Dopaminergic Suppression of Synaptic Transmission in the Lateral Entorhinal Cortex. (1st July 2008)

• Record Type: Journal Article
• Authors: Caruana, Douglas A.; Chapman, C. Andrew
• Other Names: Jones Roland S. G. Academic Editor.
• Is Part Of: Journal of neural transplantation & plasticity. Volume 2008(2008)
• Publication Date: 2008-07-01
• Subjects: Nerve tissue -- Transplantation -- Periodicals; Neuroplasticity -- Periodicals; Nerve tissue -- Transplantation; Neuroplasticity; Neuronal Plasticity -- Periodicals; Computer network resources; Periodicals; Electronic journals; 612.82
• DOI: 10.1155/2008/203514
• Languages: English
• ISSNs: 0792-8483

Abstract

Abstract : Dopaminergic projections to the superficial layers of the lateral entorhinal cortex can modulate the strength of olfactory inputs to the region. We have found that low concentrations of dopamine facilitate field EPSPs in the entorhinal cortex, and that higher concentrations of dopamine suppress synaptic responses. Here, we have used whole-cell current clamp recordings from layer II neurons to determine the mechanisms of the suppression. Dopamine (10 to 50 μ M) hyperpolarized membrane potential and reversibly suppressed the amplitude of EPSPs evoked by layer I stimulation. Both AMPA- and NMDA-mediated components were suppressed, and paired-pulse facilitation was also enhanced indicating that the suppression is mediated largely by reduced glutamate release. Blockade ofD 2 -like receptors greatly reduced the suppression of EPSPs. Dopamine also lowered input resistance, and reduced the number of action potentials evoked by depolarizing current steps. The drop in input resistance was mediated by activation ofD 1 -like receptors, and was prevented by blockingK + channels with TEA. The dopaminergic suppression of synaptic transmission is therefore mediated by aD 2 receptor-dependent reduction in transmitter release, and aD 1 receptor-dependent increase in aK + conductance. This suppression of EPSPs may dampen the strength of sensory inputs during periods of elevated mesocortical dopamine activity.