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This Article Full Text Full Text (PDF) All Versions of this Article: 98/5/2868    most recent 00679.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (7) Citing Articles via Google Scholar Google Scholar Articles by Lei, S. Articles by Shin, H.-S. Search for Related Content PubMed PubMed Citation Articles by Lei, S. Articles by Shin, H.-S.

Adrenergic Facilitation of GABAergic Transmission in Rat Entorhinal Cortex

¹Department of Pharmacology, Physiology and Therapeutics, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, North Dakota; and ²Center for Neural Science, Korea Institute of Science and Technology, Seoul, Republic of Korea

Submitted 19 June 2007; accepted in final form 5 September 2007

Whereas the entorhinal cortex (EC) receives noradrenergic innervations from the locus coeruleus of the pons and expresses adrenergic receptors, the function of norepinephrine (NE) in the EC is still elusive. We examined the effects of NE on GABA_A receptor–mediated synaptic transmission in the superficial layers of the EC. Application of NE dose-dependently increased the frequency and amplitude of spontaneous inhibitory postsynaptic currents (IPSCs) recorded from the principal neurons in layer II/III through activation of ₁ adrenergic receptors. NE increased the frequency and not the amplitude of miniature IPSCs (mIPSCs) recorded in the presence of TTX, suggesting that NE increases presynaptic GABA release with no effects on postsynaptic GABA_A receptors. Application of Ca²⁺ channel blockers (Cd²⁺ and Ni²⁺), omission of Ca²⁺ in the extracellular solution, or replacement of extracellular Na⁺ with N-methyl-D-glucamine (NMDG) failed to alter NE-induced increase in mIPSC frequency, suggesting that Ca²⁺ influx through voltage-gated Ca²⁺ or other cationic channels is not required. Application of BAPTA-AM, thapsigargin, and ryanodine did not change NE-induced increase in mIPSC frequency, suggesting that Ca²⁺ release from intracellular stores is not necessary for NE-induced increase in GABA release. Whereas ₁ receptors are coupled to G_q/11 resulting in activation of the phospholipase C (PLC) pathway, NE-mediated facilitation of GABAergic transmission was independent of PLC, protein kinase C, and tyrosine kinase activities. Our results suggest that NE-mediated facilitation of GABAergic function contributes to its antiepileptic effects in the EC.

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