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Alpha-1A adrenergic receptor activation increases inhibitory tone in CA1 hippocampus by Kristin L. Hillman; Saobo Lei; Van A. Doze; James E. Porter is a Medicine article available to read on EtoBox.

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The endogenous catecholamine norepinephrine (NE) exhibits anti-epileptic properties, however it is not well understood which adrenergic receptor (AR) mediates this effect. The aim of this study was to investigate alpha(1)-adrenergic receptor activation in region CA1 of the hippocampus, a subcortical structure often implicated in temporal lobe epilepsies. Using cell-attached and whole-cell recordings in rat hippocampal slices, we confirmed that selective alpha(1)-AR activation increases action potential firing in a subpopulation of CA1 interneurons. We found that this response is mediated via the alpha(1A)-AR subtype, initiated by sodium influx, and appears independent of second messenger signaling. In CA1 pyramidal cells, alpha(1A)-AR activation decreases activity due to increased pre-synaptic GABA and somatostatin release. Examination of post-synaptic receptor involvement revealed that while GABA(A) receptors mediate the majority of alpha(1A)-adrenergic effects on CA1 pyramidal cells, significant contributions are also made by GABA(B) and somatostatin receptors. Finally, to test whether alpha(1A)-AR activation could have potential therapeutic implications, we performed AR agonist

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Author

Kristin L. Hillman; Saobo Lei; Van A. Doze; James E. Porter

Publisher

Elsevier Science; Elsevier ; Elsevier BV (ISSN 0920-1211)

Published

2009

Language

EN

Field

Medicine (Health Sciences)