Dopamine control of pyramidal neuron activity in the primary motor cortex via D2 receptors
Frontiers in Neural Circuits. 2014-01-01; 8:
DOI: 10.3389/fncir.2014.00013
Vitrac C(1), Péron S(1), Frappé I(2), Fernagut PO(3), Jaber M(2), Gaillard A(1),
Benoit-Marand M(1).
Author information:
(1)Laboratoire de Neurosciences Expérimentales et Cliniques, INSERM, U1084
Poitiers, France ; Laboratoire de Neurosciences Expérimentales et Cliniques,
Université de Poitiers Poitiers, France.
(2)Laboratoire de Neurosciences Expérimentales et Cliniques, INSERM, U1084
Poitiers, France ; Laboratoire de Neurosciences Expérimentales et Cliniques,
Université de Poitiers Poitiers, France ; CHU de Poitiers Poitiers, France.
(3)Institut des Maladies Neurodégénératives, UMR 5293, Université de Bordeaux
Bordeaux, France ; CNRS, Institut des Maladies Neurodégénératives, UMR 5293
Bordeaux, France.
The primary motor cortex (M1) is involved in fine voluntary movements control.
Previous studies have shown the existence of a dopamine (DA) innervation in M1
of rats and monkeys that could directly modulate M1 neuronal activity. However,
none of these studies have described the precise distribution of DA terminals
within M1 functional region nor have quantified the density of this innervation.
Moreover, the precise role of DA on pyramidal neuron activity still remains
unclear due to conflicting results from previous studies regarding D2 effects on
M1 pyramidal neurons. In this study we assessed in mice the neuroanatomical
characteristics of DA innervation in M1 using unbiased stereological
quantification of DA transporter-immunostained fibers. We demonstrated for the
first time in mice that DA innervates the deep layers of M1 targeting
preferentially the forelimb representation area of M1. To address the functional
role of the DA innervation on M1 neuronal activity, we performed
electrophysiological recordings of single neurons activity in vivo and
pharmacologically modulated D2 receptor activity. Local D2 receptor activation
by quinpirole enhanced pyramidal neuron spike firing rate without changes in
spike firing pattern. Altogether, these results indicate that DA innervation in
M1 can increase neuronal activity through D2 receptor activation and suggest a
potential contribution to the modulation of fine forelimb movement. Given the
demonstrated role for DA in fine motor skill learning in M1, our results suggest
that altered D2 modulation of M1 activity may be involved in the pathophysiology
of movement disorders associated with disturbed DA homeostasis.
DOI: 10.3389/fncir.2014.00013
PMCID: PMC3937764
PMID: 24616667 [Indexed for MEDLINE]