Although studies of classical conditioning in humans began to wane in the 1960s, particularly for eyeblink classical conditioning, within the past 10 years there has been a resurgence of experimental work that can largely be attributed to the success of classical conditioning as a tool to study brain function in the experimental animal. Currently, our understanding of how different human brain structures contribute to classical condition lags far behind what is known in the animal and will likely never approach the level of precision that is possible with animal studies. Nevertheless, there has recently been much progress with relating classical conditioning to brain function in humans.
Recent findings from human studies have been remarkably consistent with previous work with animal studies of conditioning. For example, work in rats has convincingly demonstrated the importance of the amygdala in fear classical conditioning. Studies using brain imagining methods such as positron emission tomography (PET) and functional magnetic resonance image (fMRI) have shown that fear classical conditioning activates the amygdala. Additionally, humans with bilateral degeneration of the amygdala, as a result of Urbach-Wiethe disease, show an impaired ability to acquire fear classical conditioning.
Results from human studies of eyeblink classical conditioning have also been remarkably consistent with those of studies in rabbits. For example, work with rabbits clearly indicates that the cerebellum is critical for acquisition of delay classical conditioning. Humans with cerebellar damage are also severely impaired on eyeblink classical conditioning. Humans with bilateral hippocampal damage due to anoxia are normal at acquiring CRs in the delay classical conditioning paradigm, but they are impaired when tested on trace classical conditioning. These results are entirely consistent with the animal work. Imagining studies using PET and fMRI have also consistently identified the cerebellum and hippocampus as being activated during classical conditioning of the eyeblink response.
In addition to supporting previous work in animals, human eyeblink conditioning studies have also extended our understanding of brain function in several interesting ways. For example, it has been reported that the knowledge that humans sometime acquire about the stimulus contingencies of the conditioning experiment (e.g., the CS predicts the US) is an important variable for trace conditioning but irrelevant or superfluous for delay eyeblink conditioning. Humans with hippocampal damage fail to acquire this knowledge and accordingly fail to acquire trace conditioning while being unaffected on delay conditioning.
It has repeatedly been reported that subjects with Alzheimer's disease and those with probable Alzheimer's disease are impaired on delay classical conditioning of the eyeblink response. At first, this finding did not appear to be congruent with the animal work because Alzheimer's disease does not affect the cerebellum or other brain stem structures that are critical for delay conditioning. However, work in rabbits has shown that although the hippocampus can be removed without affecting acquisition in the delay paradigm, disrupting the hippocampus by inactivating the cholinergic input to the hippocampus can disrupt delay conditioning. Alzheimer's disease disrupts the septohippocampal cholinergic system and it is this disruption that likely causes the impairment in delay eyeblink conditioning. If fact, this classical conditioning paradigm is so sensitive to the early effects of Alzheimer's disease that, it has been proposed as a simple neuropsychological test for Alzheimer's. Finally, humans with autism, a developmental disorder characterized by severe impairments in communication and social relating and by ritualistic and repetitive patterns of behavior, also show abnormalities in the cerebellum. Subjects with autism also show abnormal acquisition and extinction of the CR. This finding further supports the involvement of the cerebellum in classical eyeblink conditioning.
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