A golgi analysis of cortical pyramidal cells in the unilateral parkinson rat: absence of change in the affected hemisphere vs hypertrophy in the intact hemisphere.
OBJECTIVE
Unilateral dopamine (DA) depletion in the rat provides an analog of human Parkinson's disease. The classic view of DA loss is that it produces changes in the activity of striatal-cortical circuitry that results in reduced frontal cortex neural activity. This "functional deafferent" view is consistent with findings that animals display sensorimotor deficits in the contralateral-to-lesion side of the body and compensatory behavior adjustments in the ipsilateral-to-lesion side of the body. The present study examined how DA depletion and the associated sensorimotor changes affect the morphology of the ipsilateral or contralateral neocortex neurons as assessed by dendritic morphology in Golgi-stained tissue.


METHODS
Rats were given unilateral 6-hydroxydopamine (6-OHDA) or sham lesions in the nigrostriatal bundle. Lesion success was confirmed by enduring bilateral motor impairments in a skilled-reaching task, compensatory use of the ipsilateral-to-lesion limbs, and by increases in amphetamine and apomorphine-induced rotational behavior.


RESULTS
Brains processed for Golgi-Cox staining at 1, 3, 8, or 24 months after the lesion showed no changes in dendritic arborization or synapse number in layer V pyramidal cells of motor cortex ipsilateral to the 6-OHDA lesion (DA-depleted hemisphere) at any postsurgical recovery stage. There was an increase in dendritic arborization in all lesion groups in the hemisphere contralateral to the lesion (good hemisphere).


CONCLUSIONS
The results are inconsistent with the classical view of frontal cortex functional deafferentiation due to DA loss but do suggest that compensatory behavior leads to dendritic hypertrophy in the good hemisphere.
Miklyaeva
Elena I
EI
Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, AB, T1K 3M4, Canada.
Whishaw
Ian Q
IQ
Kolb
Bryan
B
D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D002540:Cerebral Cortex / Q000473:pathology*; D003712:Dendrites / Q000648:ultrastructure; D049229:Dendritic Spines / Q000648:ultrastructure; D003913:Dextroamphetamine / Q000494:pharmacology; D005260:Female; D005552:Forelimb / Q000503:physiopathology; D006056:Golgi Apparatus / Q000648:ultrastructure*; D006984:Hypertrophy; D009043:Motor Activity / Q000187:drug effects; D009044:Motor Cortex / Q000473:pathology; D016627:Oxidopamine; D010302:Parkinson Disease, Secondary / Q000139:chemically induced / Q000473:pathology* / Q000503:physiopathology; D011597:Psychomotor Performance; D017966:Pyramidal Cells / Q000648:ultrastructure*; D051381:Rats; D020318:Rats, Long-Evans; D012399:Rotation; D013569:Synapses / Q000648:ultrastructure
D016627:Oxidopamine; D001058:Apomorphine; D003913:Dextroamphetamine