Nicotinic acetylcholine receptor β2 subunits in the medial prefrontal cortex control attention.

K. Guillem, B. Bloem, R. B. Poorthuis, M. Loos, A. B. Smit, U. Maskos, S. Spijker, H. D. Mansvelder
Science. 2011-08-11; 333(6044): 888-891
DOI: 10.1126/science.1207079

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1. Science. 2011 Aug 12;333(6044):888-91. doi: 10.1126/science.1207079.

Nicotinic acetylcholine receptor β2 subunits in the medial prefrontal cortex
control attention.

Guillem K(1), Bloem B, Poorthuis RB, Loos M, Smit AB, Maskos U, Spijker S,
Mansvelder HD.

Author information:
(1)Department of Integrative Neurophysiology, Center for Neurogenomics and
Cognitive Research (CNCR), Neuroscience Campus Amsterdam, VU University, 1081 HV
Amsterdam, Netherlands.

More than one-third of all people are estimated to experience mild to severe
cognitive impairment as they age. Acetylcholine (ACh) levels in the brain
diminish with aging, and nicotinic ACh receptor (nAChR) stimulation is known to
enhance cognitive performance. The prefrontal cortex (PFC) is involved in a range
of cognitive functions and is thought to mediate attentional focus. We found that
mice carrying nAChR β2-subunit deletions have impaired attention performance.
Efficient lentiviral vector-mediated reexpression of functional
β2-subunit-containing nAChRs in PFC neurons of the prelimbic area (PrL)
completely restored the attentional deficit but did not affect impulsive and
motivational behavior. Our findings show that β2-subunit expression in the PrL
PFC is sufficient for endogenous nAChR-mediated cholinergic regulation of
attentional performance.

DOI: 10.1126/science.1207079
PMID: 21836018 [Indexed for MEDLINE]


Auteurs Bordeaux Neurocampus