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phrenia to a breakdown between monitoring attention-related activity and endogenous
thought or motor programs (Gray et al., 1990).
Selective attention processing has long been described as impaired in psychotic patients
(Shakow, 1936) but descriptions of the psychological or neurobiological mechanisms
responsible have remained elusive (Oades, 1982). However as some patients (e.g. with
paranoid hallucinatory symptoms) have a more tractable form of illness (i.e. better prog-
nosis) and respond better clinically to neuroleptic medication (Straube & Oades, 1992) we
hypothesized that a subgroup analysis of CB performance in terms of active symptoms and
monoaminergic metabolic status might reveal features on which this cognitive adaptiveness
depends. The nature of these is, in part, predicted by the results of animal studies of learned
inattention.
In animals, latent inhibition is disrupted by amphetamine and facilitated by haloperidol
after acute∕subchronic systemic treatment (Solomon et al., 1981; Weineret al., 1988; Feldon
& Weiner, 1991). Local mesolimbic dopaminergic (DA) stimulation also disrupts (Solomon
& Staton, 1982). Serotonergic (5HT) activity in the raphe-hippocampal system has been
implicated (Solomon et al., 1978; 1980; Cassaday et al., 1993) and noradrenergic (NA)
function has been found to be relevant to the contextual sensitivity of latent inhibition
(Mohammed et al., 1986; Honey & Good, 1993). Many studies have implicated the ana-
tomical substrates of the hippocampus and nucleus accumbens (Ackil et al., 1969; Schmajuk
et al.. 1994; Tai et al., 1995). For rats an intact hippocampus is necessary for CB measured
in different task forms (Solomon, 1977; Rickert et al., 1978) but lesion of the dorsal NA
bundle rather than ascending 5HT projections attenuates CB (Lorden et al., 1980). Indeed
by pharmacologically changing the balance between α- and /J-NA interactions, CB can be
attenuated (Caza, 1984). The DA balance in mesolimbic and mesocortical areas is also
important for the expression of CB. Thus, amphetamine produces a haloperidol-reversible
attenuation of CB (Crider et al., 1982) but haloperidol-induced DA supersensitivity reduces
CB (Crider et al., 1986). Prefrontal 6-OHDA lesions that increase DA turnover disturb CB
(Oades et al., 1987).
Learned inattention in healthy human subjects tends to be reduced if they show psychotic
personality features. Latent inhibition attenuation has been reported in those with high
psychoticism scores on the Eysenck (Baruch et al., 1988a) and MMPI scales (De la Casa et
al., 1993). However, this reduction is sensitive to the personality scale used (Baruch et al.,
1988a), experimental parameters (Lubow et al., 1992) and test form (Lipp & Vaitl, 1992).
However, for CB an initial report suggested that neurotic rather than psychotic features
may lead to an attenuation (Jones et al., 1990). This raises the question of whether certain
personality features are indicative of a trait contribution to psychopathological forms of
information processing.
In an audiovisual test acute schizophrenics initially showed attenuated latent inhibition
but normal performance in a later phase of the illness (Baruch et al., 1988b; Gray et al.,
1992). This applied to paranoid and non-paranoid subtypes (Lubow et al., 1987). While
the severity of symptoms probably played a role (Baruch et al., 1988b), these reports remain
equivocal on the role of symptom-type and medication, which we would predict to be
central to CB expression.
CB was examined by Jones et al. (1990; 1992), first, in a visual reaction time paradigm