Intratelencephalic corticostriatal neurons equally excite striatonigral and striatopallidal neurons and their discharge activity is selectively reduced in experimental parkinsonism.
European Journal of Neuroscience. 2008-04-25; 27(9): 2313-2321
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1. Eur J Neurosci. 2008 May;27(9):2313-21. doi: 10.1111/j.1460-9568.2008.06192.x.
Intratelencephalic corticostriatal neurons equally excite striatonigral and
striatopallidal neurons and their discharge activity is selectively reduced in
Ballion B(1), Mallet N, Bézard E, Lanciego JL, Gonon F.
(1)Centre National de la Recherche Scientifique UMR 5227, case 63, Université
Victor Segalen Bordeaux 2, 33076 Bordeaux, France.
Striatonigral and striatopallidal neurons form distinct populations of striatal
projection neurons. Their discharge activity is imbalanced after dopaminergic
degeneration in Parkinson’s disease. Striatal projection neurons receive massive
cortical excitatory inputs from bilateral intratelencephalic (IT) neurons
projecting to both the ipsilateral and contralateral striatum and from collateral
axons of ipsilateral neurons that send their main axon through the pyramidal
tract (PT). Previous anatomical studies in rats suggested that IT and PT inputs
preferentially excite striatonigral and striatopallidal neurons, respectively.
Here we used electrophysiological criteria to identify them with antidromic
stimulations. We show that the spontaneous discharge activity of IT neurons is
depressed, whereas that of PT neurons is not affected in the rat cortex
ipsilateral to 6-hydroxydopamine injection. However, our functional experiments
do not support the hypothesis of a differential cortical input to striatal
pathways. Firstly, although the conduction velocity of PT neurons is 4.6 times
faster than that of IT neurons, identified striatopallidal and striatonigral
neurons exhibit identical latencies of their spike responses to electrical
stimulation of the ipsilateral cortex. Secondly, although PT neurons are
ipsilateral, both striatal populations exhibit similar sensitivity to the
stimulation of the ipsilateral and contralateral cortex. We suggest that IT
neurons provide the main excitatory input to both striatal populations and that
the corticostriatal PT input is weaker. Therefore, our functional data do not
support our previous hypothesis that the deficit of IT neurons associated with
the dopaminergic depletion might contribute to the striatal imbalance. This
imbalance might rather result from intrinsic striatal mechanisms.
PMID: 18445222 [Indexed for MEDLINE]