Summary:Purpose: To determine whether seizure activity, repeatedly elicited in the hippocampus, could alter the functional organization of neocortical movement representations (motor maps) and whether a relation exists between the number of afterdischarges recorded in the sensorimotor neocortex and the size of the motor maps.Methods: We electrically kindled the right ventral hippocampus of Long-Evans hooded rats, twice daily, for 40 sessions and recorded the afterdischarges in the stimulated hippocampus and right sensorimotor neocortex. Between 3 and 7 days after the last seizure, we used high-resolution intracortical microstimulation to derive the forelimb-movement representations in the left (un-implanted) sensorimotor neocortex.Results: In the hippocampal kindled rats, we observed a dramatic expansion of the area of neocortex that would elicit forelimb movements compared with sham-kindled controls. The number of afterdischarges recorded in the neocortex was significantly and positively correlated with the size of the motor maps.Conclusions: Seizures propagating from the hippocampus have long-distance effects on the functional organization of motor maps.

Long-term depression (LTD) is one of the most widely investigated models of the synaptic mechanisms underlying learning and memory. Previous research has shown that induction of LTD in the neocortex decreases measures of pyramidal cell dendritic morphology in both layers III and V. Here, we investigated the effects of LTD induction on 1) the time course of recovery of synaptic efficacy, 2) movement representations, 3) cortical thickness and layer V neuron density, and 4) the density of excitatory and inhibitory synapses in layer V of sensorimotor neocortex. Rats carried a stimulating electrode in the midline corpus callosum and a recording electrode in the right sensorimotor neocortex. Each rat received either low-frequency stimulation composed of 900 pulses at 1 Hz or handling daily for a total of 20-25 days. Callosal-neocortical evoked potentials were recorded in the right hemisphere before and after stimulation or handling. Our results show that LTD induction lasts for 3 weeks and results in smaller motor maps of the caudal forelimb area. We did not observe any reduction in neocortical thickness or neuron density. There was a reduction in the density of excitatory perforated synapses and an increase in the density of inhibitory synapses in layer V of the sensorimotor neocortex, thereby providing a general mechanism for the reduction in motor map size. This study sheds light on the interaction between an artificial model of learning, receptive field characteristics, and synaptic number in the sensorimotor cortex.

Atypically organised motor maps have been described in some people with epilepsy and we have modelled this in rats. Our goal is to more fully understand the mechanisms responsible for seizure-induced functional brain reorganisation and to reverse their effects. Here we present an overview of the relationship between neocortical motor maps, seizures, and interictal behaviour. To begin we summarise the observations of atypical motor maps with epilepsy and in animal models following experimentally induced seizures. Our novel experiments have established that motor map expansion is linked to a functional alteration of motor behaviour. Evidence for some of the putative brain mechanisms responsible for motor map size is discussed. Our successes reversing seizure-induced map expansion by two different methods are also briefly reviewed. Lastly, unanswered questions for possible future experimentation are posed.