scholarly journals Large-conductance calcium-dependent potassium channels prevent dendritic excitability in neocortical pyramidal neurons

2008 ◽  
Vol 457 (5) ◽  
pp. 1133-1145 ◽  
Author(s):  
Narimane Benhassine ◽  
Thomas Berger
Keyword(s):  
Potassium Channels ◽  
Pyramidal Neurons ◽  
Calcium Dependent ◽  
Dendritic Excitability ◽  
Neocortical Pyramidal Neurons

scholarly journals Somatic and dendritic GABAB receptors regulate neuronal excitability via different mechanisms

2012 ◽  
Vol 108 (10) ◽  
pp. 2810-2818 ◽  
Author(s):  
Jean-Didier Breton ◽  
Greg J. Stuart
Keyword(s):  
Potassium Channels ◽  
Neuronal Excitability ◽  
Pyramidal Neurons ◽  
Barrel Cortex ◽  
Receptor Activation ◽  
Gabab Receptors ◽  
Membrane Properties ◽  
Dendritic Excitability ◽  
The Impact ◽  
Neuronal Output

GABAB receptors play a key role in regulating neuronal excitability in the brain. Whereas the impact of somatic GABAB receptors on neuronal excitability has been studied in some detail, much less is known about the role of dendritic GABAB receptors. Here, we investigate the impact of GABAB receptor activation on the somato-dendritic excitability of layer 5 pyramidal neurons in the rat barrel cortex. Activation of GABAB receptors led to hyperpolarization and a decrease in membrane resistance that was greatest at somatic and proximal dendritic locations. These effects were occluded by low concentrations of barium (100 μM), suggesting that they are mediated by potassium channels. In contrast, activation of dendritic GABAB receptors decreased the width of backpropagating action potential (APs) and abolished dendritic calcium electrogenesis, indicating that dendritic GABAB receptors regulate excitability, primarily via inhibition of voltage-dependent calcium channels. These distinct actions of somatic and dendritic GABAB receptors regulated neuronal output in different ways. Activation of somatic GABAB receptors led to a reduction in neuronal output, primarily by increasing the AP rheobase, whereas activation of dendritic GABAB receptors blocked burst firing, decreasing AP output in the absence of a significant change in somatic membrane properties. Taken together, our results show that GABAB receptors regulate somatic and dendritic excitability of cortical pyramidal neurons via different cellular mechanisms. Somatic GABAB receptors activate potassium channels, leading primarily to a subtractive or shunting form of inhibition, whereas dendritic GABAB receptors inhibit dendritic calcium electrogenesis, leading to a reduction in bursting firing.

scholarly journals The Molecular Basis for the Calcium-Dependent Slow Afterhyperpolarization in CA1 Hippocampal Pyramidal Neurons

2021 ◽  
Vol 12 ◽  
Author(s):  
Giriraj Sahu ◽  
Ray W. Turner
Keyword(s):  
Potassium Channels ◽  
Pyramidal Neurons ◽  
Signal Transmission ◽  
Ryanodine Receptors ◽  
Pyramidal Cells ◽  
Frequency Pattern ◽  
Hippocampal Pyramidal Neurons ◽  
Calcium Dependent ◽  
Ionic Basis ◽  
Hippocampal Pyramidal Cells

Neuronal signal transmission depends on the frequency, pattern, and timing of spike output, each of which are shaped by spike afterhyperpolarizations (AHPs). There are classically three post-spike AHPs of increasing duration categorized as fast, medium and slow AHPs that hyperpolarize a cell over a range of 10 ms to 30 s. Intensive early work on CA1 hippocampal pyramidal cells revealed that all three AHPs incorporate activation of calcium-gated potassium channels. The ionic basis for a fAHP was rapidly attributed to the actions of big conductance (BK) and the mAHP to small conductance (SK) or Kv7 potassium channels. In stark contrast, the ionic basis for a prominent slow AHP of up to 30 s duration remained an enigma for over 30 years. Recent advances in pharmacological, molecular, and imaging tools have uncovered the expression of a calcium-gated intermediate conductance potassium channel (IK, KCa3.1) in central neurons that proves to contribute to the slow AHP in CA1 hippocampal pyramidal cells. Together the data show that the sAHP arises in part from a core tripartite complex between Cav1.3 (L-type) calcium channels, ryanodine receptors, and IK channels at endoplasmic reticulum-plasma membrane junctions. Work on the sAHP in CA1 pyramidal neurons has again quickened pace, with identified contributions by both IK channels and the Na-K pump providing answers to several mysteries in the pharmacological properties of the sAHP.

