Amygdala inactivation impairs eyeblink conditioning in developing rats

Abstract

The amygdala facilitates acquisition of eyeblink conditioning in adult animals by enhancing conditioned stimulus (CS) inputs to the cerebellum and the unconditioned response circuitry. Ontogenetic changes in amygdala modulation of eyeblink conditioning have not been investigated directly. We examined the effects of amygdala inactivation on the ontogeny of eyeblink conditioning and conditioned freezing in rat pups. Rat pups received bilateral infusions of saline or bupivacaine into the central nucleus of the amygdala before each of the first 5 training sessions, which consisted of paired CS-US trials on postnatal days (P)17-19, P21-23, or P24-26. The final session consisted of CS-alone test trials to assess the effect of amygdala inactivation during training on conditioned freezing. Amygdala inactivation impaired acquisition of eyeblink conditioning in all of the age groups and impaired freezing to the context during the extinction test. The results indicate that the amygdala modulates cerebellar learning as soon as it begins to emerge ontogenetically.

Central amygdala lesions inhibit pontine nuclei acoustic reactivity and retard delay eyeblink conditioning acquisition in adult rats

“…The increase in UR amplitude provided by the CS (i.e., relative to US-alone trials) was negligible (5.0 %) compared to the increase seen in sham rats (42.7 %). This result runs counter to two prior EBC studies, which found no reliable experimental group differences in UR amplitude (based on CS-US trials), when the CEA was pharmacologically inactivated in young rats or, in adult rats, the whole amygdala was damaged (Lee & Kim, 2004;Ng & Freeman, 2014). Nevertheless, current data indicate that the loss of potentiated freezing and reflexive responding observed in lesion rats was, in both cases, most pronounced on the first training session.…”

“…Rats exhibit conditioned fear to the training context early in EBC in that they show elevated freezing before and after CS-US presentations (Britton & Astheimer, 2004;Ng & Freeman, 2014). We propose that the context-US memory grows in strength over training, such that subsequent exposures to the context-which includes both the physical chamber and the handling required to attach each subject's headstage-leads to faster retrieval and higher baseline freezing rates (see Fig.…”

Medial auditory thalamus is necessary for acquisition and retention of eyeblink conditioning to cochlear nucleus stimulation

“…6; LeDoux et al 1991;Blair et al 2005). Amygdala modulation of cerebellar-dependent motor learning could therefore be influenced from either the direct amygdala projection to LPN or from the reciprocal connection between the amygdala and MATN (Prince and Amaral 1981;Maren et al 2001;Poremba and Gabriel 2001;Taub and Mintz 2010;Ng and Freeman 2013).…”

Ontogeny of septohippocampal modulation of delay eyeblink conditioning

“…This moderate level of associative learning would presumably be susceptible to disruption. Indeed, we previously found that the modest level of eyeblink conditioning in pups trained on P17–19 can be reduced substantially (< 10% CRs) by amygdala inactivation (Ng & Freeman, 2013). The amygdala inactivation data suggest that the floor for CR percentage in infant eyeblink conditioning is substantially lower than the CR percentage in the lesion groups or the P17–19 control group in the current study.…”