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Afterhyperpolarization

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Elspeth M. Mclachlan – One of the best experts on this subject based on the ideXlab platform.

  • Diversity of Channels Involved in Ca2+ Activation of K+ Channels During the Prolonged AHP in Guinea-Pig Sympathetic Neurons
    Journal of neurophysiology, 2000
    Co-Authors: Juan Martinez-pinna, Philip J. Davies, Elspeth M. Mclachlan
    Abstract:

    The types of Ca2+-dependent K+ channel involved in the prolonged Afterhyperpolarization (AHP) in a subgroup of sympathetic neurons have been investigated in guinea pig celiac gangganglia in vitro. The …

  • potassium currents contributing to action potential repolarization and the Afterhyperpolarization in rat vagal motoneurons
    Journal of Neurophysiology, 1992
    Co-Authors: Pankaj Sah, Elspeth M. Mclachlan
    Abstract:

    1. Intracellular recordings were made from neurons in the dorsal motor nucleus of the vagus (DMV) in transverse slices of rat medulla maintained in vitro at 30 degrees C. Neurons had a resting potential of -59.8 +/- 1.4 (SE) mV (n = 39) and input resistance of 293 +/- 23 M omega (n = 44). 2. Depolarization elicited overshooting action potentials that were blocked by tetrodotoxin (TTX; 1 microM). In the presence of TTX, two types of action potentials having low and high thresholds could be elicited. The action potentials were blocked by cobalt (2 mM) indicating they were mediated by calcium currents. 3. Under voltage clamp, depolarization of the cell from membrane potentials negative of the resting potential activated a transient potassium current. This current was selectively blocked by 4-aminopyridine (4-AP) (5 mM) and catechol (5 mM) indicating that it is an A-type current. This current inactivated with a time constant of 420 ms and recovered from inactivation with a time constant of 26 ms. 4. When calcium currents were blocked by cadmium or cobalt, the rate of action potential repolarization was slower. In the presence of tetraethylammonium (TEA; 200-400 microM) or charybdotoxin (CTX; 30 nM) a small “hump” appeared on the repolarizing phase of the action potential that was abolished by addition of cadmium. These results indicate that a calcium-activated potassium current (IC) contributes to action potential repolarization. 5. Actions potentials elicited from hyperpolarized membrane potentials repolarized faster than those elicited from resting membrane potential. This effect could be blocked by catechol, indicating that voltage-dependent potassium currents (IA) can also contribute to action-potential repolarization. In the presence of catechol and calcium channel blockers, action potentials still had a significant early Afterhyperpolarization suggesting that another calcium independent outward current is also active during repolarization. This fast Afterhyperpolarizations (AHP) was not blocked by TEA. 6. Action potentials were followed by prolonged AHPs, which had two phases. The initial part of the AHP was blocked by apamin (100 nM) indicating that it results from activation of SK type calcium-activated potassium channels. The slow phase was selectively blocked by catechol suggesting that it is due to activation of IA. 7. It is concluded that a TTX-sensitive sodium current and two calcium currents contribute to the action potential in rat DMV neurons. At least three different currents contribute to action-potential repolarization: IC, IA, and a third unidentified calcium-insensitive outward current.(ABSTRACT TRUNCATED AT 400 WORDS)

John B. Furness – One of the best experts on this subject based on the ideXlab platform.

  • Intermediate-conductance calcium-activated potassium channels in enteric neurones of the mouse: pharmacological, molecular and immunochemical evidence for their role in mediating the slow Afterhyperpolarization
    Journal of neurochemistry, 2004
    Co-Authors: Craig B. Neylon, Kulmira Nurgali, Billie Hunne, Heather L. Robbins, Moore Stephen, Mao Xiang Chen, John B. Furness
    Abstract:

    Calcium-activated potassium channels are critically important in modulating neuronal cell excitability. One member of the family, the intermediate-conductance potassium (IK) channel, is not thought to play a role in neurones because of its predominant expression in non-excitable cells such as erythrocytes and lymphocytes, in smooth muscle tissues, and its lack of apparent expression in brain. In the present study, we demonstrate that IK channels are localized on specific neurones in the mouse enteric nervous system where they mediate the slow Afterhyperpolarization following an action potential. IK channels were localized by immunohistochemistry on intrinsic primary afferent neurones, identified by their characteristic Dogiel type II morphology. The slow Afterhyperpolarization recorded from these cells was abolished by the IK channel blocker clotrimazole. RT-PCR and western analysis of extracts from the colon revealed an IK channel transcript and protein identical to the IK channel expressed in other cell types. These results indicate that IK channels are expressed in neurones where they play an important role in modulating firing properties.

