Glutamic acid decarboxylase activity decreases in mouse neocortex after lesions of the basal forebrain.
Glutamic acid decarboxylase (GAD) activity was measured in the cerebral cortex of animals after acute and chronic lesions to basal forebrain cholinergic nuclei. Such lesions were shown to result in an extensive depletion of cholinergic markers in parietal cerebral cortex. A statistically significant 30% decrease in GAD activity was first detected at 6 weeks postlesion and was still measurable 8 months after the lesion. These results suggest that cholinergic inputs to cortex indirectly or directly influence GABAergic transmission in cortex.
Höhmann
C F
CF
Bear
M F
MF
Ebner
F F
FF
D000818:Animals; D002540:Cerebral Cortex / Q000201:enzymology* / Q000502:physiology; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D005917:Globus Pallidus / Q000502:physiology*; D005968:Glutamate Decarboxylase / Q000378:metabolism*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009434:Neural Pathways / Q000502:physiology; D009435:Synaptic Transmission; D005680:gamma-Aminobutyric Acid / Q000502:physiology
D005680:gamma-Aminobutyric Acid; D002795:Choline O-Acetyltransferase; D005968:Glutamate Decarboxylase