Functions and Modulation of Neuronal SK Channels

Faber, E. S. L.

doi:10.1007/s12013-009-9062-7

Cited by 76 publications

(35 citation statements)

References 172 publications

(279 reference statements)

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“…Interestingly, PKA dependent endocytosis of synaptic SK2 channels (Lin et al, 2010) can regulate, both, the efficiency of LTP induction and firing patterns in the postsynaptic neuron (Faber, 2009). Similar to our observation of parallel modulation of spike properties and t-LTP efficiency, these data indicate that cAMP dependent regulation of action potential properties and efficiency of LTP induction can occur in parallel, although both processes are not necessarily causally connected.…”

Section: Discussionmentioning

confidence: 99%

Dopamine Modulates Spike Timing-Dependent Plasticity and Action Potential Properties in CA1 Pyramidal Neurons of Acute Rat Hippocampal Slices

Edelmann¹,

Leßmann²

2011

Front. Syn. Neurosci.

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Spike timing-dependent plasticity (STDP) is a cellular model of Hebbian synaptic plasticity which is believed to underlie memory formation. In an attempt to establish a STDP paradigm in CA1 of acute hippocampal slices from juvenile rats (P15–20), we found that changes in excitability resulting from different slice preparation protocols correlate with the success of STDP induction. Slice preparation with sucrose containing ACSF prolonged rise time, reduced frequency adaptation, and decreased latency of action potentials in CA1 pyramidal neurons compared to preparation in conventional ASCF, while other basal electrophysiological parameters remained unaffected. Whereas we observed prominent timing-dependent long-term potentiation (t-LTP) to 171 ± 10% of controls in conventional ACSF, STDP was absent in sucrose prepared slices. This sucrose-induced STDP deficit could not be rescued by stronger STDP paradigms, applying either more pre- and/or postsynaptic stimuli, or by a higher stimulation frequency. Importantly, slice preparation with sucrose containing ACSF did not eliminate theta-burst stimulation induced LTP in CA1 in field potential recordings in our rat hippocampal slices. Application of dopamine (for 10–20 min) to sucrose prepared slices completely rescued t-LTP and recovered action potential properties back to levels observed in ACSF prepared slices. Conversely, acute inhibition of D1 receptor signaling impaired t-LTP in ACSF prepared slices. No similar restoring effect for STDP as seen with dopamine was observed in response to the β-adrenergic agonist isoproterenol. ELISA measurements demonstrated a significant reduction of endogenous dopamine levels (to 61.9 ± 6.9% of ACSF values) in sucrose prepared slices. These results suggest that dopamine signaling is involved in regulating the efficiency to elicit STDP in CA1 pyramidal neurons.

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Section: Discussionmentioning

confidence: 99%

Dopamine Modulates Spike Timing-Dependent Plasticity and Action Potential Properties in CA1 Pyramidal Neurons of Acute Rat Hippocampal Slices

Edelmann¹,

Leßmann²

2011

Front. Syn. Neurosci.

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“…In support of their view, the direct phosphorylation of SK channels by protein kinase A (PKA) and casein kinase 2 (CK2) can, respectively, cause channel internalization (Kohler et al, 1996; Ren et al, 2006; Fakler and Adelman, 2008; Faber, 2009) and reduced Ca 2+ sensitivity (Bildl et al, 2004; Allen et al, 2007). Moreover, neurotransmitter-initiated signaling cascades have been shown to modulate SK channel gating through CK2- or protein kinase C (PKC)-mediated phosphorylation (Maingret et al, 2008; Buchanan et al, 2010; Giessel and Sabatini, 2010).…”

Section: Swimming Forward: a Mechanism For Cholinergic Modulationmentioning

confidence: 98%

Swimming against the tide: investigations of the C-bouton synapse

Deardorff

Romer

Sonner

et al. 2014

Front. Neural Circuits.

111

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C-boutons are important cholinergic modulatory loci for state-dependent alterations in motoneuron firing rate. m2 receptors are concentrated postsynaptic to C-boutons, and m2 receptor activation increases motoneuron excitability by reducing the action potential afterhyperpolarization. Here, using an intensive review of the current literature as well as data from our laboratory, we illustrate that C-bouton postsynaptic sites comprise a unique structural/functional domain containing appropriate cellular machinery (a “signaling ensemble”) for cholinergic regulation of outward K+ currents. Moreover, synaptic reorganization at these critical sites has been observed in a variety of pathologic states. Yet despite recent advances, there are still great challenges for understanding the role of C-bouton regulation and dysregulation in human health and disease. The development of new therapeutic interventions for devastating neurological conditions will rely on a complete understanding of the molecular mechanisms that underlie these complex synapses. Therefore, to close this review, we propose a comprehensive hypothetical mechanism for the cholinergic modification of α-MN excitability at C-bouton synapses, based on findings in several well-characterized neuronal systems.

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“…SK channels (K Ca 2.1, K Ca 2.2, K Ca 2.3) are widely expressed throughout the central and peripheral nervous system where they act as key modulators of neuronal excitability [94, 95]. They control intrinsic excitability and pacemaking, dendritic integration, postsynaptic responses as well as synaptic plasticity [84].…”

Section: Tonic Versus Bursts Firing Mode In Chromaffin Cells: Basic Rmentioning

confidence: 99%

Ca<sub>v</sub>1.3 Channels as Key Regulators of Neuron-Like Firings and Catecholamine Release in Chromaffin Cells

Vandael¹,

Marcantoni²,

Carbone

2015

CMP

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Neuronal and neuroendocrine L-type calcium channels (Cav1.2, Cav1.3) open readily at relatively low membrane potentials and allow Ca2+ to enter the cells near resting potentials. In this way, Cav1.2 and Cav1.3 shape the action potential waveform, contribute to gene expression, synaptic plasticity, neuronal differentiation, hormone secretion and pacemaker activity. In the chromaffin cells (CCs) of the adrenal medulla, Cav1.3 is highly expressed and is shown to support most of the pacemaking current that sustains action potential (AP) firings and part of the catecholamine secretion. Cav1.3 forms Ca2+-nanodomains with the fast inactivating BK channels and drives the resting SK currents. These latter set the inter-spike interval duration between consecutive spikes during spontaneous firing and the rate of spike adaptation during sustained depolarizations. Cav1.3 plays also a primary role in the switch from “tonic” to “burst” firing that occurs in mouse CCs when either the availability of voltage-gated Na channels (Nav) is reduced or the β2 subunit featuring the fast inactivating BK channels is deleted. Here, we discuss the functional role of these “neuron-like” firing modes in CCs and how Cav1.3 contributes to them. The open issue is to understand how these novel firing patterns are adapted to regulate the quantity of circulating catecholamines during resting condition or in response to acute and chronic stress.

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Functions and Modulation of Neuronal SK Channels

Cited by 76 publications

References 172 publications

Dopamine Modulates Spike Timing-Dependent Plasticity and Action Potential Properties in CA1 Pyramidal Neurons of Acute Rat Hippocampal Slices

Dopamine Modulates Spike Timing-Dependent Plasticity and Action Potential Properties in CA1 Pyramidal Neurons of Acute Rat Hippocampal Slices

Swimming against the tide: investigations of the C-bouton synapse

Ca<sub>v</sub>1.3 Channels as Key Regulators of Neuron-Like Firings and Catecholamine Release in Chromaffin Cells

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