scholarly journals Active dendrites, potassium channels and synaptic plasticity

2003 ◽  
Vol 358 (1432) ◽  
pp. 667-674 ◽  
Author(s):  
Daniel Johnston ◽  
Brian R. Christie ◽  
Andreas Frick ◽  
Richard Gray ◽  
Dax A. Hoffman ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Potassium Channels ◽  
Potassium Channel ◽  
Pyramidal Neurons ◽  
Back Propagation ◽  
Dendritic Tree ◽  
Long Term Potentiation ◽  
Synaptic Potentials ◽  
Dendritic Excitability

The dendrites of CA1 pyramidal neurons in the hippocampus express numerous types of voltage-gated ion channel, but the distributions or densities of many of these channels are very non-uniform. Sodium channels in the dendrites are responsible for action potential (AP) propagation from the axon into the dendrites (back-propagation); calcium channels are responsible for local changes in dendritic calcium concentrations following back-propagating APs and synaptic potentials; and potassium channels help regulate overall dendritic excitability. Several lines of evidence are presented here to suggest that back-propagating APs, when coincident with excitatory synaptic input, can lead to the induction of either long-term depression (LTD) or long-term potentiation (LTP). The induction of LTD or LTP is correlated with the magnitude of the rise in intracellular calcium. When brief bursts of synaptic potentials are paired with postsynaptic APs in a theta-burst pairing paradigm, the induction of LTP is dependent on the invasion of the AP into the dendritic tree. The amplitude of the AP in the dendrites is dependent, in part, on the activity of a transient, A-type potassium channel that is expressed at high density in the dendrites and correlates with the induction of the LTP. Furthermore, during the expression phase of the LTP, there are local changes in dendritic excitability that may result from modulation of the functioning of this transient potassium channel. The results support the view that the active properties of dendrites play important roles in synaptic integration and synaptic plasticity of these neurons.

scholarly journals Early Exposure to Alcohol Leads to Permanent Impairment of Dendritic Excitability in Neocortical Pyramidal Neurons

2012 ◽  
Vol 32 (4) ◽  
pp. 1377-1382 ◽  
Author(s):  
A. Granato ◽  
L. M. Palmer ◽  
A. De Giorgio ◽  
D. Tavian ◽  
M. E. Larkum
Keyword(s):  
Pyramidal Neurons ◽  
Early Exposure ◽  
Dendritic Excitability ◽  
Neocortical Pyramidal Neurons

Voltage-Gated Potassium Channels Activated During Action Potentials in Layer V Neocortical Pyramidal Neurons

2000 ◽  
Vol 83 (1) ◽  
pp. 70-80 ◽  
Author(s):  
Jian Kang ◽  
John R. Huguenard ◽  
David A. Prince
Keyword(s):  
Potassium Channels ◽  
Action Potentials ◽  
Pyramidal Neurons ◽  
Bk Channels ◽  
Repetitive Firing ◽  
Delayed Rectifier ◽  
Voltage Gated ◽  
Voltage Dependent ◽  
Layer V ◽  
Neocortical Pyramidal Neurons

