Disruption of sensory gating by the α2 selective noradrenergic antagonist yohimbine
1993; Elsevier BV; Volume: 33; Issue: 2 Linguagem: Inglês
10.1016/0006-3223(93)90313-3
ISSN1873-2402
AutoresKaren E. Stevens, J. Meltzer, Gregory M. Rose,
Tópico(s)Neuroscience and Neuropharmacology Research
ResumoSchizophrenia is a disease marked by abnormalities in sensory processing that are thought to be involved in the development of the disease. Specifically, it has been suggested that schizophrenics are unable to adequately filter incoming stimuli, which leads to sensory overload or flooding, and thence to disorganization and decompensation (Venebles 1964). Central filtering mechanisms have been demonstrated in the laboratory in both humans (Fruhstorfer et al 1970) and animals (Knight et al 1985). Additionally, it has been shown that these filtering mechanisms are aberrant in schizophrenics (Adler et al 1982; Braff and Geyer 1990) and in amphetamine-treated or phencyclidine-treated laboratory rats (Adler et al 1986; Stevens et al 1991). Sensory filtering, or is easily demonstrated using a condition-test auditory paradigm (Braff and Geyer 1990). In this paradigm, click pairs are delivered at a 0.5-sec interval. Normal humans and unmedicated rats show a reduced auditory evoked potential to the second of these closely paired stimuli (Freedman et al 1987; Adler et al 1982; Stevens et al 1991). Previous work has indicated that central noradrenergic pathways are important in the gating process (Adler et al 1988; Stevens et al 1991). To more directly examine the noradrenergic contribution to sensory gating, we have employed the selective or2 antagonist, yohimbine, to enhance noradrenergic tone via the blockade of inhibitory feedback autoreceptors (Fludder and Leonard 1979). Our results demonstrate that this treatment can disrupt sensory gating.
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