Long-term potentiation of the amygdalo-striatal synaptic transmission in the course of development of amygdaloid kindling in cats.

Limbic projection from the amygdala to the basal forebrain and the neostriatum was studied physiologically during development of amygdaloid kindling in cats. Stimulation of the basolateral amygdaloid nucleus (BL) produced the negative field potential monosynaptically in the nucleus accumbens (Acb), while in the caudate nucleus (Cd) it produced a slight negative deflection with a longer latency. The latter is produced disynaptically as it showed marked facilitation in its amplitude when two stimuli were applied at short intervals. After a single period of tetanic stimulation of the BL with a 2-s train of 50-Hz pulses, there was a long-term potentiation (LTP) of both Acb and Cd responses in amplitude to test pulses to the same electrode. These responses increased up to 140% of the pre-tetanus control for 1 h following tetanic stimulation and declined gradually back to the baseline thereafter. However, a slight or moderate increase in the response was observed even 24 h later. Therefore, trains of stimuli presented once per day had a cumulative effect on the negative field potentials evoked in the Acb and the Cd in the early stage of kindling development. In particular, the disynaptic response in the Cd increased markedly to over 10 times as the prekindled control. These findings suggest that LTP in amygdalo-striatal synaptic transmission following tetanic stimulation represents an example of plastic changes in a neuronal chain within the neostriatum, which would underlie the pathophysiological mechanism for developing motor seizures of amygdaloid kindling.