To investigate voltage-gated potassium channels underlying action potentials (APs), we simultaneously recorded neuronal APs and single K+ channel activities, using dual patch-clamp recordings (1 whole cell and 1 cell-attached patch) in single-layer V neocortical pyramidal neurons of rat brain slices. A fast voltage-gated K+ channel with a conductance of 37 pS (Kf) opened briefly during AP repolarization. Activation of Kf channels also was triggered by patch depolarization and did not require Ca2+influx. Activation threshold was about −20 mV and inactivation was voltage dependent. Mean duration of channel activities after single APs was 6.1 ± 0.6 ms (mean ± SD) at resting membrane potential (−64 mV), 6.7 ± 0.7 ms at −54 mV, and 62 ± 15 ms at −24 mV. The activation and inactivation properties suggest that Kf channels function mainly in AP repolarization but not in regulation of firing. Kf channels were sensitive to a low concentration of tetraethylammonium (TEA, 1 mM) but not to charybdotoxin (ChTX, 100 nM). Activities of A-type channels (KA) also were observed during AP repolarization. KA channels were activated by depolarization with a threshold near −45 mV, suggesting that KA channels function in both repolarization and timing of APs. Inactivation was voltage dependent with decay time constants of 32 ± 6 ms at −64 mV (rest), 112 ± 28 ms at −54 mV, and 367 ± 34 ms at −24 mV. KA channels were localized in clusters and were characterized by steady-state inactivation, multiple subconductance states (36 and 19 pS), and inhibition by 5 mM 4-aminopyridine (4-AP) but not by 1 mM TEA. A delayed rectifier K+ channel (Kdr) with a unique conductance of 17 pS was recorded from cell-attached patches with TEA/4-AP-filled pipettes. Kdrchannels were activated by depolarization with a threshold near −25 mV and showed delayed long-lasting activation. Kdr channels were not activated by single action potentials. Large conductance Ca2+-activated K+ (BK) channels were not triggered by neuronal action potentials in normal slices and only opened as neuronal responses deteriorated (e.g., smaller or absent spikes) and in a spike-independent manner. This study provides direct evidence for different roles of various K+ channels during action potentials in layer V neocortical pyramidal neurons. Kf and KA channels contribute to AP repolarization, while KA channels also regulate repetitive firing. Kdr channels also may function in regulating repetitive firing, whereas BK channels appear to be activated only in pathological conditions.

scholarly journals Acetylcholine boosts dendritic NMDA spikes in a CA3 pyramidal neuron model

2021 ◽  
Author(s):  
Rachel Humphries ◽  
Jack R. Mellor ◽  
Cian O’Donnell
Keyword(s):  
Potassium Channels ◽  
Computational Models ◽  
Pyramidal Neurons ◽  
Input Resistance ◽  
Synaptic Integration ◽  
Stratum Radiatum ◽  
List Type ◽  
Spike Generation ◽  
Dendritic Excitability ◽  
Nmdar Activation

AbstractAcetylcholine has been proposed to facilitate the formation of memory ensembles within the hippocampal CA3 network, by enhancing plasticity at CA3-CA3 recurrent synapses. Regenerative NMDA receptor (NMDAR) activation in CA3 neuron dendrites (NMDA spikes) increase synaptic Ca2+ influx and can trigger this synaptic plasticity. Acetylcholine inhibits potassium channels which enhances dendritic excitability and therefore could facilitate NMDA spike generation. Here, we investigate NMDAR-mediated nonlinear synaptic integration in stratum radiatum (SR) and stratum lacunosum moleculare (SLM) dendrites in a reconstructed CA3 neuron computational model and study the effect of acetylcholine on this nonlinearity. We found that distal SLM dendrites, with a higher input resistance, had a lower threshold for NMDA spike generation compared to SR dendrites. Simulating acetylcholine by blocking potassium channels (M-type, A-type, Ca2+-activated, and inwardly-rectifying) increased dendritic excitability and reduced the number of synapses required to generate NMDA spikes, particularly in the SR dendrites. The magnitude of this effect was heterogeneous across different dendritic branches within the same neuron. These results predict that acetylcholine facilitates dendritic integration and NMDA spike generation in selected CA3 dendrites which could strengthen connections between specific CA3 neurons to form memory ensembles.Highlights-Using biophysical computational models of CA3 pyramidal neurons we estimated the quantitative effects of acetylcholine on nonlinear synaptic integration.-Nonlinear NMDA spikes can be triggered by fewer synapses in distal dendrites due to increased local input resistance.-Acetylcholine broadly reduces the number of synapses needed to trigger NMDA spikes, but the magnitude of the effect varies across dendrite branches within a single neuron.-No single potassium channel type is the dominant mediator of the excitability effects of acetylcholine.

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