Ultrastructural and metabolic changes in the neuropeptide Y-containing striatal neuronal network after thermocoagulatory cortical lesion in adult rat

Citation
P. Kachidian et al., Ultrastructural and metabolic changes in the neuropeptide Y-containing striatal neuronal network after thermocoagulatory cortical lesion in adult rat, SYNAPSE, 34(3), 1999, pp. 208-221
Citations number
66
Categorie Soggetti
Neurosciences & Behavoir
Journal title
SYNAPSE
ISSN journal
08874476 → ACNP
Volume
34
Issue
3
Year of publication
1999
Pages
208 - 221
Database
ISI
SICI code
0887-4476(199912)34:3<208:UAMCIT>2.0.ZU;2-J
Abstract
This study examined the effects of unilateral thermocoagulatory cortical le sion on the pattern of neuropeptide Y immunostaining in the rat ipsilateral striatum at 4 and 21 days post-lesion. Light microscopic analysis showed a significant increase in the number of neuropeptide Y-positive neurons vs. control at both time points; paradoxically, the intraneuronal level of labe lling significantly decreased at 4 days post-lesion but increased at 21 day s post-lesion. Ultrastructural analysis in control condition showed a highe r proportion of dendritic versus axonal labelled processes (3.5 ratio); all the neuropeptide Y synaptic terminals formed symmetrical contacts, mostly onto unlabelled dendrites. At 4 days post-lesion, the neuropeptide Y-positi ve axon density dramatically increased (+ 576%) without significant change in the labelled dendrite density, vs. control values; the density of neurop eptide Y synaptic terminals increased in parallel, by 233%. In addition, a significant proportion of large neuropeptide Y boutons forming asymmetrical synapses onto unlabelled spines were observed. At 21 days post-lesion, den sities of neuropeptide Y dendrites, axons, and synaptic terminals increased by 68, 246 and 125%, respectively, vs, control. But, the morphological fea tures of the neuropeptide Y axonal processes and synaptic specializations o f the boutons were similar to those observed in control condition. These da ta (1) raise an important issue regarding the origin of the terminals formi ng asymmetrical synapses in the striatum, (2) suggest that adaptative chang es in the neuropeptide Y neuronal network may be a main component of striat al remodelling resulting from the progressive loss of cortical inputs, and (3) reinforce the view that neuropeptide Y and excitatory amino acid functi ons may be tightly linked in the striatum. Synapse 34:208-221, 1999. (C) 19 99 Wiley-Liss, Inc.