Rationale of systematic desensitization and covert positive reinforcement.
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Based on a critical review of the literature, Davey (1994) [Behaviour Research and Therapy, 32, 291-299] concludes that there is no sufficient evidence to support the theoretical position that evaluative conditioning is a qualitatively different form of classical conditioning. In the present manuscript, we will try to show that Davey's conclusion is biased by: (a) an overemphasis on what he believes to be problematic procedural aspects of previous evaluative conditioning studies; and (b) a selective reading of the available evidence. Finally, an attempt is made to characterize evaluative conditioning phenomena as the output of a Referential Learning System, which can be distinguished from an Expectancy Learning System.
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Rats were trained to discriminate d-amphetamine (1.0 mg/kg) or clonidine (0.06 mg/kg) from saline in a standard, two-lever procedure with food reinforcement (n = 6). The similarity between the discriminable properties of amphetamine and clonidine was both partial and asymmetrical. Cross tests with amylobarbitone and chlordiazepoxide in rats trained with clonidine suggested that a major component of the clonidine stimulus may be general sedation. Pretreatment with the alpha 2-adrenoreceptor antagonist, piperoxane partially antagonized the discriminative stimulus produced by clonidine. The alpha 1 antagonist, phenoxybenzamine failed to alter the clonidine stimulus. Although amphetamine and clonidine may share some elements in common, this may not represent a noradrenergic component in the amphetamine discriminative stimulus since noradrenergic mediation of the clonidine stimulus was not established.
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Rats were trained to discriminate intraperitoneally administered mescaline from saline in a two-lever operant chamber for food reinforcement. Reward was contingent upon responses made greater than 15 sec apart (DRL-15) on the appropriate lever paired with either drug or saline administration. Following the establishment of discriminative response control by mescaline, the animals were tested for stimulus generalization produced by mescaline after: (a) blockade of periphreral and central serotonin (5-HT) receptors with cinanserin, methysergide, or cyproheptadine; (b) blockade of peripheral 5-HT receptors with xylamidine tosylate; and (c) depletion of brain 5-HT with the tryptophan hydroxylase inhibitor p-chlorophenylalanine (PCPA). The results show that all three central 5-HT antagonists greatly reduced the discriminability of mescaline while the peripheral antagonist, xylamidine tosylate, was without effect. Furthermore, these agents at the doses employed did not effect the discriminability of saline. Depletion of 5-HT with PCPA potentiated the effects of a sub-threshold dose of mescaline and slightly reduced the discriminability of saline. The results indicate that mescaline produces its discriminative stimulus properties by directly stimulating central serotonergic receptors.
An NMDA antagonist, ketamine, at the highest dose tested (15 mg/kg), impaired the acquisition of a hole-board spatial learning task but not the acquisition of a left-right alternation task. A non-NMDA (quisqualate) antagonist, L-glutamic acid diethyl ester (LGDE), did not impair the acquisition of either task. Both drugs had effects on different aspects of a go-no go discrimination task and a straight runway task, ketamine tending to activate and LGDE tending to slow rats. These results concur with previous research regarding the sensitivity of some spatial tasks to NMDA antagonism. Non-NMDA antagonists affect behavior without causing spatial deficits.
In order to localize the site of action of neuropeptides in relation to their effects on behavior and memory various approaches have been used. As a result of studies using rats bearing lesions in different areas of the limbic system as well as of studies in which neuropeptides were locally applied into various areas of the brain it appeared that the limbic system (amygdala, hippocampus, septum and some thalamic areas) plays an essential role in the effect of vasopressin and ACTH and their derivatives on behavior and memory. Neurochemical studies generally indicate that changes occur in catecholamine utilization in these various limbic regions upon administration of these neuropeptides. It can be concluded that the effects of vasopressin in the terminal regions of the coeruleo-telencephalic noradrenalin system correlate with its effects on consolidation of memory. It is likely that the effects of vasopressin on other transmitter systems (e.g. dopamine in the amygdala and serotonin in the hippocampus) correspond with the effect of this neuropeptide on retrieval processes. In addition, regional differences in biotransformation of the neurohypophyseal hormones suggest that different patterns of behaviorally active fragments of these peptides may be present locally in the brain.