Abstract

Startle amplitude and startle-stimulus-induced freezing were measured in a standard acoustic startle response (ASR) paradigm in rats. Subsequently conditioned freezing was measured to an auditory conditioned stimulus (CS) with a foot-shock unconditioned stimulus (US). In Experiment 1, lesions to the brachium of the inferior colliculus (BIC) increased ASR amplitude and freezing. Lesions to the nucleus of the trapezoid body abolished ASR and marginally reduced freezing. Neither lesioned group differed from controls in conditioned freezing to the auditory CS. In Experiment 2, lesions to the medial geniculate nucleus (MGN) increased ASR amplitude, as did BIC lesions, but reduced freezing, while BIC lesions increased freezing. MGN lesions, unlike BIC lesions, significantly attenuated freezing to the auditory CS, as compared with controls. Both groups startled less than controls to a weak shock stimulus. The data suggest an ascending auditory pathway medial to BIC that carries the fear-inducing dimension of an acoustic stimulus and a descending pathway in BIC that provides tonic inhibition of the acoustic input to the ASR circuitry.

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