
Mean amplitudes of the different components of theevoked potential complexat the first stimulus of the train (first response) and during stimulus repetition (mean of second-fourth response) in control and in ethanol experiment. All subjects pooled. The bars indicate the standard error of the mean. Nl = N120, P2 = P200, SP = sustained potential, OFF = off response N120-P200 peak-totrough.
Fig. 3. N120 and P200 latency changes with ethanol
100
NI
1.
2.
3.
’ stim. 4.
The mean peak latencies of the N120 and P200 components of the transient on response at consecutive stimuli of the train in control and ethanol experiment. All subjects pooled. The bars indicate the standard error of the mean.
311 Background Activity. In half of the recordings, occasional alpha activity was seen during the stimulus trains. In two recordings (of one subject) the frequency of alpha was 0.5 Hz and in one recording 1.0 Hz higher under the influence of ethanol. In three recordings a slowing of 0.5 Hz was seen. In all recordings where alpha activity was seen during ethanol experiments, it was seen in control experiments, too. Only slight unsystematic variations in the amount and amplitude of alpha activity from train to train were observed. Discussion The present results show that even small doses of ethanol have a marked influence on the evoked electrical activity of the brain. Ethanol depressed the transient responses both at the first stimulus of the train and during stimulus repetition. These findings are similar to those of earlier investigations of the effects of larger doses on transient auditory, visual and somatosensory responses elicited by short stimuli (Lewis et al., 1970; Perrin et al., 1974; Salamy and Williams, 1973). The slight shortening of the peak latencies of the components of the transient on and off responses under the influence of ethanol is probably due to the markedly decreased amplitudes of these potentials. The SPs recorded at the first stimulus of the train were not affected by ethanol. During stimulus repetition, however, amplitude of SP was significantly larger in the ethanol than in the control experiment. This opposite effect of ethanol on auditory evoked transient and sustained potentials elicited by repetitive stimuli further supports the hypothesis that there are different neural generators of these potentials (Picton et al., 1978). Drowsiness may contribute to some extent to the effects attributed to ethanol. Begleiter and Platz (1972), for example, stated that the amount of alpha activity increases and its frequency slows down under the influence of ethanol. These changes are further regarded as signs of decreased vigilance. In the present study, subjects were instructed to read a magazine during the control and during the ethanol experiment in order to maintain the activation level as stable as possible. Studies of the relationship between vigilance and auditory evoked transient responses (Fruhstorfer and Bergstrom, 1969) suggest that the decrease of the amplitude of the N120 component observed in the present study-if it were solely due to a decrease in vigilance-should have been accompanied by an EEG change from low voltage fast activity to continuous rhythmical alpha activity. However, such changes were never seen in the present recordings. Current evidence indicates that the central nervous system (CNS) effect ofethanol is mainly due to actions on neuronal membranes (Kalant, 1975). Ethanol hinders ionic conductances underlying neuronal synaptic and action potentials and thus results in decreased neuronal excitability (Faber and Klee, 1977). The CNS effect of ethanol is biphasic so that low blood ethanol levels are associated with a transient excitation at both a behavioral and an electrophysiological level while various signs of central depression become evident with higher blood ethanol levels (Pohorecky, 1977). The excitatory phase may be due more to suppression of inhibitory events than to excitatory effects (Person and Gunn, 1974; Hari, 1979). The present testing period (40 minutes) evidently includes both the excitatory phase and the beginning of the
312 depressing phase because small doses of ethanol were used and registration began soon after the end of the drinking. The effect of ethanol on different brain areas largely depends on the intrinsic organization of the neural networks concerned. If the principal site of action of small doses of ethanol is at the mesencephalic reticular formation (Perrin et al., 1974), then the decreased amplitude of the transient evoked potential under the influence of ethanol might be due to decreased extralemniscal afferent activity to the cortex. Sustained potentials may reflect more tonic intracortical events than the transient evoked potentials. Because of the numerous inhibitory connections in the cortex in comparison to the reticular formation, the ethanol-induced excitatory phase lasts longer at the cortical level than in the reticular formation (Hari, 1979). The increase in SP amplitude might therefore be due to the release of intracortical inhibition.
References Begleiter, H., and Platz, A. The effects of ethanol on the central nervous system in humans. Gross, M.M., ed. Advances in Experimental Medicine and Biology: Alcohol and Withdrawal-Experimental Studies. Plenum Press, New York (1972).
In: Intoxication
Faber, D.S., and Klee, M.R. Actions of ethanol on neuronal membrane properties and synaptic transmission. In: Blum, K., ed. Alcohol and Opiates. Neurochemical and Behavioral Mechanisms. Academic Press, New York (1977). Fruhstorfer, H., and Bergstrijm, R.M. Human vigilance and auditory evoked responses. Electroencephalography and Clinical Neurophysiology, 27, 346 (1969). Hari, R. Biphasic effect of ethanol on behavioral and electrophysiological parameters can be explained by functional organization of neural networks. TIT Journal of Life Sciences: Tower International Technomedical Institute. 9, 15 (1979). Hari, R., Sams, M., and JPrvilehto, T. Opposite effects of ethanol on auditory evoked transient and sustained potentials. Neuroscience Letters, Suppl. 1, S5 (1978). Hari, R., Sams, M., and JPrvilehto, T. Auditory evoked transient and sustained potentials. 1. Effects of expectation of stimuli. Psychiatry Research, 1, 297 (1979). Hari, R., Sams, M., and Jlrvilehto, T. Effects of small ethanol doses on the auditory evoked transient and sustained potentials in the human EEG. In: Begleiter, H., ed. Biological Effects of Alcohol. Plenum Press, New York (in press). Kalant, H. Direct effects of ethanol on the nervous system. Federation Proceedings, 34, 1930 (1975). Lewis, E.G., Dustman, R.E., and Beck, E.C. The effects of alcohol on visual and somatosensory evoked responses. Electroencephalography and Clinical Neurophysiolog_v, 28, 202 ( 1970). Perrin, R.G., Hockman, C.H., Kalant, H., and Livingston, K.E. Acute effects of ethanol on spontaneous and auditory evoked electrical activity in cat brain. Electroencephalography and Clinical Neurophysiology. 36, 19 (1974). Person, R.J., and Gunn, C.G. Effects of ethanol on recruiting, augmenting and reticular activation response thresholds. Quarter[v Journal of Studies on Alcohol, 35, 987 (I 974). Picton, T.W., Woods, D.L., and Proulx, G.B. Human auditory sustained potentials: 1. The nature of the response. Electroencephalography and Clinical Neuroph_vsiology, 45, 186 (1978). Pohorecky, L.A. Biphasic action of ethanol. Biobehavioral Review, 1, 231 (1977). Salamy, A., and Williams, H.L. The effects of alcohol on sensory evoked and spontaneous cerebral potentials in man. Electroencephalography and Clinical Neurophysiology. 35, 3 (1973). This study was supported
by the Finnish
Foundation
for Alcohol
Studies.