Amphetamine and the multitrial Partial Reinforcement Extinction Effect (PREE) in an operant chamber: Procedural modifications that lead to an attenuation of the PREE

The neuropsychology of schizophrenia

“…Experimental analysis of this issue makes it clear that neuroleptics do have behavioural effects on performance in these tasks by normal animals that are the opposite of the effects of amphetamine. Thus, haloperidol treatment produces latent inhibition after only 10 exposures (Weiner & Feldon 1987); enhances latent inhibition after 40 exposures (Feldon & Weiner 1988;Weiner & Feldon 1987;Weiner et al 1987c); and gives rise to a larger FREE (Feldon et al 1988) than is seen in controls. As the dopamine system moves from functional hypoactivity through to hyperactivity, so learning to disattend in these tasks changes from more to less efficient than normal.…”

The genetic structure of personality and learning: a phylogenetic model

“…The other PREE mechanism was described by E. J. Capaldi (1966) and occurs when several trials are massed within a single day (Feldon & Weiner 1992). It is facilitated by giving rewards during the intertrial intervals that are not response contingent, involves sensory carry-over or after-effects rather than frustrative contrast (Gonzalez & Bitterman 1967, and is not blocked by anxiolytic or stimulant drugs (Feldon & Weiner 1992, Capaldi & Sparling 197 1, Ziff & Capaldi 197 1) or hippocampal lesions (Rawlins et al 1985).…”

“…One PREE mechanism was described by A. Amsel (1962) and occurs with trials spaced once per day for many days (Gray 1975, Rawlins et al 1985; it involves formation of conditioned signals of frustrative non-reward (Amsel 1962, Owen et al 1982, Gonzalez & Bitterman 1969, and can be blocked by a variety of drugs during acquisition that either prevent anxiety during acquisition or block REM sleep during the circadian intertrial interval (i.e., anti-anxiety, antidepressant, and stimulant drugs) (Pearlman & Becker 1974, Feldon & Weiner 1992, Halevy et al 1986, Gray 1975. It is also blocked by destruction of the dorsal noradrenergic bundle projection from the locus ceruleus to the septo-hippocampal system (Owen et al 1982) or hippocampal lesions (Rawlins et al 1985).…”

The neuropsychology of schizophrenia: A perspective from neurobehavioral genetics

“…Male rats that are nonhandled throughout infancy (i.e., entirely undisturbed from birth to weaning on Day 22) fail to exhibit either LI or the partial reinforcement extinction effect (FREE) as adults 1987d;1987e;. Remarkably, this behavioral deficit is reversed by neuroleptic treatment (Feldon & Weiner 1988). These results suggest that infantile nonhandling leads to a DA-mediated deficit that mimics the deficit induced by amphetamine in normal adult rats.…”

“…These results suggest that infantile nonhandling leads to a DA-mediated deficit that mimics the deficit induced by amphetamine in normal adult rats. It is interesting to note that nonhandling produces alterations in the neural organisation and development of the hippocampus (Altman et al 1968;Cain & Routtenberg 1983;Meaney et al 1985;Wilson et al 1986); it is therefore possible that the hippocampusaccumbens circuit is involved in the behavioural deficits of nonhandled males (Feldon & Weiner 1988; in press a). Thus, nonhandling in infancy may provide an animal neurodevelopmental model of those schizophrenic-like cognitive abnormalities that are modelled in normal animals by amphetamine administration or manipulation of the hippocampal system.…”