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The Journal of Neuroscience, October 25, 2006, 26(43):11072-11082; doi:10.1523/JNEUROSCI.3229-06.2006

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Behavioral/Systems/Cognitive
Estrogen Upregulates T-Type Calcium Channels in the Hypothalamus and Pituitary

Jian Qiu,^1 * Martha A. Bosch,^1,2 * Khalid Jamali,¹ Changhui Xue,¹ Martin J. Kelly,¹ and Oline K. Rønnekleiv^1,2

¹Department of Physiology and Pharmacology and ²Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, Portland, Oregon 97239-3098

Correspondence should be addressed to Dr. Oline K. Rønnekleiv, Department of Physiology and Pharmacology, L334, Oregon Health and Science University, Portland, OR 97239-3098. Email: ronnekle{at}ohsu.edu

Low voltage-activated (T-type) Ca²⁺ channels are responsible for generating low-threshold spikes (LTS) that facilitate burst firing and transmitter release in neurons. The T-type Ca²⁺ channels contain a regulatory 1 subunit, and several isoforms of the 1 subunit (Cav3.1, 3.2, 3.3) have been cloned. The Cav 3.1 1 subunit is abundantly expressed in the hypothalamus. Previously, we found that 17 -estradiol (E2) increased the number of arcuate neurons expressing LTS. Therefore, we used an ovariectomized female guinea pig model to measure the distribution and regulation of Cav3.1 mRNA expression by E2. Guinea pig Cav3.1 1 subunit sequences, which were cloned by PCR, were used in ribonuclease protection (RPA) and in situ hybridization assays to evaluate mRNA expression. Based on a RPA, E2 significantly increased the mRNA expression of Cav3.1 1 subunit in the mediobasal hypothalamus and the pituitary. In situ hybridization analysis revealed that E2 significantly increased Cav 3.1 mRNA expression in medial preoptic nuclei, bed nuclei stria terminalis, and the arcuate nucleus. Whole-cell patch recordings in arcuate neurons revealed that E2 treatment significantly increased the peak T-type Ca²⁺ current density by twofold without affecting the activation/inactivation characteristics and augmented the rebound excitation by threefold to fourfold. These results suggest that estrogen regulates the mRNA expression of T-type calcium channels, which leads to increased functional expression of the channel. Increased expression of T-type channels could be one mechanism by which estrogen augments burst firing and transmitter release in hypothalamic neurons.

Key words: estrogen regulation; Cav3.1 mRNA; T-current amplitude; rebound burst firing; dopamine; POMC; neurons

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Received March 23, 2006; revised Sept. 15, 2006; accepted Sept. 19, 2006.

Correspondence should be addressed to Dr. Oline K. Rønnekleiv, Department of Physiology and Pharmacology, L334, Oregon Health and Science University, Portland, OR 97239-3098. Email: ronnekle{at}ohsu.edu

This article has been cited by other articles:

				T. A. Roepke, A. Malyala, M. A. Bosch, M. J. Kelly, and O. K. Ronnekleiv Estrogen Regulation of Genes Important for K+ Channel Signaling in the Arcuate Nucleus Endocrinology, October 1, 2007; 148(10): 4937 - 4951. [Abstract] [Full Text] [PDF]

				S. E. Hammack, I. Mania, and D. G. Rainnie Differential Expression of Intrinsic Membrane Currents in Defined Cell Types of the Anterolateral Bed Nucleus of the Stria Terminalis J Neurophysiol, August 1, 2007; 98(2): 638 - 656. [Abstract] [Full Text] [PDF]

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