作者: Patrizia Aracri , Alida Amadeo , Maria Enrica Pasini , Umberto Fascio , Andrea Becchetti
DOI: 10.1002/SYN.21655
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摘要: We studied how nicotinic acetylcholine receptors (nAChRs) regulate glutamate release in the secondary motor area (Fr2) of dorsomedial murine prefrontal cortex, presence steady agonist levels. Fr2 mediates response to behavioral situations that require immediate attention and is a candidate for generating seizures frontal epilepsies caused by mutant nAChRs. Morphological analysis showed peculiar chemoarchitecture laminar distribution pyramidal cells interneurons. Tonic application 5 µM nicotine on Layer V neurons strongly increased frequency spontaneous glutamatergic excitatory postsynaptic currents. The effect was inhibited 1 dihydro-β-erythroidine (which blocks α4-containing nAChRs) but not 10 nM methyllicaconitine α7-containing receptors). Excitatory currents s were also stimulated 5-iodo-3-[2(S)-azetidinylmethoxy]pyridine, selective β2-containing receptors, -sensitive way. next association α4 with different populations terminals, using as markers vesicular transporter type (VGLUT) corticocortical synapses VGLUT2 thalamocortical projecting fibers. Immunoblots higher expression Fr2, compared somatosensory cortex. Immunofluorescence intense VGLUT1 staining throughout cortical layers, whereas immunoreactivity displayed more distinct distribution. In V, colocalization nAChR subunit both considerably stronger than Thus, α4β2 nAChRs are expressed intrinsic extrinsic terminals give major contribution control tonic Synapse 00:000–000, 2013. © 2013 Wiley Periodicals, Inc.