The amplitude of the acoustic startle response (ASR) in rats is increased in the presence of a cue which has previously been paired with an electric footshock. This phenomenon is termed fear-potentiated startle and is a useful model to investigate the neural systems underlying fear and anxiety. A series of studies have shown, that the amygdaloid complex is necessary for the acquisition and the expression of conditioned fear. Further experiments have delineated an efferent amygdalofugal pathway to the primary startle circuit, at the level of the caudal pontine reticular formation, which mediates the expression of conditioned fear [10]. Yet it was unclear, whether this amygdaloreticular pathway directly transfers the effects of conditioned fear from the amygdala to the primary startle circuit or whether there exist one or more relay nuclei within this pathway or even additional parallel circuits. Based on our previous finding that the midbrain central gray (CG) is involved in the mediation of the facilitatory effects on the ASR of unconditioned aversive events, the present study tested the hypothesis that the CG is important for the potentiation of the ASR by conditioned fear. Therefore, we lesioned the CG before and after fear-conditioning and examined the effects of these lesions on fear-potentiated startle. Pre- and post-training lesions of the CG totally blocked the potentiation of the ASR amplitude by conditioned fear, which was seen in sham-lesioned rats, indicating that CG lesions affected the expression of conditioned fear. The baseline ASR amplitude was not influenced by CG lesions. We discuss possible pathways and mechanisms underlying the expression of conditioned and unconditioned fear in rats.