Short-term facilitation in the anterior cingulate cortex following stimulation of the medial thalamus in the rat

The present study examined the distribution and localization of synaptic activities (field potentials, multiunit activities and sink source currents) evoked in the anterior cingulate cortex (ACC) by electrical paired pulse stimulation of the ipsilateral medial thalamus (MT). Male Sprague–Dawley rats were anesthetized with halothane (1.0–1.5%), and electrical paired pulses stimuli (100–300 μA, inter-pulse interval, 100 ms) were delivered to the MT. Tungsten microelectrodes and a multichannel Michigan probe were used to record the evoked field potentials and multiunit activities in the ACC. Paired pulse stimulation facilitated field potentials and multiunit activities elicited from several MT nuclei. The second component of the negative field potential (com2) was augmented to about 2.5 times that of the first component (com1), and the integrated multiunit activities were facilitated by about 1.6-fold. Paired stimulation produced an expansion of the maximal negative potential from layer II/III into the deeper layers of the cingulate cortex area 1 (Cg1). Furthermore, the potentiated activity spread into adjacent secondary motor cortex (M2) and prelimbic cortex (PrL). Meanwhile, the area covered by the maximal integrated multiunit activities expanded from layer V (com1) to layers II–V (com2) in M2, Cg1 and PrL. The current source density (CSD) analysis revealed that the short latency sinks were located in layer II/III and layer V/VI. The sink currents were potentiated and expanded to more superficial and to deeper layers when a second pulse was delivered with a 100-ms time delay. Sink currents and the paired pulse facilitation (PPF) were reduced by morphine treatment (5 mg/kg, i.v.), and this effect could be blocked by naloxone. Electrical stimulation at 10 Hz in the MT induced more pronounced c-fos immunolabeling of neurons in the medial prefrontal cortex than did 1-Hz stimulation. The short-term facilitation occurred in the middle layers and expanded to the deeper layers of the ACC. These changes may mediate the effective signal transference in the specific frequency associated with painful responses.