NK-3 receptor activation depolarizes and induces an after-depolarization in pyramidal neurons in gerbil cingulate cortex

Abstract

The involvement of tachykinins in cortical function is poorly understood. To study the actions of neurokinin-3 (NK3) receptor activation in frontal cortex, whole cell patch clamp recordings were performed from pyramidal neurons in slices of cingulate cortex from juvenile gerbils. Senktide (500 nM), a selective NK3 receptor agonist, induced a transient increase in spontaneous EPSPs in layer V pyramidal neurons, accompanied by a small depolarization (∼4 mV). EPSPs during senktide had a larger amplitude and faster 10–90% rise time than during control. Senktide induced a transient depolarization in layer II/III pyramidal neurons, which often reached threshold for spikes. The depolarization (∼6 mV) persisted in TTX, and was accompanied by an increase in input resistance. Senktide also transiently induced a slow after-depolarization, which appeared following a depolarizing pulse. The slow after-depolarization persisted in TTX. These data suggest that activation of NK3 receptors on layer II/III pyramidal neurons induce post-synaptic depolarization and an after-depolarization, which could be mediated by blockade of a leak potassium conductance and a non-selective cation conductance, respectively.