Format

Send to

Choose Destination
Prog Brain Res. 2005;147:285-93.

Physiological studies of information processing in the normal and Parkinsonian basal ganglia: pallidal activity in Go/No-Go task and following MPTP treatment.

Author information

1
Department of Physiology, Hadassah Medical School, The Hebrew University, Jerusalem, Israel.

Abstract

Understanding the role of the basal ganglia in day to day behavior is critical for a better understanding of the role of these structures in pathological states--such as Parkinson's disease. To elucidate this connection, we studied pallidal activity in a monkey performing a delayed release Go/No-Go task and in monkeys treated with the dopaminergic neurotoxin--MPTP. We compared the results with the predictions of the action selection and reinforcement driven dimensionality reduction models of the basal ganglia. The fraction of responding pallidal neurons, as well as the ratio of positive to negative responses, were equal in the Go and the No-Go modes. The fraction of pallidal neurons with significant responses following the trigger signal (19/26) was higher than that following the visual cue (11/26); however, the fraction of negative responses was significantly higher following the cue signal (47%) than that following the trigger signal (22%). Most (80%) of the cue responses were sensitive to the laterality of the cue, whereas only 25% of the responses following the trigger signal were sensitive to the cue or movement direction. Finally, pallidal spiking activity was not correlated in the normal behaving monkey, and became highly synchronized following MPTP treatment. We conclude that pallidal activity in the normal monkey is consistent with the model of action selection, assuming that action is selected following the visual cue. However, the reinforcement driven dimensionality reduction model is consistent with both the Go/No-Go responses and the normal/MPTP correlation studies.

PMID:
15581713
DOI:
10.1016/S0079-6123(04)47021-6
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center