Abstract
Pyramidal neurons were acutely isolated from neocortex slices of 14- to 20-day-old rats and patch-clamped under physiological conditions. Current-clamp recordings revealed firing patterns corresponding to those previously reported in slices as regular spiking (RS) and intrinsically bursting (IB). i.e., single action potentials (AP), trains of regular spikes and bursts with depolarizing after-potentials (DAP). In IB neurons, intracellular perfusion with KF blocked the high-voltage-activated Ca2+ and the Ca2+-dependent K+ currents, revealing APs with a 10-30 ms shoulder at -35 mV (shoulder AP), which was the supporting plateau of the intraburst spikes. The use of the A channel blocker, 4-aminopyridine, caused a three-fold reduction in the AP repolarizing rate. A study of the de- and repolarizing rates modulating the spike shape (sboulder AP, burst or single APs) suggested that the percentage of available A channels could play a crucial role in burst formation. Blockade of the residual T-type Ca2+ current by Ni2+ did not inhibit the AP shoulder, whereas it was completely and reversibly inhibited by 30 nM TTX, which did not affect AP amplitude. The AP rising rate was only halved by 100 nM TTX. The data concerning the A channel-mediated burst formation and the role of the TTX-sensitive conductance have been successfully simulated in a model cell. We suggest that bursting is an intrinsic property of the membrane of neocortex neurons, and is sustained by TTX-sensitive slowly inactivating and/or persistent Na+ conductances.
| Original language | English |
|---|---|
| Pages (from-to) | 1-12 |
| Number of pages | 12 |
| Journal | Brain Research |
| Volume | 741 |
| Issue number | 1-2 |
| DOIs | |
| Publication status | Published - Nov 25 1996 |
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Keywords
- burst firing
- pyramidal neuron
- sensorimotor cortex
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
A TTX-sensitive conductance underlying burst firing in isolated pyramidal neurons from rat neocortex. / Guatteo, Ezia; Franceschetti, Silvana; Bacci, Alberto; Avanzini, Giuliano; Wanke, Enzo.
In: Brain Research, Vol. 741, No. 1-2, 25.11.1996, p. 1-12.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - A TTX-sensitive conductance underlying burst firing in isolated pyramidal neurons from rat neocortex
AU - Guatteo, Ezia
AU - Franceschetti, Silvana
AU - Bacci, Alberto
AU - Avanzini, Giuliano
AU - Wanke, Enzo
PY - 1996/11/25
Y1 - 1996/11/25
N2 - Pyramidal neurons were acutely isolated from neocortex slices of 14- to 20-day-old rats and patch-clamped under physiological conditions. Current-clamp recordings revealed firing patterns corresponding to those previously reported in slices as regular spiking (RS) and intrinsically bursting (IB). i.e., single action potentials (AP), trains of regular spikes and bursts with depolarizing after-potentials (DAP). In IB neurons, intracellular perfusion with KF blocked the high-voltage-activated Ca2+ and the Ca2+-dependent K+ currents, revealing APs with a 10-30 ms shoulder at -35 mV (shoulder AP), which was the supporting plateau of the intraburst spikes. The use of the A channel blocker, 4-aminopyridine, caused a three-fold reduction in the AP repolarizing rate. A study of the de- and repolarizing rates modulating the spike shape (sboulder AP, burst or single APs) suggested that the percentage of available A channels could play a crucial role in burst formation. Blockade of the residual T-type Ca2+ current by Ni2+ did not inhibit the AP shoulder, whereas it was completely and reversibly inhibited by 30 nM TTX, which did not affect AP amplitude. The AP rising rate was only halved by 100 nM TTX. The data concerning the A channel-mediated burst formation and the role of the TTX-sensitive conductance have been successfully simulated in a model cell. We suggest that bursting is an intrinsic property of the membrane of neocortex neurons, and is sustained by TTX-sensitive slowly inactivating and/or persistent Na+ conductances.
AB - Pyramidal neurons were acutely isolated from neocortex slices of 14- to 20-day-old rats and patch-clamped under physiological conditions. Current-clamp recordings revealed firing patterns corresponding to those previously reported in slices as regular spiking (RS) and intrinsically bursting (IB). i.e., single action potentials (AP), trains of regular spikes and bursts with depolarizing after-potentials (DAP). In IB neurons, intracellular perfusion with KF blocked the high-voltage-activated Ca2+ and the Ca2+-dependent K+ currents, revealing APs with a 10-30 ms shoulder at -35 mV (shoulder AP), which was the supporting plateau of the intraburst spikes. The use of the A channel blocker, 4-aminopyridine, caused a three-fold reduction in the AP repolarizing rate. A study of the de- and repolarizing rates modulating the spike shape (sboulder AP, burst or single APs) suggested that the percentage of available A channels could play a crucial role in burst formation. Blockade of the residual T-type Ca2+ current by Ni2+ did not inhibit the AP shoulder, whereas it was completely and reversibly inhibited by 30 nM TTX, which did not affect AP amplitude. The AP rising rate was only halved by 100 nM TTX. The data concerning the A channel-mediated burst formation and the role of the TTX-sensitive conductance have been successfully simulated in a model cell. We suggest that bursting is an intrinsic property of the membrane of neocortex neurons, and is sustained by TTX-sensitive slowly inactivating and/or persistent Na+ conductances.
KW - burst firing
KW - pyramidal neuron
KW - sensorimotor cortex
UR - http://www.scopus.com/inward/record.url?scp=0030602068&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0030602068&partnerID=8YFLogxK
U2 - 10.1016/S0006-8993(96)00866-9
DO - 10.1016/S0006-8993(96)00866-9
M3 - Article
C2 - 9001698
AN - SCOPUS:0030602068
VL - 741
SP - 1
EP - 12
JO - Brain Research
JF - Brain Research
SN - 0006-8993
IS - 1-2
ER -