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Involvement of the medial geniculate body in prepulse inhibition of acoustic startle.

Journal article
Authors Jianhua Zhang
Jörgen Engel
Mia Ericson
Lennart Svensson
Published in Psychopharmacology
Volume 141
Issue 2
Pages 189-96
ISSN 0033-3158
Publication year 1999
Published at Institute of Physiology and Pharmacology
Institute of Physiology and Pharmacology, Dept of Pharmacology
Pages 189-96
Language en
Keywords Acoustic Stimulation, Animals, Baclofen, pharmacology, Calcium Channel Blockers, pharmacology, GABA Agonists, pharmacology, Geniculate Bodies, drug effects, physiology, Inhibition (Psychology), Male, Microdialysis, Muscimol, pharmacology, Rats, Rats, Sprague-Dawley, Reflex, Startle, drug effects, physiology, Tetrodotoxin, pharmacology
Subject categories Pharmacology, Neurobiology, Neuroscience


Prepulse inhibition of acoustic startle is the normal reduction in startle response to an intense auditory stimulus when this stimulus is immediately preceded by a weaker prestimulus. Previous studies have shown that several neuroanatomical structures and pathways in the brain are involved in the modulation of prepulse inhibition. In the present study, the functional importance of the medial geniculate body (MG) in the modulation of prepulse inhibition was investigated. To this end, in vivo brain microdialysis probes were used to infuse drugs locally into the MG of awake, freely moving rats simultaneously with startle response and prepulse inhibition measurements in the same animals. Intrageniculate infusion of the sodium channel blocker, tetrodotoxin, significantly reduced prepulse inhibition without affecting baseline startle amplitude. A similar effect was obtained after intrageniculate infusion of the GABA(B) receptor agonist, baclofen. In addition, intrageniculate infusion of muscimol, an agonist at the GABA(A) receptor complex, reduced prepulse inhibition, although this effect was obtained at a higher concentration of the drug compared to that of baclofen. These studies suggest that the MG is involved in the modulation of prepulse inhibition and that auditory signals relayed via the MG may be subjected to inhibitory control at this level, involving GABA neurotransmission.

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