Behavioral disinhibition following basal forebrain excitotoxin lesions: alcohol consumption, defensive aggression, impulsivity and serotonin levels.

Research on alcoholism have identified a subgroup in which the drinking problem is associated with high rates of violence, an impulsive disposition and signs of reduced serotonin functioning in the brain. The present study reports that male Wistar rats with ibotenic acid-induced (5 micrograms/0.5 microliter) neuron loss in the basal forebrain (ventral striatum, septal area and adjacent structures) showed behavioral and neurochemical signs not unlike this subtype of alcoholics. Thus, rats with this lesion exhibited excessive 6% alcohol drinking in a two-bottle choice test and showed augmentation of certain defensive behaviors, including defensive aggression and increased activity-during signal. In the punished drinking test, a passive avoidance task which taps psychological mechanisms underlying impulsivity [56], experimental rats were not different from sham-operated controls with regard to the number of punished licks, but punishment evoked less disruption of ongoing behavior in subjects with basal forebrain damage. The virtual absence of food hoarding in the face of normal feeding may constitute yet another sign of increased impulsivity, indicating as it does a diminished influence of future rewards on behavior. As expected, in view of ibotenic acid's selectivity for neuronal perikarya, the concentrations of dopamine, serotonin and norepinephrine were normal in the lesioned area. However, the levels of serotonin and norepinephrine in the cortex were reduced. A separate experiment examined the extent to which serotonin depletion alone reproduced the behavioral profile induced by basal forebrain neuron loss. However, measures of alcohol consumption, defensive behavior and impulsivity were not different from controls in rats given intracerebroventricular 5,7-DHT (150 micrograms/20 microliters), except for a modest increase in defensive aggression.