fg-9041 and 1-ethyl-2-benzimidazolinone

Climbing fiber input to the cerebellum is believed to serve as a teaching signal during associative, cerebellum-dependent forms of motor learning. However, it is not understood how this neural pathway coordinates changes in cerebellar circuitry during learning. Here, we use pharmacological manipulations to prolong the postcomplex spike pause, a component of the climbing fiber signal in Purkinje neurons, and show that these manipulations enhance the rate of learning in classical eyelid conditioning. Our findings elucidate an unappreciated aspect of the climbing fiber teaching signal, and are consistent with a model in which convergent postcomplex spike pauses drive learning-related plasticity in the deep cerebellar nucleus. They also suggest a physiological mechanism that could modulate motor learning rates.

Topics: Analysis of Variance; Animals; Benzimidazoles; Blinking; Calcium Channel Agonists; Cardiovascular Agents; Cerebellar Nuclei; Cerebellum; Conditioning, Eyelid; Electric Stimulation; Excitatory Amino Acid Antagonists; Excitatory Postsynaptic Potentials; GABA Antagonists; Learning; Mice; Nerve Fibers; Picrotoxin; Purkinje Cells; Pyrimidines; Quinoxalines; Rats; Rats, Sprague-Dawley; Time Factors