Corticotrophin-releasing hormone decreases synaptic transmission in rat sensorimotor cortex in vivo.

Corticotrophin-releasing hormone is a key regulator of the mammalian stress response. Although its actions on behavior are well documented, the actions of corticotrophin-releasing hormone in cortical neuronal systems are poorly understood. In the present experiments, adult male Sprague-Dawley rats were anesthetized and field excitatory post-synaptic potential recordings were made from sensorimotor cortex layer II/III and layer V cells. Infusions of corticotrophin-releasing hormone (100 ng/nl) directly into the sensorimotor cortex produced a significant depression of the initial excitatory component of evoked responses that could be prevented by prior administration of a corticotrophin-releasing hormone antagonist. Although requiring the activation of corticotrophin-releasing hormone receptors, the depression was also dependent upon N-methyl-D-aspartate receptor activity and could be blocked by the competitive N-methyl-D-aspartate antagonist -3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonate. These findings demonstrate that corticotrophin-releasing hormone has a novel depressant-like action in sensorimotor cortex in vivo that may play a role in modulating motor activity during periods of stress.