Kenneth C. Mills

Shock induced ethanol consumption in rats.

Two experiments are presented which describe the temporal and volumetric changes in ethanol consumption by rats exposed to recurring schedules of inescapable random shock. The animals in Experiment 1, which had a choice between ethanol and water, increased their voluntary ethanol consumption immediately after the shock schedule. The postshock changes occurred with both 5% and 10% V/V ethanol, were specific to the presence of shock and were not reflected by measures of total daily ethanol intake. Experiment 2 exposed rats to extended 22 hr stress sessions, during which each animal had four simultaneous fluid choices available: water, saccharin 0.1% W/V, ethanol 5% V/V, and ethanol 10% V/V. Temporal intake patterns for both 5% and 10% ethanol showed pronounced peaks for the interval immediately following the shock schedule. A shift of intake from 5% to 10% ethanol was also demonstrated with increasing time under shock, while saccharin and water intake decreased. The results are interpreted as a relationship between voluntary ethanol intake and escape from the consequences of stress.

ALCOHOL AS A EUPHORIANT DRUG: SEARCHING FOR A NEUROCHEMICAL BASIS*

Although alcohol is almost certainly the drug in longest use and although the ethanol molecule is a relatively simple one, the effects of alcohol upon living organisms are enormously complex. For the most complex organism, man, we know remarkably little about how alcohol produces its effects. Ethanol has long been known to be a general depressant of activity in all living cells.’ However, a naive observer of a cocktail party. as he noticed the increasing euphoria and general uproariousness of the participants, would find it difficult to accept that this is the behavior of depressed people, or at least that of people with depressed central nervous systems (CNS). Thus, it is not surprising that lay people often label alcohol as a “stimulant.” Of course, the standard medical explanation for this phenomenon is disinhibition: alcohol, like other CNS depressants, first affects. the phylogenetically newer parts of the brain. those concerned with self-evaluation and control, particularly in the social setting. By selectively depressing or inhibiting such centers, alcohol appears to promote the release of behavior that otherwise would be suppressed.? However, there is increasing interest in the possibility that alcohol can produce direct stimulation effects, including euphoria in man. A major issue that remains to be elucidated is the relative role of acetaldehyde, the first metabolic breakdown product of alcohol.3 This highly reactive substance appears to be significantly more toxic than alcohol itself.4 Evidence suggests that certain organisms may metabolize acetaldehyde less efficiently than others, thus possibly being subject to more of the effects of acetaldehyde, whatever they may be.s Also, although earlier studies found no difference in blood acetaldehyde levels in alcoholics and n o n a l c o h ~ l i c s , ~ ~ ~ Korsten et al. recently reported data that showed higher levels in alcoholics that did not merely represent more rapid metabolism.” Thus, this subject must be studied in more detail.

A compact and inexpensive drinkometer for use with small animals

Abstract A compact and low cost solid state drinkometer design is presented permitting electrical isolation of the animal from the recording system. Data correlating licks with daily water intake (ml) and temporal consumption patterns are provided for several Long Evans rats.

The Effect of Low Dose Intravenous Alcohol on Human Information Processing

A model of multiple-stage information processing predicts alcohol to have a selective effect on mechanisms involving central processing rather than sensory input. However, behavioral effects at low alcohol doses administered orally can be overshadowed by fluctuations in gastrointestinal absorption and metabolism rate. Paid volunteers, who therefore received intravenous doses of alcohol and a barbiturate, were tested on tasks varying in sensory discriminability and in central processing difficulty. The low drug doses did not affect errors of stimulus encoding but increased error rate in memory comparison tasks. These results confirmed the predictions based on the mutiple-stage model.

The Temporal and Volumetric Components of Stress Induced Drinking in Rats

Two experiments are presented which describe the temporal and volumetric changes in ethanol consumption with rats exposed to recurring schedules of inescapable random shock stress. The animals in Experiment I had an ethanol and water choice and the data demonstrated cumulative increases in voluntary ethanol consumption which occurred immediately after the shock schedule. The post shock changes occurred with both 5% and 10% V/V ethanol, were specific to the appearance of shock and were not reflected by measures of total daily ethanol intake. Experiment II exposed rats to extended 22 hr. stress sessions and each animal had four simultaneous fluid choices available: water, saccharin. 1% W/V, ethanol 5% V/V, and ethanol 10% V/V. Temporal intake patterns for both 5% and 10% ethanol showed pronounced peaks for the interval immediately following the shock schedule. A progressive shift of intake from 5% to 10% ethanol was also evidenced with increasing time under shock, while saccharin and water intake decreased. Blood ethanol levels during shock increased significantly from baseline for all animals and ranged from 30 to 162 mg/100 ml. The results are interpreted as a relationship between voluntary ethanol intake and escape from the consequences of stress.