Cholinergic control of firing pattern and neurotransmission in rat neostriatal projection neurons: Role of CaV2.1 and CaV2.2 Ca2+ channels

Tamara Perez-Rosello, Alejandra Figueroa, Humberto Salgado, Carmen Vilchis, Fatuel Tecuapetla, Jaime N. Guzman, Elvira Galarraga, Jose Bargas*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

88 Scopus citations

Abstract

Besides a reduction of L-type Ca2+-currents (CaV1), muscarine and the peptidic M1-selective agonist, MT-1, reduced currents through CaV2.1 (P/Q) and CaV2.2 (N) Ca 2+ channel types. This modulation was strongly blocked by the peptide MT-7, a specific muscarinic M1-type receptor antagonist but not significantly reduced by the peptide MT-3, a specific muscarinic M 4-type receptor antagonist. Accordingly, MT-7, but not MT-3, blocked a muscarinic reduction of the afterhyperpolarizing potential (AHP) and decreased the GABAergic inhibitory postsynaptic currents (IPSCs) produced by axon collaterals that interconnect spiny neurons. Both these functions are known to be dependent on P/Q and N types Ca2+ channels. The action on the AHP had an important effect in increasing firing frequency. The action on the IPSCs was shown to be caused presynaptically as it coursed with an increase in the paired-pulse ratio. These results show: first, that muscarinic M 1-type receptor activation is the main cholinergic mechanism that modulates Ca2+ entry through voltage-dependent Ca2+ channels in spiny neurons. Second, this muscarinic modulation produces a postsynaptic facilitation of discharge together with a presynaptic inhibition of the GABAergic control mediated by axon collaterals. Together, both effects would tend to recruit more spiny neurons for the same task.

Original languageEnglish (US)
Pages (from-to)2507-2519
Number of pages13
JournalJournal of neurophysiology
Volume93
Issue number5
DOIs
StatePublished - May 2005

ASJC Scopus subject areas

  • Neuroscience(all)
  • Physiology

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