Key pointsThe mammalian pineal gland is a neuroendocrine organ that responds to circadian and seasonal rhythms. Its major function is to secrete melatonin as a hormonal night signal in response to nocturnal delivery of noradrenaline from sympathetic neurons.Culturing rat pinealocytes in noradrenaline for 24 h induced a low‐voltage activated transient Ca2+current whose pharmacology and kinetics corresponded to a CaV3.1 T‐type channel.The upregulation of the T‐type Ca2+current is initiated by β‐adrenergic receptors, cyclic AMP and cyclic AMP‐dependent protein kinase.Messenger RNA for CaV3.1 T‐type channels is significantly elevated by noradrenaline at 8 h and 24 h.The noradrenaline‐induced T‐type channel mediated an increased Ca2+entry and supported modest transient electrical responses to depolarizing stimuli, revealing the potential for circadian regulation of pinealocyte electrical excitability and Ca2+signalling.AbstractOur basic hypothesis is that mammalian pinealocytes have cycling electrical excitability and Ca2+signalling that may contribute to the circadian rhythm of pineal melatonin secretion. This study asked whether the functional expression of voltage‐gated Ca2+channels (CaVchannels) in rat pinealocytes is changed by culturing them in noradrenaline (NA) as a surrogate for the night signal. Channel activity was assayed as ionic currents under patch clamp and as optical signals from a Ca2+‐sensitive dye. Channel mRNAs were assayed by quantitative polymerase chain reaction. Cultured without NA, pinealocytes showed only non‐inactivating L‐type dihydropyridine‐sensitive Ca2+current. After 24 h in NA, additional low‐voltage activated transient Ca2+current developed whose pharmacology and kinetics corresponded to a T‐type CaV3.1 channel. This change was initiated by β‐adrenergic receptors, cyclic AMP and protein kinase A as revealed by pharmacological experiments. mRNA for CaV3.1 T‐type channels became significantly elevated, but mRNA for another T‐type channel and for the major L‐type channel did not change. After only 8 h of NA treatment, the CaV3.1 mRNA was already elevated, but the transient Ca2+current was not. Even a 16 h wait without NA following the 8 h NA treatment induced little additional transient current. However, these cells were somehow primed to make transient current as a second NA exposure for only 60 min sufficed to induce large T‐type currents. The NA‐induced T‐type channel mediated an increased Ca2+entry during short depolarizations and supported modest transient electrical responses to depolarizing stimuli. Such experiments reveal the potential for circadian regulation of excitability.