Synaptic reorganization in the feline ventral anterior thalamic nucleus induced by lesions in the basal ganglia.
This report presents the results of quantitative analysis of synaptic coverage of the dendrites of thalamocortical projection neurons in the adult cat ventral anterior thalamic nucleus (VA) and its changes at short (4 days)- and long-term (1 year) survival times after combined unilateral kainic acid lesions in the substantia nigra pars reticularis and entopeduncular nucleus. The study showed that deafferentation induced an increase in the appositional length of the dendrites of GABAergic local circuit neurons along projection neuron dendrites, accompanied by an increase in the number of dendrodendritic synapses. Dendritic or axonic origin of other unusual presynaptic structures at 1 year postlesion could not be established with certainty. All of them displayed some features of growth cones, such as an abundance of tubular and vesicular structures many with electron-dense contents. Projection neuron dendrites postsynaptic to these profiles contained numerous coated vesicles at the same survival time. The findings suggest that (i) the lesioning of the two basal ganglia output structures induces synaptic reorganization in the VA, (ii) this process appears to be active at 1 year after deafferentation, and (iii) all reactive systems display symmetric contacts and positive GAD immunoreactivity suggesting that homotypic remodeling is taking place. Despite the signs of remodeling, the density of presynaptic terminals with symmetric contacts on primary and secondary projection neuron dendrites in the VA remained below the control level at 1 year postlesion suggesting that an imbalance of excitatory and inhibitory inputs on thalamocortical projection neurons may persist for long periods after deafferentation.
Kultas-Ilinsky
K
K
Department of Anatomy, University of Iowa College of Medicine, Iowa City 52242.
De Boom
T
T
Ilinsky
I A
IA
D000818:Animals; D001479:Basal Ganglia / Q000473:pathology*; D002415:Cats; D005260:Female; D008297:Male; D009474:Neurons / Q000473:pathology; D013569:Synapses / Q000473:pathology / Q000648:ultrastructure*; D013787:Thalamic Nuclei / Q000473:pathology / Q000648:ultrastructure*