Person:

Fortier, Catherine

Chronic alcoholism has profound effects on the brain, including volume reductions in regions critical for eyeblink classical conditioning (EBCC). The current study challenged abstinent alcoholics using delay (n = 20) and trace (n = 17) discrimination/reversal EBCC. Comparisons revealed a significant difference between delay and trace conditioning performance during reversal (t (35) = 2.08, p < 0.05). The difference between the two tasks for discrimination was not significant (p = 0.44). These data support the notion that alcoholics are increasingly impaired in the complex task of reversing a previously learned discrimination when a silent trace interval is introduced. Alcoholics’ impairment in flexibly altering learned associations may be central to their continued addiction.

Background: Converging evidence from varied experimental paradigms has demonstrated that the cerebellum is involved in the timing of learned behavior. Given the documented neurological changes secondary to chronic alcoholism, particularly cerebellar degeneration, the ability of recovered chronic alcoholics to learn a temporal discrimination was assessed by using delayed eyeblink classical conditioning.

Methods: Twelve abstinent alcoholic participants and 12 matched control participants were randomly presented 2 clearly discriminable tone conditioned stimuli that were individually paired with 2 different interstimulus intervals.

Results: The data revealed a significant alteration in the abstinent alcoholics’ peak latency measure at the long interstimulus intervals and an overall impairment in their level of acquisition of conditioned responses. No group differences in extinction were observed.

Conclusions: It was speculated that cerebellar cortical atrophy caused by years of alcohol abuse resulted in the peak latency alteration and that atrophy extending into deep cerebellar nuclei caused the overall impairment in conditioned response acquisition.

Evidence has shown that alcoholism leads to volume reductions in brain regions critical for associative learning using the eyeblink classical conditioning paradigm (EBCC). Evidence indicates that cerebellar shrinkage causes impairment in simple forms of EBCC, whereas changes in forebrain structures result in impairment in more complex tasks. In this study, the ability of abstinent alcoholics and matched control participants to acquire learned responses during delay discrimination and discrimination reversal was examined and related to severity of drinking history and neuropsychological performance. During discrimination learning, one tone (CS+) predicted the occurrence of an airpuff (unconditioned stimulus), and another tone (CS−) served as a neutral stimulus; then the significance of the tones was reversed. Alcoholics who learned the initial discrimination were impaired in acquiring the new CS+ after the tones reversed; this is a function that has previously been linked to forebrain structures. It is suggested that a factor important to alcoholic addiction may be the presence of alcoholic-related associative responses that interfere with the ability to learn new more adaptive associations.

The ability of bilateral medial temporal lobe amnesic patients (MT; n = 8) and normal participants (NC; n = 8) to acquire a conditional discrimination in trace and delay eyeblink conditioning paradigms was investigated. Experiment 1 assessed trace conditional discrimination learning by using a light conditional stimulus (S+/S−) and tone conditioned stimulus (CS) separated by a 1-s trace. NCs responded differentially on S+ trials (mean percent conditioned responses = 66) versus S− trials (30), whereas MTs were impaired in their acquisition of the conditional discrimination (S+ = 51, S− = 43). In Experiment 2, the temporal separation was eliminated. NCs acquired the conditional discrimination (S+ = 70, S− = 29). MTs were unable to respond differentially (S+ = 42, S− = 37). The findings indicate that the hippocampal system is essential in acquiring a conditional discrimination, even in a delay paradigm.

A number of studies investigating trace eyeblink conditioning have found impaired, but not eliminated, acquisition of conditioned responses (CRs) in both animals and humans with hippocampal removal or damage. The underlying mechanism of this residual learning is unclear. The present study investigated whether the impaired level of learning is the product of residual hippocampal function or whether it is mediated by another memory system that has been shown to function normally in delay eyeblink conditioning. Performance of bilateral medial temporal lobe amnesic patients who had a prior history of participating in eyeblink conditioning studies was compared to a control group with a similar training history and to an untrained control group in a series of single cue trace conditioning tasks with 500 ms, 250 ms, and 0 ms trace intervals. Overall, patients acquired CRs to a level similar to the untrained controls, but were significantly impaired compared to the trained controls. The pattern of acquisition suggests that amnesic patients may be relying on the expression of previously acquired, likely cerebellar based, procedural memory representations in trace conditioning.