  • Regulation of K+ channels underlying the slow Afterhyperpolarization in enteric Afterhyperpolarization‐generating myenteric neurons: Role of calcium and phosphorylation
    Clinical and experimental pharmacology & physiology, 2002
    Co-Authors: Fivos Vogalis, Craig B. Neylon, John R. Harvey, John B. Furness
    Abstract:

    1. Myenteric Afterhyperpolarization-generating myenteric (AH) neurons serve as intrinsic primary afferent neurons of the enteric nervous system and generate prolonged or slow afterhyperpolarizing potentials (slow AHP). The slow AHP is generated by an increase in a Ca2+-activated K+ conductance (gK-Ca) and is inhibited by enteric neurotransmitters leading to increased excitability. 2. Using cell-attached patch-clamp recordings from AH neurons, we have shown that K+ channels with an intermediate unitary conductance (IK channels) open following action potential firing. 3. In excised patches from AH neurons, we have identified an IK-like channel that can be activated by submicromolar levels of cytoplasmic Ca2+ and is not voltage dependent. 4. Application of the catalytic subunit of cAMP-dependent protein kinase to the cytoplasmic surface of inside-out patches inhibits the opening of IK-like channels previously activated by Ca2+. 5. The IK-like channels are resistant to external tetraethylammonium (5 mmol/L) and apamin (0.3-1 micro mol/L), but are inhibited by clotrimazole (10 micro mol/L). 6. Our present data support the idea that an increase in the open probability of IK-like channels in AH neurons following an increase in cytoplasmic [Ca2+] is responsible for the slow AHP and their opening is modulated by kinases.

Miloslav Kolaj – One of the best experts on this subject based on the ideXlab platform.

  • properties of a t type ca2 channel activated slow Afterhyperpolarization in thalamic paraventricular nucleus and other thalamic midline neurons
    Journal of Neurophysiology, 2009
    Co-Authors: Li Zhang, Leo P. Renaud, Miloslav Kolaj
    Abstract:

    Burst firing mediated by a low-threshold spike (LTS) is the hallmark of many thalamic neurons. However, postburst Afterhyperpolarizations (AHPs) are relatively uncommon in thalamus. We now report d…

  • Properties of a T-type Ca2+channel-activated slow Afterhyperpolarization in thalamic paraventricular nucleus and other thalamic midline neurons.
    Journal of neurophysiology, 2009
    Co-Authors: Li Zhang, Leo P. Renaud, Miloslav Kolaj
    Abstract:

    Burst firing mediated by a low-threshold spike (LTS) is the hallmark of many thalamic neurons. However, postburst Afterhyperpolarizations (AHPs) are relatively uncommon in thalamus. We now report d…

John P Adelman – One of the best experts on this subject based on the ideXlab platform.

  • Activation kinetics of the slow Afterhyperpolarization in hippocampal CA1 neurons.
    Pflugers Archiv : European journal of physiology, 2004
    Co-Authors: Aaron C. Gerlach, James Maylie, John P Adelman
    Abstract:

    The activation of the slow Afterhyperpolarization (sAHP) in CA1 neurons was studied using whole-cell recordings in the presence of inhibitors of the fast and medium-duration AHPs. The amplitude of the slow Afterhyperpolarization current (IsAHP) increased as a function of duration and magnitude of the depolarizing voltage pulse reflecting graded increases in Ca2+ influx through voltage-dependent Ca2+ channels. Therefore, the time constant for activation, τmax, determined from a family of IsAHPs as a function of pulse duration, was voltage dependent decreasing several-fold within the range of −20 to 20 mV and was dependent on extracellular [Ca2+]. The IsAHP displayed a pronounced rising phase that was well fit by a single exponential with a time constant, τrise, that was invariant of pulse duration, voltage, IsAHP amplitude, or external [Ca2+] and was significantly slower than the τmax. In current clamp, the magnitude of the sAHP increased with the number of evoked action potentials, yet τrise of the sAHP was invariant of action potential number and was similar to the τrise of the IsAHP recorded in voltage-clamp. The results suggest that there are two components to the development of the IsAHP, a rapid, voltage- and Ca2+-dependent step, the magnitude and rate of which reflects the voltage dependence of the Ca2+ channels, that triggers a second rate-limiting, voltage-independent process that dictates the slow IsAHP rise kinetics.

  • Gene structure and chromosome mapping of the human small-conductance calcium-activated potassium channel SK1 gene (KCNN1).
    Cytogenetic and Genome Research, 1999
    Co-Authors: Michael Litt, Dante M. Lamorticella, Chris T Bond, John P Adelman
    Abstract:

    Abstract. Small-conductance, calcium-activated potassium channels contribute to the Afterhyperpolarization in central neurons and other cell types. Because these channels regulate neurona

Svetlana Lutsenko – One of the best experts on this subject based on the ideXlab platform.

  • Mechanism of calcium gating in small-conductance calcium-activated potassium channels
    Nature, 1998
    Co-Authors: Bernd Fakler, Chris T Bond, A. Rivard, Gary A. Wayman, Teresa L. Johnson-pais, J. E. Keen, Takahiro M. Ishii, Birgit Hirschberg, Svetlana Lutsenko
    Abstract:

    The slow Afterhyperpolarization that follows an action potential is generated by the activation of small-conductance calcium-activated potassium channels (SK channels). The slow Afterhyperpolarization limits the firing frequency of repetitive action potentials (spike-frequency adaption) and is essential for normal neurotransmission1,2,3. SK channels are voltage-independent and activated by submicromolar concentrations of intracellular calcium1. They are high-affinity calcium sensors that transduce fluctuations in intracellular calcium concentrations into changes in membrane potential. Here we study the mechanism of calcium gating and find that SK channels are not gated by calcium binding directly to the channel α-subunits. Instead, the functional SK channels are heteromeric complexes with calmodulin, which is constitutively associated with the α-subunits in a calcium-independent manner. Our data support a model in which calcium gating of SK channels is mediated by binding of calcium to calmodulin and subsequent conformational alterations in the channel protein.