scholarly journals Ca2+-activated KCa3.1 potassium channels contribute to the slow afterhyperpolarization in L5 neocortical pyramidal neurons

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
M. V. Roshchin ◽  
V. N. Ierusalimsky ◽  
P. M. Balaban ◽  
E. S. Nikitin
Keyword(s):  
Potassium Channels ◽  
Pyramidal Neurons ◽  
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 Ciliary neuropeptidergic signaling dynamically regulates excitatory synapses in postnatal neocortical pyramidal neurons

2020 ◽  
Author(s):  
Lauren Tereshko ◽  
Ya Gao ◽  
Brian A. Cary ◽  
Gina G. Turrigiano ◽  
Piali Sengupta
Keyword(s):  
Primary Cilia ◽  
Neuronal Development ◽  
Pyramidal Neurons ◽  
Somatostatin Receptor ◽  
Cognitive Disorders ◽  
Mammalian Brain ◽  
Excitatory Synapses ◽  
Ciliary Signaling ◽  
Neocortical Pyramidal Neurons

ABSTRACTPrimary cilia are compartmentalized sensory organelles present on the majority of neurons in the mammalian brain throughout adulthood. Recent evidence suggests that cilia regulate multiple aspects of neuronal development, including the maintenance of neuronal connectivity. However, whether ciliary signals can dynamically modulate postnatal circuit excitability is unknown. Here we show that acute cell-autonomous knockdown of ciliary signaling rapidly strengthens glutamatergic inputs onto cultured neocortical pyramidal neurons, and increases spontaneous firing. This increased excitability occurs without changes to passive neuronal properties or intrinsic excitability. Further, the neuropeptide receptor somatostatin receptor 3 (SSTR3) is localized nearly exclusively to pyramidal neuron cilia both in vivo and in culture, and pharmacological manipulation of SSTR3 signaling bidirectionally modulates excitatory synaptic inputs onto these neurons. Our results indicate that ciliary neuropeptidergic signaling dynamically modulates excitatory synapses, and suggest that defects in this regulation may underlie a subset of behavioral and cognitive disorders associated with ciliopathies.

Specificity in the Interaction of HVA Ca2+ Channel Types With Ca2+-Dependent AHPs and Firing Behavior in Neocortical Pyramidal Neurons

1998 ◽  
Vol 79 (5) ◽  
pp. 2522-2534 ◽  
Author(s):  
Juan Carlos Pineda ◽  
Robert S. Waters ◽  
Robert C. Foehring
Keyword(s):  
Brain Slice ◽  
Pyramidal Neurons ◽  
Repetitive Firing ◽  
Channel Blockers ◽  
Firing Behavior ◽  
Inward Currents ◽  
Functional Consequences ◽  
P Type ◽  
Brain Slice Preparation ◽  
Neocortical Pyramidal Neurons

Pineda, Juan Carlos, Roberts S. Waters, and Robert C. Foehring. Specificity in the interaction of HVA Ca2+ channel types with Ca2+-dependent AHPs and firing behavior in neocortical pyramidal neurons. J. Neurophysiol. 79: 2522–2534, 1998. Intracellular recordings and organic and inorganic Ca2+ channel blockers were used in a neocortical brain slice preparation to test whether high-voltage–activated (HVA) Ca2+ channels are differentially coupled to Ca2+-dependent afterhyperpolarizations (AHPs) in sensorimotor neocortical pyramidal neurons. For the most part, spike repolarization was not Ca2+ dependent in these cells, although the final phase of repolarization (after the fast AHP) was sensitive to block of N-type current. Between 30 and 60% of the medium afterhyperpolarization (mAHP) and between ∼80 and 90% of the slow AHP (sAHP) were Ca2+ dependent. Based on the effects of specific organic Ca2+ channel blockers (dihydropyridines, ω-conotoxin GVIA, ω-agatoxin IVA, and ω-conotoxin MVIIC), the sAHP is coupled to N-, P-, and Q-type currents. P-type currents were coupled to the mAHP. L-type current was not involved in the generation of either AHP but (with other HVA currents) contributes to the inward currents that regulate interspike intervals during repetitive firing. These data suggest different functional consequences for modulation of Ca2+ current subtypes.

Relationships Between Intracellular Calcium and Afterhyperpolarizations in Neocortical Pyramidal Neurons

2004 ◽  
Vol 91 (1) ◽  
pp. 324-335 ◽  
Author(s):  
H. J. Abel ◽  
J.C.F. Lee ◽  
J. C. Callaway ◽  
R. C. Foehring
Keyword(s):  
Intracellular Calcium ◽  
Linear Relationship ◽  
Pyramidal Neurons ◽  
Pyramidal Cells ◽  
Firing Frequency ◽  
Discharge Activity ◽  
Apical Dendrites ◽  
Neocortical Pyramidal Neurons

We examined the effects of recent discharge activity on [Ca2+]i in neocortical pyramidal cells. Our data confirm and extend the observation that there is a linear relationship between plateau [Ca2+]i and firing frequency in soma and proximal apical dendrites. The rise in [Ca2+] activates K+ channels underlying the afterhyperpolarization (AHP), which consists of 2 Ca2+-dependent components: the medium AHP (mAHP) and the slow AHP (sAHP). The mAHP is blocked by apamin, indicating involvement of SK-type Ca2+-dependent K+ channels. The identity of the apamin-insensitive sAHP channel is unknown. We compared the sAHP and the mAHP with regard to: 1) number and frequency of spikes versus AHP amplitude; 2) number and frequency of spikes versus [Ca2+]i; 3) IAHP versus [Ca2+]i. Our data suggest that sAHP channels require an elevation of [Ca2+]i in the cytoplasm, rather than at the membrane, consistent with a role for a cytoplasmic intermediate between Ca2+ and the K+ channels. The mAHP channels appear to respond to a restricted Ca2+ domain.

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