Determination of acetylcholine and dopamine content in thalamus and striatum after excitotoxic lesions of the pedunculopontine tegmental nucleus in rats

Trisha Anne Jenkins, Mary Patricia Latimer, Helen Louise Alderson, Philip Winn

Research output: Contribution to journalArticlepeer-review

8 Citations (Scopus)

Abstract

The pedunculopontine tegmental nucleus (PPTg) contains cholinergic neurons whose principal ascending connections are with thalamic nuclei and structures associated with the striatum. It has been hypothesized that PPTg neurons are more closely associated with the substantia nigra (and therefore striatal motor systems) than with the ventral tegmental area (and therefore limbic striatal functions). In the present experiments we have examined the hypothesis that the PPTg is similarly associated with motor nuclei in the thalamus. Rats received unilateral ibotenate lesions of PPTg and were sacrificed 1, 2, 4 or 7 days later. Discrete thalamic nuclei, and samples of caudate-putamen and nucleus accumbens, were punched out and thalamic acetylcholine (ACh) and striatal ACh and dopamine (DA) content examined. Anteroventral nucleus had decreased ACh content after PPTg lesion, but a time dependent increase was found in mediodorsal nucleus; ACh concentration was unchanged in thalamic reticular nucleus or medial geniculate. No long-term lesion-dependent changes in striatal ACh or DA content were found. The effects of PPTg lesion on thalamic ACh content are consistent with the hypothesis that it has effects on motor nuclei, but also indicate that PPTg lesions have complex and dynamic effects on thalamic ACh content. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.

Original languageEnglish
Pages (from-to)45-48
Number of pages4
JournalNeuroscience Letters
Volume322
Issue number1
DOIs
Publication statusPublished - 29 Mar 2002

Keywords

  • acetylcholine
  • caudate-putamen
  • dopamine
  • nucleus accumbens
  • CHOLINERGIC STIMULATION
  • D-AMPHETAMINE
  • EFFLUX
  • MODULATION
  • ACCUMBENS
  • INTACT

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