Mechanisms underlying activation of the slow AHP in rat hippocampal neurons

Lima, Pedro U.; Marrion, Neil V.

doi:10.1016/j.brainres.2007.02.067

Cited by 48 publications

(52 citation statements)

References 36 publications

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“…6). A number of locations for the sI AHP have been proposed, including the soma (Lima and Marrion, 2007), apical dendrites (Sah and Bekkers, 1996), or basal dendrites (Bekkers, 2000). To determine the possible distributions of the sAHP that may explain these data, we used simulated results using a computational model of a BLA projection neuron (see Materials and Methods).…”

Section: Ahp Reduces the Ap-evoked Calcium Risementioning

confidence: 99%

“…Studies in hippocampal pyramidal neurons have indicated that both SK (Lima and Marrion, 2007) and KCNQ (Tzingounis and Nicoll, 2008;Tzingounis et al, 2010) potassium channels, which mediate I AHP and I M , respectively (Hille, 2001), also contribute to the sAHP/sI AHP . However, specific blockers of SK and KCNQ channels have only a minor impact on the sAHP in BLA projection neurons (Womble and Moises, 1993;Power and Sah, 2008), and their molecular identity remains a mystery.…”

Section: Introductionmentioning

confidence: 99%

“…In hippocampal pyramidal neurons, in which they have been studied extensively, their location remains controversial. Some studies have placed these channels on the soma (Lima and Marrion, 2007), whereas other reports suggest that they are localized on the dendritic tree (Andreasen and Lambert, 1995;Sah and Bekkers, 1996;Bekkers, 2000). A dendritic location suggests that the role of the sI AHP is not restricted to spike-frequency adaptation but that it may also be involved in shaping synaptic potentials.…”

Section: Introductionmentioning

confidence: 99%

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Location and Function of the Slow Afterhyperpolarization Channels in the Basolateral Amygdala

Power

Bocklisch²,

Curby³

et al. 2011

J. Neurosci.

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The basolateral amygdala (BLA) assigns emotional significance to sensory stimuli. This association results in a change in the output (action potentials) of BLA projection neurons in response to the stimulus. Neuronal output is controlled by the intrinsic excitability of the neuron. A major determinant of intrinsic excitability in these neurons is the slow afterhyperpolarization (sAHP) that follows action potential (AP) trains and produces spike-frequency adaptation. The sAHP is mediated by a slow calcium-activated potassium current (sI AHP ), but little is known about the channels that underlie this current. Here, using whole-cell patch-clamp recordings and high-speed calcium imaging from rat BLA projection neurons, we examined the location and function of these channels. We determined the location of the sI AHP by applying a hyperpolarizing voltage step during the sI AHP and measuring the time needed for the current to adapt to the new command potential, a function of its electrotonic distance from the somatic recording electrode. Channel location was also probed by focally uncaging calcium using a UV laser. Both methodologies indicated that, in BLA neurons, the sI AHP is primarily located in the dendritic tree. EPSPs recorded at the soma were smaller, decayed faster, and showed less summation during the sAHP. Adrenergic stimulation and buffering calcium reduced the sAHP and the attenuation of the EPSP during the sAHP. The sAHP also modulated the AP in the dendrite, reducing the calcium response evoked by a single AP. Thus, in addition to mediating spike-frequency adaptation, the sI AHP modulates communication between the soma and the dendrite.

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Section: Ahp Reduces the Ap-evoked Calcium Risementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Location and Function of the Slow Afterhyperpolarization Channels in the Basolateral Amygdala

Power

Bocklisch²,

Curby³

et al. 2011

J. Neurosci.

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“…This kind of regulation of VGCC bears much importance in many physiological processes especially in neuronal excitability as an increase in the L type VGCC will enhance AHP which keeps the cell in more hyperpolarized state and thus decrease excitability [19,20]. This aspect is also very important in memory formation [17].…”

Section: Discussionmentioning

confidence: 99%

“…In their seminal work Chameau et al [18] has reported that out of two VGCC namely the L type and N type, Glucocorticoid specifically enhance L type VGCC over N type. Studies [19,20] have reported that increase in L type VGCC can lead to more hyperpolarized stage of hippocampal neurons. Chameau et al has shown that the alpha subunit of N type alpha subunit (CaV2.2) of VGCC is down regulated while L type alpha subunit 1C(CaV1.2) remains unaffected and L type alpha subunit 1D(CaV1.3) is up regulated in response to increased Glucocorticoid.…”

