A TTX-sensitive conductance underlying burst firing in isolated pyramidal neurons from rat neocortex

1996 ◽  
Vol 741 (1-2) ◽  
pp. 1-12 ◽  
Author(s):  
Ezia Guatteo ◽  
Silvana Franceschetti ◽  
Alberto Bacci ◽  
Giuliano Avanzini ◽  
Enzo Wanke
Keyword(s):  
Pyramidal Neurons ◽  
Burst Firing ◽  
Rat Neocortex

scholarly journals Dendritic Voltage-Gated Ion Channels Regulate the Action Potential Firing Mode of Hippocampal CA1 Pyramidal Neurons

1999 ◽  
Vol 82 (4) ◽  
pp. 1895-1901 ◽  
Author(s):  
Jeffrey C. Magee ◽  
Michael Carruth
Keyword(s):  
Ion Channels ◽  
Action Potential ◽  
Large Amplitude ◽  
Action Potentials ◽  
Pyramidal Neurons ◽  
Burst Firing ◽  
Voltage Gated ◽  
Ca1 Pyramidal Neurons ◽  
Firing Mode ◽  
Voltage Gated Ion Channels

The role of dendritic voltage-gated ion channels in the generation of action potential bursting was investigated using whole cell patch-clamp recordings from the soma and dendrites of CA1 pyramidal neurons located in hippocampal slices of adult rats. Under control conditions somatic current injections evoked single action potentials that were associated with an afterhyperpolarization (AHP). After localized application of 4-aminopyridine (4-AP) to the distal apical dendritic arborization, the same current injections resulted in the generation of an afterdepolarization (ADP) and multiple action potentials. This burst firing was not observed after localized application of 4-AP to the soma/proximal dendrites. The dendritic 4-AP application allowed large-amplitude Na+-dependent action potentials, which were prolonged in duration, to backpropagate into the distal apical dendrites. No change in action potential backpropagation was seen with proximal 4-AP application. Both the ADP and action potential bursting could be inhibited by the bath application of nonspecific concentrations of divalent Ca2+ channel blockers (NiCl and CdCl). Ca2+ channel blockade also reduced the dendritic action potential duration without significantly affecting spike amplitude. Low concentrations of TTX (10–50 nM) also reduced the ability of the CA1 neurons to fire in the busting mode. This effect was found to be the result of an inhibition of backpropagating dendritic action potentials and could be overcome through the coordinated injection of transient, large-amplitude depolarizing current into the dendrite. Dendritic current injections were able to restore the burst firing mode (represented as a large ADP) even in the presence of high concentrations of TTX (300–500 μM). These data suggest the role of dendritic Na+ channels in bursting is to allow somatic/axonal action potentials to backpropagate into the dendrites where they then activate dendritic Ca2+ channels. Although it appears that most Ca2+ channel subtypes are important in burst generation, blockade of T- and R-type Ca2+ channels by NiCl (75 μM) inhibited action potential bursting to a greater extent than L-channel (10 μM nimodipine) or N-, P/Q-type (1 μM ω-conotoxin MVIIC) Ca2+ channel blockade. This suggest that the Ni-sensitive voltage-gated Ca2+ channels have the most important role in action potential burst generation. In summary, these data suggest that the activation of dendritic voltage-gated Ca2+ channels, by large-amplitude backpropagating spikes, provides a prolonged inward current that is capable of generating an ADP and burst of multiple action potentials in the soma of CA1 pyramidal neurons. Dendritic voltage-gated ion channels profoundly regulate the processing and storage of incoming information in CA1 pyramidal neurons by modulating the action potential firing mode from single spiking to burst firing.

Muscarinic Inhibition of Persistent Na+ Current in Rat Neocortical Pyramidal Neurons

1998 ◽  
Vol 79 (3) ◽  
pp. 1579-1582 ◽  
Author(s):  
Thomas Mittmann ◽  
Christian Alzheimer
Keyword(s):  
Pyramidal Neurons ◽  
Pyramidal Cells ◽  
Cholinergic Innervation ◽  
Voltage Range ◽  
Rat Neocortex ◽  
The Rich ◽  
Subthreshold Voltage ◽  
Whole Cell Recordings ◽  
Muscarinic Modulation ◽  
Neocortical Pyramidal Neurons

Mittmann, Thomas and Christian Alzheimer. Muscarinic inhibition of persistent Na+ current in rat neocortical pyramidal neurons. J. Neurophysiol. 79: 1579–1582, 1998. Muscarinic modulation of persistent Na+ current ( I NaP) was studied using whole cell recordings from acutely isolated pyramidal cells of rat neocortex. After suppression of Ca2+ and K+ currents, I NaP was evoked by slow depolarizing voltage ramps or by long depolarizing voltage steps. The cholinergic agonist, carbachol, produced an atropine-sensitive decrease of I NaP at all potentials. When applied at a saturating concentration (20 μM), carbachol reduced peak I NaP by 38% on average. Carbachol did not alter the voltage dependence of I NaP activation nor did it interfere with the slow inactivation of I NaP. Our data indicate that I NaP can be targeted by the rich cholinergic innervation of the neocortex. Because I NaP is activated in the subthreshold voltage range, cholinergic inhibition of this current would be particularly suited to modulate the electrical behavior of neocortical pyramidal cells below and near firing threshold.

