Burst firing mediated by the low threshold spike (LTS) is a hallmark of many thalamic neurons. However, post-burst 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 seconds and has a novel pharmacology, with resistance to tetrodotoxin and cadmium, and reduction by Ni²⁺ or nominally zero [Ca²⁺]_o which also attenuate both the LTS and sAHP. The sAHP is inhibited by 10mM 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 -78mV in 10.1mM [K⁺]_o and is reduced by Ba²⁺ or TEA. While 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 -adrenoceptor agonist isoproterenol, a serotonin 5-HT₇ receptor agonist 5-CT, a neuropeptide orexin-A, and by stimulation of cAMP/protein kinase-A pathway with 8-Br-cAMP and forskolin. The data suggest that PVT and certain midline thalamic neurons possess a LTS-induced sAHP that is pharmacologically distinct, and may be important for information transfer in thalamic-limbic circuitry during states of attentiveness and motivation.