Section: Introductionmentioning

confidence: 99%

Glucocorticoid mediated Specific Regulation of Calcium Channel: An in silico study

2017

IJAPSA

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The role played by steroid hormones in managing stress and homeostasis is extremely important from physiological perspective. Glucorticoid, one of the main steroid hormones bears an important position in this respect. Glucocorticoid confers its activity by precise and specific regulation of certain genes. It adopts a mechanism where it binds to its receptor in the cytosol and translocates to the nucleus and hereby activates or represses particular genes. The voltage gated calcium channels (VGCC) play important roles in neuronal firing. Between the L type and N type VGCC, Glucocorticoid specifically enhance the L type. This is important in regulating the neuronal excitability as enhanced L type current leads the cell to more hyperpolarized state and thus reducing excitability. Here we have studied the factors governing the glucocorticoid mediated control of VGCC. We found that the locus of the glucocorticoid receptor response elements (GRE) and negative GRE (nGRE), nucleosome positioning, the binding affinity of Glucocorticoid receptor (GR) to GRE and nGRE are the factors that lead to specific enhancement of L type over N type VGCC mediated by GR.

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Deletion of the L‐type calcium channel Ca_V1.3 but not Ca_V1.2 results in a diminished sAHP in mouse CA1 pyramidal neurons

et al. 2011

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Trains of action potentials in CA1 pyramidal neurons are followed by a prolonged calciumdependent post-burst afterhyperpolarization (AHP) that serves to limit further firing to a sustained depolarizing input. A reduction in the AHP accompanies acquisition of several types of learning and increases in the AHP are correlated with age-related cognitive impairment. The AHP develops primarily as the result of activation of outward calcium-activated potassium currents; however the precise source of calcium for activation of the AHP remains unclear. There is substantial experimental evidence suggesting that calcium influx via voltage-gated L-type calcium channels (L-VGCCs) contributes to the generation of the AHP. Two L-VGCC subtypes are predominately expressed in the hippocampus, Ca V 1.2 and Ca V 1.3, however it is not known which L-VGCC subtype is involved in generation of the AHP. This ambiguity is due in large part to the fact that at present there are no subunit-specific agonists or antagonists. Therefore, using mice in which the gene encoding Ca V 1.2 or Ca V 1.3 was deleted, we sought to determine the impact of alterations in levels of these two L-VCGG subtypes on neuronal excitability. No differences in any AHP measure were seen between neurons from Ca V 1.2 knockout mice and controls. However, the total area of the AHP was significantly smaller in neurons from Ca V 1.3 knockout mice as compared to neurons from wildtype controls. A significant reduction in the amplitude of the AHP was also seen at the 1 sec time point in neurons from Ca V 1.3 knockout mice as compared to those from controls. Reductions in both the area and 1 sec amplitude suggest the involvement of calcium influx via Ca V 1.3 in the slow AHP (sAHP). Thus, the results of our study demonstrate that deletion of Ca V 1.3, but not Ca V 1.2, significantly impacts the generation of the sAHP.

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Mechanisms underlying activation of the slow AHP in rat hippocampal neurons

Cited by 48 publications

References 36 publications

Location and Function of the Slow Afterhyperpolarization Channels in the Basolateral Amygdala

Location and Function of the Slow Afterhyperpolarization Channels in the Basolateral Amygdala

Glucocorticoid mediated Specific Regulation of Calcium Channel: An in silico study

Deletion of the L‐type calcium channel Ca_V1.3 but not Ca_V1.2 results in a diminished sAHP in mouse CA1 pyramidal neurons

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Mechanisms underlying activation of the slow AHP in rat hippocampal neurons

Cited by 48 publications

References 36 publications

Location and Function of the Slow Afterhyperpolarization Channels in the Basolateral Amygdala

Location and Function of the Slow Afterhyperpolarization Channels in the Basolateral Amygdala

Glucocorticoid mediated Specific Regulation of Calcium Channel: An in silico study

Deletion of the L‐type calcium channel CaV1.3 but not CaV1.2 results in a diminished sAHP in mouse CA1 pyramidal neurons

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Deletion of the L‐type calcium channel Ca_V1.3 but not Ca_V1.2 results in a diminished sAHP in mouse CA1 pyramidal neurons