Abstract

The globus pallidus (GP) plays a key role in the overall basal ganglia (BG) activity. Despite evidence of cholinergic inputs to GP, their role in the spiking activity of GP neurons has not received attention. We examine the effect of local activation and blockade of muscarinic receptors (MRs) in the spontaneous firing of GP neurons both in normal and ipsilateral striatum-lesioned rats. We found that activation of MRs produces heterogeneous responses in both normal and ipsilateral striatum-lesioned rats: in normal rats the response evoked by MRs depends on the predrug basal firing rate; the inhibition evoked by MRs is higher in normal rats than in striatum-lesioned rats; the number of neurons that undergo inhibition is lower in striatum-lesioned rats than in normal rats. Our data suggest that modulation of MRs in the GP depends on the firing rate before their activation and on the integrity of the striato-pallidal pathway.

Highlights

  • The use of antimuscarinic drugs in the management of Parkinson’s disease either as monotherapy or as an adjunct to other drugs is still in wide practice [1, 2]

  • The effect of a wide variety of neurotransmitters on the electrical activity of globus pallidus (GP) neurons has been studied [11,12,13,14,15,16], yet, despite the presence of cholinergic fibers in the GP coming from the pedunculopontine nucleus (PPN) [17,18,19,20], there are no studies on the effect of acetylcholine on the spiking activity of GP neurons

  • The spontaneous firing rate of 97 neurons recorded from normal rats ranged from 6.3 to 98.7 spikes/s

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Summary

Introduction

The use of antimuscarinic drugs in the management of Parkinson’s disease either as monotherapy or as an adjunct to other drugs is still in wide practice [1, 2]. The presence of MRs modifies the activity of other BG nuclei [5,6,7]. The GP plays a key role in the global activity of basal ganglia [8]. Variations in the basal spontaneous firing rate of pallidal neurons are related to movement disorders both in humans and in animal models of Parkinson’s disease [9, 10]. The effect of a wide variety of neurotransmitters on the electrical activity of GP neurons has been studied [11,12,13,14,15,16], yet, despite the presence of cholinergic fibers in the GP coming from the pedunculopontine nucleus (PPN) [17,18,19,20], there are no studies on the effect of acetylcholine on the spiking activity of GP neurons

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