INVESTIGADORES
ZOLD Camila Lidia
congresos y reuniones científicas
Título:
Abnormal responses of globus pallidus units to cortical stimulation in experimental parkinsonism
Autor/es:
ZOLD, CAMILA; MURER, GUSTAVO; RIQUELME, LUIS
Lugar:
Mar del PLata, Buenos Aires, Argentina
Reunión:
Congreso; Congreso Conjunto de Sociedades Biomédicas; 2004
Resumen:
The normal operation of the basal ganglia (BG) requires the
processing of cortical information through segregated parallel channels along
with the integration of cortical-striatal and cortical-subthalamic inputs.
Nigrostriatal lesions would alter essential aspects of information processing
in the BG causing the clinical signs of parkinsonism. As the globus pallidus
(GP) receives cortical inputs through the striatum (inhibitory) and subthalamus
(excitatory), we decided to study the effects of nigrostriatal lesions on the
responses of GP units to electrical stimulation of the motor cortex. In
6-OHDA-lesioned rats (a widespread model of parkinsonism) 26 of 27 (98%) GP
units responded to motor cortex stimulation against 23% (4 of 17 units) in
control animals (p<0.001, Fisher exact test). This increased responsiveness
was due to a greater incidence of both excitations (96% vs 23%, p<0.001) and
inhibitions (40% vs 12%, p<0.05).
We also found an abnormal integration of inhibitory
(cortical-striatum-GP) and excitatory (cortical-subthalamus-GP) responses in GP
units: none of the neurons of control rats showed
excitation-inhibition-excitation responses against 6 of 27 in the 6-OHDA rats
(p<0.05).
These
results indicate that: i) the representation of a focus of cortical activity is
distributed more extensively in the GP in experimental parkinsonism, suggesting
a degradation of the capacity of parallel processing; ii) this alteration could
be explained by an increased transfer of activity through both the
cortical-striatum-GP and cortical-subthalamus-GP pathways; iii) the presence of
greater number of triphasic responses in 6-OHDA rats suggests increased
convergence cortical-striatum-GP and cortical-subthalamus-GP inputs in
parkinsonian rats.