title: Motor effects of GABA(A) antagonism in globus pallidus: studies of locomotion and tremulous jaw movements in rats.
abstract: BACKGROUND
  Although most rodent studies related to parkinsonian symptoms have focused on locomotion, tremulous jaw movements also have been used as a rodent model of tremor for investigating the circuitry of the basal ganglia.
  
  
  OBJECTIVE
  There are multiple pathways involved in the generation of parkinsonian symptoms. The globus pallidus is a basal ganglia relay nucleus, and the present study was conducted to investigate the effect of pallidal GABA antagonism on locomotion and tremulous jaw movements.
  
  
  METHODS
  Suppression of locomotion and induction of tremulous jaw movements were produced by repeated (i.e., 14 day) systemic administration of the dopamine D2 antagonist haloperidol, and by acute systemic injection of the muscarinic agonist pilocarpine. The GABA(A) antagonist bicuculline was injected into the globus pallidus, and its effects on locomotion in haloperidol- and pilocarpine-treated rats were assessed in the first group of experiments. In the second group of experiments, the effects of intrapallidal infusions of bicuculline on haloperidol- and pilocarpine-induced jaw movements were observed.
  
  
  RESULTS
  Pallidal GABA antagonism stimulated locomotion when no other treatment was present, and also when animals were coadministered haloperidol or pilocarpine. Bicuculline suppressed haloperidol-induced jaw movements in a dose-related manner, and had no effect on pilocarpine-induced jaw movements.
  
  
  CONCLUSIONS
  These results support the notion that there are distinct pathways conveying basal ganglia outflow and demonstrate that the striatopallidal pathway is involved in the generation of the haloperidol-induced tremulous jaw movements. These findings are consistent with some features of current models of basal ganglia function and may lead to an understanding of the specific mechanisms that generate parkinsonian symptoms.
authors.affiliation: Department of Psychology, University of Connecticut, Storrs, CT 06269-1020, USA.
authors.forename: Anna
authors.initials: A
authors.lastname: Wisniecki
authors.forename: Merce
authors.initials: M
authors.lastname: Correa
authors.forename: Maria N
authors.initials: MN
authors.lastname: Arizzi
authors.forename: Keitha
authors.initials: K
authors.lastname: Ishiwari
authors.forename: John D
authors.initials: JD
authors.lastname: Salamone
mesh_terms: D000818:Animals; D001522:Behavior, Animal; D001640:Bicuculline / Q000494:pharmacology; D003864:Depression, Chemical; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions; D018756:GABA Antagonists / Q000494:pharmacology*; D005917:Globus Pallidus / Q000187:drug effects* / Q000502:physiology; D006220:Haloperidol; D007568:Jaw / Q000187:drug effects / Q000294:innervation; D008124:Locomotion / Q000187:drug effects*; D008297:Male; D009068:Movement / Q000187:drug effects*; D010862:Pilocarpine / Q000031:analogs & derivatives*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014202:Tremor / Q000139:chemically induced
chemical_list: D018756:GABA Antagonists; D010862:Pilocarpine; C029118:pilocarpic acid; D006220:Haloperidol; D001640:Bicuculline