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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

Simulations with little or no BK conductanceA, basal spiking activity in the absence of BK conductance. B, CRH/AVP increases spike frequency without bursting when there is no BK conductance. C, when some BK conductance remains, CRH/AVP elicits some bursting mixed with fast spiking.
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fig06: Simulations with little or no BK conductanceA, basal spiking activity in the absence of BK conductance. B, CRH/AVP increases spike frequency without bursting when there is no BK conductance. C, when some BK conductance remains, CRH/AVP elicits some bursting mixed with fast spiking.

Mentions: In the model, BK channels have almost no effect on the spontaneous low-frequency spiking activity. Figure6A shows spontaneous activity in the absence of BK conductance. When application of CRH and AVP together is simulated the spike frequency greatly increases and the model cell is depolarised, but there is no bursting (Fig.6B). However, when even a small fraction (15%) of BK conductance remains there is a mixture of bursting and fast spiking (Fig.6C).


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)

Simulations with little or no BK conductanceA, basal spiking activity in the absence of BK conductance. B, CRH/AVP increases spike frequency without bursting when there is no BK conductance. C, when some BK conductance remains, CRH/AVP elicits some bursting mixed with fast spiking.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig06: Simulations with little or no BK conductanceA, basal spiking activity in the absence of BK conductance. B, CRH/AVP increases spike frequency without bursting when there is no BK conductance. C, when some BK conductance remains, CRH/AVP elicits some bursting mixed with fast spiking.
Mentions: In the model, BK channels have almost no effect on the spontaneous low-frequency spiking activity. Figure6A shows spontaneous activity in the absence of BK conductance. When application of CRH and AVP together is simulated the spike frequency greatly increases and the model cell is depolarised, but there is no bursting (Fig.6B). However, when even a small fraction (15%) of BK conductance remains there is a mixture of bursting and fast spiking (Fig.6C).

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