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Large conductance Ca²⁺-activated K⁺ (BK) channels promote secretagogue-induced transition from spiking to bursting in murine anterior pituitary corticotrophs.

Duncan PJ, Şengül S, Tabak J, Ruth P, Bertram R, Shipston MJ - J. Physiol. (Lond.) (2015)

Bottom Line: Anterior pituitary corticotroph cells are a central component of the hypothalamic-pituitary-adrenal (HPA) axis essential for the neuroendocrine response to stress.We reveal that BK channels do not play a significant role in the generation of spontaneous activity but are critical for the transition to bursting in response to CRH.In contrast, AVP promotes an increase in single spike frequency, a mechanism independent of BK channels but dependent on background non-selective conductances.

View Article: PubMed Central - PubMed

Affiliation: Centre for Integrative Physiology, College of Medicine and Veterinary Medicine, University of Edinburgh, Edinburgh, EH8 9XD, UK.

No MeSH data available.


Related in: MedlinePlus

Pharmacological blockade of BK channels reduces bursting activityA, representative traces of corticotrophs pretreated with 1 μm paxilline, which reduces CRH/AVP-evoked bursting behaviour (B). C, paxilline has no effect on the ability of CRH/AVP to increase event frequency but significantly reduces event duration (D). Data are means ± SEM (n = 7 per group). *P < 0.05, **P < 0.01, ANOVA compared to respective base values.
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fig07: Pharmacological blockade of BK channels reduces bursting activityA, representative traces of corticotrophs pretreated with 1 μm paxilline, which reduces CRH/AVP-evoked bursting behaviour (B). C, paxilline has no effect on the ability of CRH/AVP to increase event frequency but significantly reduces event duration (D). Data are means ± SEM (n = 7 per group). *P < 0.05, **P < 0.01, ANOVA compared to respective base values.

Mentions: To investigate the role of BK channels in the CRH/AVP response, corticotroph cells were treated with paxilline (1 μm) for 4 min prior to CRH/AVP exposure. Paxilline remained present throughout the remainder of the recording. In comparison to control cells, paxilline-treated cells showed predominantly single-spike action potentials under basal conditions (Fig.7A). In contrast, there was a significant reduction in CRH/AVP-evoked bursting behaviour (Fig.7B). Under basal conditions, paxilline-treated cells had a resting membrane potential of −54.2 ± 2.8 mV and a spontaneous event frequency of 0.27 ± 0.20 Hz (n = 7). Paxilline-treated cells also had a mean event duration of 148 ± 39 ms and a burstiness factor of 0.23 ± 0.13. The basal properties of paxilline-treated cells were not significantly different to untreated cells for all parameters measured.


Large conductance Ca²⁺-activated K⁺ (BK) channels promote secretagogue-induced transition from spiking to bursting in murine anterior pituitary corticotrophs.

Duncan PJ, Şengül S, Tabak J, Ruth P, Bertram R, Shipston MJ - J. Physiol. (Lond.) (2015)

Pharmacological blockade of BK channels reduces bursting activityA, representative traces of corticotrophs pretreated with 1 μm paxilline, which reduces CRH/AVP-evoked bursting behaviour (B). C, paxilline has no effect on the ability of CRH/AVP to increase event frequency but significantly reduces event duration (D). Data are means ± SEM (n = 7 per group). *P < 0.05, **P < 0.01, ANOVA compared to respective base values.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4358680&req=5

fig07: Pharmacological blockade of BK channels reduces bursting activityA, representative traces of corticotrophs pretreated with 1 μm paxilline, which reduces CRH/AVP-evoked bursting behaviour (B). C, paxilline has no effect on the ability of CRH/AVP to increase event frequency but significantly reduces event duration (D). Data are means ± SEM (n = 7 per group). *P < 0.05, **P < 0.01, ANOVA compared to respective base values.
Mentions: To investigate the role of BK channels in the CRH/AVP response, corticotroph cells were treated with paxilline (1 μm) for 4 min prior to CRH/AVP exposure. Paxilline remained present throughout the remainder of the recording. In comparison to control cells, paxilline-treated cells showed predominantly single-spike action potentials under basal conditions (Fig.7A). In contrast, there was a significant reduction in CRH/AVP-evoked bursting behaviour (Fig.7B). Under basal conditions, paxilline-treated cells had a resting membrane potential of −54.2 ± 2.8 mV and a spontaneous event frequency of 0.27 ± 0.20 Hz (n = 7). Paxilline-treated cells also had a mean event duration of 148 ± 39 ms and a burstiness factor of 0.23 ± 0.13. The basal properties of paxilline-treated cells were not significantly different to untreated cells for all parameters measured.

Bottom Line: Anterior pituitary corticotroph cells are a central component of the hypothalamic-pituitary-adrenal (HPA) axis essential for the neuroendocrine response to stress.We reveal that BK channels do not play a significant role in the generation of spontaneous activity but are critical for the transition to bursting in response to CRH.In contrast, AVP promotes an increase in single spike frequency, a mechanism independent of BK channels but dependent on background non-selective conductances.

View Article: PubMed Central - PubMed

Affiliation: Centre for Integrative Physiology, College of Medicine and Veterinary Medicine, University of Edinburgh, Edinburgh, EH8 9XD, UK.

No MeSH data available.


Related in: MedlinePlus