Changes in choline acetyltransferase, glutamic acid decarboxylase, high-affinity glutamate uptake and dopaminergic activity induced by kainic acid lesion of the thalamostriatal neurons.
Kainic acid lesion of the 'centre médian'-parafascicular complex of the thalamus inducing a degeneration of the thalamostriatal neurons was followed by a decrease in choline acetyltransferase (ChAT) in the rostral part of the striatum in the rat. This decrease in ChAT was concomitant with an increase in glutamate decarboxylase, high-affinity glutamate uptake and apparent dopamine turnover. These results suggest that the thalamostriatal partly cholinergic input exerts a powerful control over GABAergic, glutamatergic and dopaminergic neurons in the basal ganglia.
Nieoullon
A
A
Scarfone
E
E
Kerkerian
L
L
Errami
M
M
Dusticier
N
N
D000818:Animals; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D002799:Cholinergic Fibers / Q000502:physiology; D003342:Corpus Striatum / Q000502:physiology*; D004298:Dopamine / Q000502:physiology; D005968:Glutamate Decarboxylase / Q000378:metabolism; D005971:Glutamates / Q000502:physiology; D018698:Glutamic Acid; D007608:Kainic Acid / Q000494:pharmacology; D009434:Neural Pathways / Q000502:physiology; D051381:Rats; D009435:Synaptic Transmission; D013787:Thalamic Nuclei / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000502:physiology
D005971:Glutamates; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D002795:Choline O-Acetyltransferase; D005968:Glutamate Decarboxylase; D007608:Kainic Acid; D004298:Dopamine