Components of after‐hyperpolarization in magnocellular neurones of the rat supraoptic nucleus in vitro

Abstract

The pharmacological sensitivity of hyperpolarizing components of spike train after‐potentials was examined in sixty‐one magnocellular neurones of the rat supraoptic nucleus using intracellular recording techniques in a brain slice preparation. In 26 % of all neurones a slow after‐hyperpolarization (AHP) was observed in addition to a fast AHP. In 31 % of all neurones a depolarizing after‐potential (DAP) was observed. The fast AHP was blocked by apamin whereas the slow AHP was blocked by charybdotoxin (ChTX). The DAP was enhanced by ChTX or a DAP was unmasked if not present during the control period. Low concentrations of TEA (0.15–1.5 mm) induced effects on the slow AHP and the DAP essentially resembling those of ChTX. The same was true for the effects of CoCl2 (1 mm). Spike train after‐potentials were not affected by either iberiotoxin (IbTX), a selective high‐conductance potassium (BK) channel antagonist, or margatoxin (MgTX), a Kv1.3 α‐subunit antagonist. Kv1.3 α‐subunit immunohistochemistry revealed that these units are not expressed in the somato‐dendritic region of supraoptic neurones. The effects of ChTX, IbTX, MgTX, TEA, CoCl2 and CdCl2 on spike train after‐potentials are interpreted in terms of an induction of the slow AHP by the activation of calcium‐dependent potassium channels of intermediate single channel conductance (IK channels). The results suggest that at least the majority of supraoptic magnocellular neurones share the capability of generating both a slow AHP and a DAP. The slow AHP may act to control the expression of the DAP, thus regulating the excitability of magnocellular neurones. The interaction of the slow AHP and the DAP may be important for the control of phasic discharge.

Burst Initiation and Termination in Phasic Vasopressin Cells of the Rat Supraoptic Nucleus: A Combined Mathematical, Electrical, and Calcium Fluorescence Study

“…4c) (Kirkpatrick and Bourque, 1996), and, furthermore, the time course of spike frequency adaptation indicates that it is strongly activated early, rather than late, in the burst. Although AVP neurons probably have an even slower, apamin-insensitive, calcium-dependent AHP, this current also appears to develop well before the end of the burst (Greffrath et al, 1998). Furthermore, our imaging data (Fig.…”

Functional coupling of intracellular calcium and inactivation of voltage-gated Kv1.1/Kvβ1.1 A-type K + channels

“…Intracellular injection of calcium activates potassium conductance in snail neurons, and the conductance is due to the opening of potassium channels gated by intracellular calcium (19). The fact that the increase in potassium conductance in response to calcium can be partially altered by charybdotoxin also suggests that other voltage-gated potassium channels might be modulated by the rise of intracellular calcium (20).…”

Somato-dendritic mechanisms underlying the electrophysiological properties of hypothalamic magnocellular neuroendocrine cells: A multicompartmental model study

“…The findings of Greffrath et al (1998) suggest that the induction, maintenance and termination of the plateau potential underlying bursting in MNCs are regulated by the balance between the DAP and the slow AHP. Experimental evidence of a contribution of the slow AHP to burst termination was presented by Ghamari-Langroudi and Bourque (2004).…”

“…Activation of the SK channels is voltage independent and highly sensitive to intracellular Ca 2+ (Hille 2001;Sah and Davies 2000); BK channel activation is both voltage-and Ca 2+ -dependent (Vergara et al 1998;Dopico et al 1999). While activation of BK channels contributes to the falling phase of individual action potentials and the generation of the fast after hyperpolarizing potential (AHP) or hyperpolarizing after potential in many types of neurons (Lancaster and Adams 1986;Lancaster and Nicoll 1987;MacDermott and Weight 1982;Womack and Khodakhah 2002), including MNCs (Dopico et al 1999), SK channel activation is responsible for the generation of the AHP following a train of action potentials (Armstrong et al 1994;Bourque and Brown 1987;Greffrath et al 1998;Kirkpatrick and Bourque 1996;Lancaster and Adams 1986;Lancaster and Nicoll 1987;Sah and Bekkers 1996). This apamin-sensitive AHP is intermediate between the fast AHP (~50 ms) and "slow" AHP (lasting >5 s) (GhamariLangroudi and Bourque 2004).…”