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Sun Apr 10 21:26:34 EST 2005

Here, I shall consider only latent inhibition (Lubow 1973; 1989). This is
an extremely simple phenomenon. If a potential conditioned stimulus (CS)
(e.g., a tone or white noise) is presented to the subject a number of
times (typically, 20-40) without consequence, this preexposure retards
subsequent learning when the stimulus does have consequence (e.g., it now
predicts the occurrence of a second stimulus: footshock if the subject is
a rat, a counter increment for human subjects). In Hemsley's (1987) terms,
a past regularity (CS with no consequence)  adversely affects the current
learning of a new association. If, therefore, one were unable normally to
integrate current learning with such past regularities, latent inhibition
should be blocked, i.e., learning to a preexposed CS should resemble
learning to a novel CS.
A number of experimental manipulations have been shown to influence latent
inhibition in ways predicted by the theory (references in Gray et al.
1991a unless others given). Thus, the indirect dopamine agonist and
psychotomimetic, amphetamine, blocks latent inhibition in both rats and
human volunteers, showing in both cases an inverse dependence upon dose
(N. S. Gray et al. 1992a); and this effect is reversed by dopamine
receptor antagonists with anti-psychotic action. Given on their own, such
anti-psychotic drugs increase latent inhibition in both animal (Dunn et
al. 1993) and human (Williams et al. 1994) subjects.  The model Gray et
al. (1991a; 1991b) model attributes the effect of amphetamine on latent
inhibition to the release of dopamine specifically in n. accumbens (Figure
8); intense dopaminergic activity in this structure is thought to
interrupt motor programming and substitute exploratory behaviour (Kelly et
al. 1975). This prediction is supported by several observations. First,
latent inhibition is abolished also by nicotine (Joseph et al. 1993), a
drug which causes dopamine release in n. accumbens but not in the
caudate-putamen (Brazell et al.  1990). Second, a CS paired with footshock
elicits conditioned dopamine release in n. accumbens, and this response is
blocked if the CS is first preexposed, paralleling behavioural latent
inhibition (Young et al. 1993). Third, amphetamine injected directly into
n. accumbens, but not into the caudate-putamen, has been reported to block
latent inhibition by Solomon & Staton (1982), although Killcross & Robbins
(1993) failed to replicate this finding. Fourth, excitotoxic lesions of
the shell of n. accumbens also blocks latent inhibition (Tai et al., in
press).  Fifth, destruction of the dopaminergic afferents to the n.
accumbens (by local injection of the catecholamine-specific neurotoxin, 6-
hydroxydopamine) has the same effect as systemic administration of
dopamine-receptor antagonists, that is, this lesion potentiates latent
inhibition (Peters et al., in preparation).

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