Literature DB >> 17596455

State-dependent modulation of amygdala inputs by dopamine-induced enhancement of sodium currents in layer V entorhinal cortex.

J Amiel Rosenkranz1, Daniel Johnston.   

Abstract

Interaction between the entorhinal cortex (EC) and basolateral amygdala (BLA) may be a fundamental component in the consolidation of many forms of affective memory, such as inhibitory avoidance. Dopamine (DA) in the EC is necessary for, and may facilitate, this form of learning. This effect of DA on affective behaviors may be accomplished in part through modulation of amygdala inputs. Although it is known that DA can modulate neuronal activity in the EC, it is not known whether DA modulates inputs from the BLA. In this study, we used in vitro patch-clamp recordings and Ca2+ imaging of layer V neurons in the rat lateral EC to determine whether DA modulates the integration of inputs from the BLA and the mechanism for this modulation. We found that DA exerted actions that depended on the neuronal state. Near resting membrane potentials, DA suppressed integration of inputs, whereas at depolarized potentials, DA enhanced integration. DA enhanced the integration by a D2-mediated enhancement of Na+ currents, via phospholipase C. These experiments demonstrate that DA can exert actions in the EC that depend on the membrane voltage. This effect of DA may affect a wide range of inputs. Functionally, by enhancement of amygdala inputs that arrive in concert with other inputs, or during depolarized states, DA can facilitate the impact of affect on memory in a subset of conditions.

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Year:  2007        PMID: 17596455      PMCID: PMC6672235          DOI: 10.1523/JNEUROSCI.1744-07.2007

Source DB:  PubMed          Journal:  J Neurosci        ISSN: 0270-6474            Impact factor:   6.167


  11 in total

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9.  Repeated restraint stress exerts different impact on structure of neurons in the lateral and basal nuclei of the amygdala.

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10.  Dopaminergic modulation of GABAergic transmission in the entorhinal cortex: concerted roles of α1 adrenoreceptors, inward rectifier K⁺, and T-type Ca²⁺ channels.

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