Role of EPSPs in initiation of spontaneous synchronized burst firing in rat hippocampal neurons bathed in high potassium

1990 ◽  
Vol 64 (3) ◽  
pp. 1000-1008 ◽  
Author(s):  
N. L. Chamberlin ◽  
R. D. Traub ◽  
R. Dingledine
Keyword(s):  
Hippocampal Neurons ◽  
Pyramidal Neurons ◽  
Hippocampal Slices ◽  
Pyramidal Cells ◽  
Burst Firing ◽  
Interictal Spikes ◽  
High Potassium ◽  
Synaptic Excitation ◽  
Ca3 Neurons

1. Spontaneous discharges that resemble interictal spikes arise in area CA3 b/c of rat hippocampal slices bathed in 8.5 mM [K+]o. Excitatory postsynaptic potentials (EPSPs) also appear at irregular intervals in these cells. The role of local synaptic excitation in burst initiation was examined with intracellular and extracellular recordings from CA3 pyramidal neurons. 2. Most (70%) EPSPs were small (less than 2 mV in amplitude), suggesting that they were the product of quantal release or were evoked by a single presynaptic action potential in another cell. It is unlikely that most EPSPs were evoked by a presynaptic burst of action potentials. Indeed, intrinsic burst firing was not prominent in CA3 b/c pyramidal cells perfused in 8.5 mM [K+]o. 3. The likelihood of occurrence and the amplitude of EPSPs were higher in the 50-ms interval just before the onset of each burst than during a similar interval 250 ms before the burst. This likely reflects increased firing probability of CA3 neurons as they emerge from the afterhyperpolarization (AHP) and conductance shunt associated with the previous burst. 4. Perfusion with 2 microM 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), a potent quisqualate receptor antagonist, decreased the frequency of EPSPs in CA3 b/c neurons from 3.6 +/- 0.9 to 0.9 +/- 0.3 (SE) Hz. Likewise, CNQX reversibly reduced the amplitude of evoked EPSPs in CA3 b/c cells. 5. Spontaneous burst firing in 8.5 mM [K+]o was abolished in 11 of 31 slices perfused with 2 microM CNQX.(ABSTRACT TRUNCATED AT 250 WORDS)

Recruitment of GABAergic Inhibition and Synchronization of Inhibitory Interneurons in Rat Neocortex

1997 ◽  
Vol 77 (6) ◽  
pp. 3134-3144 ◽  
Author(s):  
Larry S. Benardo
Keyword(s):  
Large Amplitude ◽  
Pyramidal Neurons ◽  
Excitatory Amino Acid ◽  
Lucifer Yellow ◽  
Inhibitory Neurons ◽  
Inhibitory Interneurons ◽  
Gabaergic Inhibition ◽  
Rat Neocortex ◽  
Excitatory Gaba ◽  
Spike Firing

Benardo, Larry S. Recruitment of GABAergic inhibition and synchronization of inhibitory interneurons in rat neocortex. J. Neurophysiol. 77: 3134–3144, 1997. Intracellular recordings were obtained from pyramidal and interneuronal cells in rat neocortical slices to examine the recruitment of GABAergic inhibition and inhibitory interneurons. In the presence of the convulsant agent4-aminopyridine (4-AP), after excitatory amino acid (EAA) ionotropic transmission was blocked, large-amplitude triphasic inhibitory postsynaptic potentials (IPSPs) occurred rhythmically (every 10–40 s) and synchronously in pyramidal neurons. After exposure to the γ-aminobutyric acid-A (GABAA) receptor antagonist picrotoxin, large-amplitude monophasic slow IPSPs persisted in these cells. In the presence of 4-AP and EAA blockers, interneurons showed periodic spike firing. Although some spikes rode on an underlying synaptic depolarization, much of the rhythmic firing consisted of spikes having highly variable amplitudes, arising abruptly from baseline, even during hyperpolarization. The spike firing and depolarizing synaptic potentials were completely suppressed by picrotoxin exposure, although monophasic slow IPSPs persisted in interneurons. This suggests that this subset of interneurons may participate in generating fast GABAA IPSPs, but not slow GABAB IPSPs. Cell morphology was confirmed by intracellular injection of neurobiotin or the fluorescent dye Lucifer yellow CH. Dye injection into interneurons often (>70%) resulted in the labeling of two to six cells (dye coupling). These findings suggest that GABAAergic neurons may be synchronized via recurrent collaterals through the depolarizing action of synaptically activatedGABAA receptors and a mechanism involving electrotonic coupling. Although inhibitory neurons mediating GABAB IPSPs may be entrained by the excitatory GABAA mechanism, they appear to be a separate subset of GABAergic neurons capable of functioning independently with autonomous pacing.

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