Prefrontal parvalbumin interneurons shape neuronal activity to drive fear expression
Nature. 2013-11-20; 505(7481): 92-96
DOI: 10.1038/nature12755
Read on PubMed
1. Nature. 2014 Jan 2;505(7481):92-6. doi: 10.1038/nature12755. Epub 2013 Nov 20.
Prefrontal parvalbumin interneurons shape neuronal activity to drive fear
expression.
Courtin J(1), Chaudun F(1), Rozeske RR(1), Karalis N(1), Gonzalez-Campo C(1),
Wurtz H(1), Abdi A(2), Baufreton J(2), Bienvenu TC(1), Herry C(1).
Author information:
(1)1] INSERM, Neurocentre Magendie, U862, 146 Rue Léo-Saignat, Bordeaux 33077,
France [2] University of Bordeaux, Neurocentre Magendie, U862, 146 Rue
Léo-Saignat, Bordeaux 33077, France.
(2)1] University of Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293,
Bordeaux F-33000, France [2] CNRS, Institut des Maladies Neurodégénératives, UMR
5293, Bordeaux F-33000, France.
Synchronization of spiking activity in neuronal networks is a fundamental process
that enables the precise transmission of information to drive behavioural
responses. In cortical areas, synchronization of principal-neuron spiking
activity is an effective mechanism for information coding that is regulated by
GABA (γ-aminobutyric acid)-ergic interneurons through the generation of neuronal
oscillations. Although neuronal synchrony has been demonstrated to be crucial for
sensory, motor and cognitive processing, it has not been investigated at the
level of defined circuits involved in the control of emotional behaviour.
Converging evidence indicates that fear behaviour is regulated by the dorsomedial
prefrontal cortex (dmPFC). This control over fear behaviour relies on the
activation of specific prefrontal projections to the basolateral complex of the
amygdala (BLA), a structure that encodes associative fear memories. However, it
remains to be established how the precise temporal control of fear behaviour is
achieved at the level of prefrontal circuits. Here we use single-unit recordings
and optogenetic manipulations in behaving mice to show that fear expression is
causally related to the phasic inhibition of prefrontal parvalbumin interneurons
(PVINs). Inhibition of PVIN activity disinhibits prefrontal projection neurons
and synchronizes their firing by resetting local theta oscillations, leading to
fear expression. Our results identify two complementary neuronal mechanisms
mediated by PVINs that precisely coordinate and enhance the neuronal activity of
prefrontal projection neurons to drive fear expression.
DOI: 10.1038/nature12755
PMID: 24256726 [Indexed for MEDLINE]