ReviewThe neural circuitry and molecular mechanisms underlying delay and trace eyeblink conditioning in mice

- The molecular mechanisms underlying DEC and TEC in mice differ from each other.
- Amygdala-Cerebellum-Prefrontal Cortex-Dynamic-Conditioning Model for DEC in mice is proposed.
- The forebrain regions may play an essential role in TEC of mice.
- Cerebellar cortex seems to be out of the neural circuitry of TEC in mice.

Classical eyeblink conditioning (EBC), a simple form of associative learning, has long been served as a model for motor learning and modulation. The neural circuitry of EBC has been studied in detail in rabbits. However, its underlying molecular mechanisms remain unclear. The advent of mouse transgenics has generated new perspectives on the studies of the neural substrates and molecular mechanisms essential for EBC. Results about EBC in mice differ in some aspects from those obtained in other mammals. Here, we review the current studies about the neural circuitry and molecular mechanisms underlying delay and trace EBC in mice. We conclude that brainstem-cerebellar circuit plays an essential role in DEC while the amygdala modulates this process, and that the medial prefrontal cortex (mPFC) as a candidate is involved in the extra-cerebellar mechanism underlying delay eyeblink conditioning (DEC) in mice. We propose the Amygdala-Cerebellum-Prefrontal Cortex-Dynamic-Conditioning Model (ACPDC model) for DEC in mice. As to trace eyeblink conditioning (TEC), the forebrain regions may play an essential role in it, whereas cerebellar cortex seems to be out of the neural circuitry in mice. Moreover, the molecular mechanisms underlying DEC and TEC in mice differ from each other. This review provides some new information and perspectives for further research on EBC.