Neurophysiological alterations in caudate neurons in aged cats

Abstract

These neurophysiological studies provide information on the alterations in functional capacity of neurons in the aging caudate nucleus (Cd) of the cat. The major finding is that there is a marked loss of excitation in the Cd during the aging process. This loss is most apparent in animals 11–14 years of age but is demonstrable in animals 6–7 years of age. Extracellular recording techniques were used to test the ability of Cd neurons to respond to activation of two of their major inputs, the precruciate cortex (CX) and the substantia nigra (SN). Types of responses that were evoked in both 1–3- and 11–14-year groups were similar and consisted of excitation, excitation followed by inhibition of action potentials or inhibition alone without preceding excitation. The frequency of occurrence of these responses was altered in the aged animals when either input was stimulated. In 1–3-year-old cats CX stimulation evoked initially excitatory responses in 75% of the cells tested while in 11–14-year-old cats excitatory responses occurred in 62% of the cells. When the SN was stimulated the decrease in initial excitation was greater (69% in 1–3-vs 35% in 11–14-year groups). In all aged animals but not in 1–3-year-old cats stimulation thresholds were higher (39–79%) for evoking excitatory responses than for evoking inhibitory responses. In order to assess synaptic security, the ability of Cd neurons to respond to iterative stimulation was determined. Distributions of the minimum interval necessary to evoke two excitatory responses were constructed. There was a marked increase in the proportion of longer intervals in the aged animals indicating that the synaptic response was less secure. There was a tendency for more of the responses in aged animals to have shorter latencies. This result was probably due to loss secure longer latency responses that are mediated via multisynaptic pathways. These findings indicate that there are functional changes in a population of Cd neurons in aged cats that impair their ability to process information.