Neuronal activity in the monkey motor thalamus during bicuculline-induced dystonia.
Recent data suggest that a decreased basal ganglia output may occur in dystonia, resulting in an increased thalamic drive to the mesial premotor cortex. In a previous work we found that injection of the GABAA antagonist bicuculline into the rostral motor thalamus induced contralateral dystonic postures, whereas myoclonic jerks were frequent after injection into the caudal motor thalamus. In the present study, we performed electrophysiological recordings in the rostral and caudal parts of the ventrolateral thalamus of two cynomolgus monkeys before and after bicuculline injections or saline injections. Discharge frequencies of thalamic neurons were increased after bicuculline injections vs. controls. Their discharge pattern was more bursty in the caudal part in which bursts of neuronal activity were correlated with myoclonic jerks. After bicuculline injection, neurons responded more frequently and less selectively to passive limb movements in both parts of the motor thalamus. Conversely, the response to microstimulation increased after bicuculline injection, particularly in the caudal part. Our data show that acute bicuculline-induced dystonia is associated with a reversible overactivity and disorganization of neuronal activity in the motor thalamus. Such a phenomenon might induce an overspreading of cortical activity leading to dystonia. We postulate that the distinct clinical syndromes observed after bicuculline injections into the rostral and caudal motor thalamus are due to differences both in the neuronal circuitry within each thalamic nucleus and in segregated cortical projections.
Macia
F
F
Laboratoire de Neurophysiologie, UMR CNRS 5543, Université Victor Segalen Bordeaux 2, 146, rue Léo Saignat 33076 Bordeaux, France.
Escola
L
L
Guehl
D
D
Michelet
Th
T
Bioulac
B
B
Burbaud
P
P
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects / Q000502:physiology; D001640:Bicuculline / Q000494:pharmacology; D004195:Disease Models, Animal; D004421:Dystonia / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*; D004558:Electric Stimulation; D005260:Female; D018756:GABA Antagonists / Q000494:pharmacology; D058787:GABA-A Receptor Antagonists; D008252:Macaca fascicularis / Q000033:anatomy & histology / Q000502:physiology*; D009044:Motor Cortex / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology*; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology; D009434:Neural Pathways / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology*; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D011963:Receptors, GABA-A / Q000378:metabolism; D020651:Ventral Thalamic Nuclei / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology*
D018756:GABA Antagonists; D058787:GABA-A Receptor Antagonists; D011963:Receptors, GABA-A; D001640:Bicuculline