Age-dependent impairment in learning and memory functions occurs in many animal species, including humans. Although cell death contributes to age-related cognitive impairment in pathological forms of aging, learning and memory deficiencies develop with age even without substantial cell death. The molecular and cellular basis of this biological aging process is not well understood but seems to involve a decline in the aging brain's capacity for experience-dependent plasticity. To aid in resolving this issue, we used a simple snail appetitive classical conditioning paradigm in which the underlying molecular, cellular, and neural network functions can be directly linked to age-associated learning and memory performance (i.e., the Lymnaea stagnalis feeding system). Our results indicate that age does not affect the acquisition of appetitive memory but that retention and/or consolidation of long-term memory become progressively impaired with advancing age. The latter phenomenon correlates with declining electrophysiological excitability in key neurons controlling the feeding behavior. Together, these results present the Lymnaea feeding system as a powerful paradigm for investigations of cellular and molecular foundations of biological aging in the brain.

People with epilepsy have a high incidence of interictal behavioural problems that appear to be related to the location of their seizure focus. This study investigated a novel test of the hypotheses that repeated seizures result in behavioural deficits and altered performance during the interictal state, and that those behaviours are related to the presence of more highly efficacious excitatory synapses. We tested these hypotheses by first repeatedly eliciting seizures with electric current through indwelling electrodes in the corpus callosum at the level of the caudal forelimb area of sensorimotor neocortex in the rat. We then assessed learned skilled behaviours that primarily utilize the forelimbs on tasks that are sensitive to the functional integrity of that structure. We observed both behavioural deficits and altered kinematic performance in rats that experienced repeated neocortical seizures relative to an electrode-implanted control group. From a separate set of rats, tissue was prepared for quantification of thickness and excitatory synaptic subtypes from neocortical layer V. We observed significantly increased numbers of perforated synapses that make their connections directly onto the dendritic shaft at 3 weeks following the last seizure. Altered reaching behaviours are likely due to neural reorganization in the neocortex including more efficacious synapses.