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This Article Full Text Full Text (PDF) All Versions of this Article: 101/6/2741    most recent 91183.2008v1 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 PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Zhang, L. Articles by Kolaj, M. PubMed PubMed Citation Articles by Zhang, L. Articles by Kolaj, M.

Properties of a T-Type Ca²⁺Channel–Activated Slow Afterhyperpolarization in Thalamic Paraventricular Nucleus and Other Thalamic Midline Neurons

Division of Neuroscience, Ottawa Health Research Institute and University of Ottawa, Ottawa, Ontario, Canada

Submitted 3 November 2008; accepted in final form 17 March 2009

Burst firing mediated by a low-threshold spike (LTS) is the hallmark of many thalamic neurons. However, postburst afterhyperpolarizations (AHPs) are relatively uncommon in thalamus. We now report data from patch-clamp recordings in rat brain slice preparations that reveal an LTS-induced slow AHP (sAHP) in thalamic paraventricular (PVT) and other midline neurons, but not in ventrobasal or reticular thalamic neurons. The LTS-induced sAHP lasts 8.9 ± 0.4 s and has a novel pharmacology, with resistance to tetrodotoxin and cadmium and reduction by Ni²⁺ or nominally zero extracellular calcium concentration, which also attenuate both the LTS and sAHP. The sAHP is inhibited by 10 mM intracellular EGTA or by equimolar replacement of extracellular Ca²⁺ with Sr²⁺, consistent with select activation of LVA T-type Ca²⁺ channels and subsequent Ca²⁺ influx. In control media, the sAHP reverses near E_K⁺, shifting to –78 mV in 10.1 mM [K⁺]_o and is reduced by Ba²⁺ or tetraethylammonium. Although these data are consistent with opening of Ca²⁺-activated K⁺ channels, this sAHP lacks sensitivity to specific Ca²⁺-activated K⁺ channel blockers apamin, iberiotoxin, charybdotoxin, and UCL-2077. The LTS-induced sAHP is suppressed by a β-adrenoceptor agonist isoproterenol, a serotonin 5-HT₇ receptor agonist 5-CT, a neuropeptide orexin-A, and by stimulation of the cAMP/protein kinase A pathway with 8-Br-cAMP and forskolin. The data suggest that PVT and certain midline thalamic neurons possess an LTS-induced sAHP that is pharmacologically distinct and may be important for information transfer in thalamic–limbic circuitry during states of attentiveness and motivation.