Role of globus pallidus and substantia nigra efferent pathways in striatally evoked head turning in the rat

Exp Brain Res. 1981;44(2):170-6. doi: 10.1007/BF00237338.

Abstract

These studies have examined the role of brain areas that receive efferent projections from the globus pallidus (GP) and substantia nigra (SN) in producing the contralateral head turning evoked by unilateral electrical stimulation of the neostriatum in the conscious rat. Two parameters were studied: the latency for a 90 degree head turn and changes in the normal latency evoked by administration of the GABA drugs picrotoxin and muscimol in GP. Electrolesions in the ipsilateral ventromedial and centromedian thalamic nuclei had no effect on the head turn parameters. Although small electrolesions in the SN slowed, but did not abolish the head turn, it prevented the changes in the response latency brought about by GABA drugs in GP. Treatment with 6-hydroxydopamine, which partly destroyed the nigro-striatal dopamine neurones, had no effect on the head turn. Areas of the brainstem that receive basal ganglia efferents were lesioned. An electrolesion of the nucleus tegmenti pedunculopontinus had no effect on the head turn latencies. The head turning was abolished by a lesion in the lateral periaqueductal grey (PAG); a more rostral PAG lesion, on the same level as SN, was ineffective. It is concluded that the head turning is mediated by basal ganglia efferents which pass close to the nigra without synapsing and project to the PAG. The GABA-sensitive GP efferents which modulate the response, probably project to SN.

MeSH terms

  • Animals
  • Corpus Striatum / drug effects
  • Corpus Striatum / physiology*
  • Efferent Pathways / physiology*
  • Electric Stimulation
  • Female
  • Functional Laterality
  • Globus Pallidus / physiology*
  • Head
  • Hydroxydopamines / pharmacology
  • Hypothalamus / physiology
  • Movement
  • Neurons / drug effects
  • Neurons / physiology
  • Rats
  • Rats, Inbred Strains
  • Substantia Nigra / physiology*

Substances

  • Hydroxydopamines