Development of calcium current subtypes in isolated rat hippocampal pyramidal cells (original) (raw)
Related papers
Hippocampus, 2000
Exploring the principles that govern activity-dependent changes in excitability is an essential step to understand the function of the nervous system, because they act as a general postsynaptic control mechanism that modulates the flow of synaptic signals. We show an activity-dependent potentiation of the slow Ca 2؉ -activated K ؉ current (sI AHP ) which induces sustained decreases in the excitability in CA1 pyramidal neurons. We analyzed the sI AHP using the slice technique and voltage-clamp recordings with sharp or patch-electrodes. Using sharp electrodes-repeated activation with depolarizing pulses evoked a prolonged (8-min) potentiation of the amplitude (171%) and duration (208%) of the sI AHP . Using patch electrodes, early after entering the whole-cell configuration (<20 min), responses were as those reported above. However, although the sI AHP remained unchanged, its potentiation was markedly reduced in later recordings, suggesting that the underlying mechanisms were rapidly eliminated by intracellular dialysis. Inhibition of L-type Ca 2؉ current by nifedipine (20 M) markedly reduced the sI AHP (79%) and its potentiation (55%). Ryanodine (20 M) that blocks the release of intracellular Ca 2؉ also reduced sI AHP (29%) and its potentiation (25%). The potentiation of the sI AHP induced a marked and prolonged (>50%; Ϸ8 min) decrease in excitability. The results suggest that sI AHP is potentiated as a result of an increased intracellular Ca 2؉ concentration ([Ca 2؉ ] i ) following activation of voltage-gated L-type Ca 2؉ channels, aided by the subsequent release of Ca 2؉ from intracellular stores. Another possibility is that repeated activation increases the Ca 2؉ -binding capacity of the channels mediating the sI AHP . This potentiation of the sI AHP could be relevant in hippocampal physiology, because the changes in excitability it causes may regulate the induction threshold of the long-term potentiation of synaptic efficacy. Moreover, the potentiation would act as a protective mechanism by reducing excitability and preventing the accumulation of intracellular Ca 2؉ to toxic levels when intense synaptic activation occurs. Hippocampus 2000;10:198 -206.
Calcium currents in cultured rat cortical neurons
Brain Research, 1989
Rat neocortical neurons grown in dissociated cell culture for 4-12 weeks were studied with whole-cell patch-clamp techniques in order to characterize the calcium currents present in these cells. When voltage-dependent Na and K currents were inhibited, depolarizations from negative holding potentials induced inward currents which had 3 components: a low threshold activated, small, relatively persistent component, which was completely inactivated at holding potentials more positive then-60 mV; a higher threshold, relatively persistent component (which was not inactivated at VH =-50 mV); and a higher threshold, larger, transient component. All 3 components were reduced by removal of Ca, and blocked by Cd and Ni at appropriate concentrations. The components were differentially affected by low concentrations of Ni (500/~M), nifedipine (500/~M) and Ba (1.8 mM). Only the first two components were present in very young neurons.
The Journal of Physiology, 2005
During postnatal development neurones display discharge behaviours that are not present in the adult, yet they are essential for the normal maturation of the nervous system. Neonatal CA1 pyramidal cells, like their adult counterparts, fire regularly, but excitatory GABAergic transmission drives them to generate spontaneous high-frequency bursts until postnatal day (P) 15. Using intracellular recordings in hippocampal slices from rats at P8 to P25, we show herein that as the network-driven burst activity fades out, most CA1 pyramidal cells become intrinsically bursting neurones. The incidence of intrinsic bursters begins to rise at P11 and attains a peak of 74% by P18-P19, after which it decreases over the course of a week, disappearing almost entirely at P25. Analysis of the effects of different voltage-gated Ca 2+ and Na + channel antagonists, applied focally to proximal and distal parts of developing neurones, revealed a complex burst mechanism. Intrinsic bursting in developing neurones results from 'ping-pong' interplay between a back-propagating spike that activates T/R-and L-type voltage-gated Ca 2+ channels in the distal apical dendrites and persistent voltage-gated Na + channels in the somatic region. Thus, developing pyramidal neurones transitionally express not only distinctive synaptic properties, but also unique intrinsic firing patterns, that may contribute to the ongoing formation and refinement of synaptic connections.
Pfl�gers Archiv European Journal of Physiology, 1992
The kinetic, permeability and pharmacological properties of Ca currents were investigated in primary cultures of rat hippocampal neurons. The low-voltage-activated (LVA) Ca current turned on positive to -60 mV and fully inactivated in a voltage-dependent way. This current was depressed by nickel (Ni, 40~tM) and amiloride (500 IxM) and was insensitive to 09-conotoxin (09-CgTx) (4 ~tM) and to the Ca agonist Bay K 8644 (5 ~tM). The high-voltage-activated (HVA) Ca current turned on positive to -40 mV and inactivated slowly and incompletely. This current was much less sensitive than the LVA current to Ni and amiloride but more sensitive to cadmium. r blocked only partially this current (about 50%) in an irreversible way. Bay K 8644 had a clear agonistic action almost exclusively on the 09-CgTx-resistant HVA current component. The present resuits suggest that the HVA channels, quite homogeneous for their kinetic properties and sensitivity to holding potentials, can be pharmacologically separated in two classes: (i) 09-CgTx-sensitive and Bay-K-8644-insensitive (09-S/BK-I) and (ii) 09-CgTx-insensitive and Bay-K-8644sensitive (09-I/BK-S), the latter displaying a stronger Cadependent inactivation.
European Journal of Neuroscience, 2000
The whole‐cell patch‐clamp technique was used to record Ca2+ currents in acutely dissociated neurons from layer II of guinea‐pig piriform cortex (PC). Ba2+ (5 mm) was used as charge carrier. In a subpopulation of layer II cells (≈ 22%) total Ba2+ currents (IBas) displayed a high degree (> 70%) of inactivation after 300 ms of steady depolarization. The application of L‐, N‐ and P/Q‐type Ca2+‐channel blockers to these high‐decay IBas left their fast inactivating component largely unaffected. The inactivation phase of the blocker‐resistant, fast‐decaying IBa thus isolated had a bi‐exponential time course, with a fast time constant of ≈ 20 ms and a slower time constant of ≈ 100 ms at voltage levels positive to −10 mV. The voltage dependence of activation of the blocker‐resistant, fast‐decaying IBa was shifted by ≈ 7–9 mV in the negative direction in comparison with those of other pharmacologically and/or kinetically different high‐voltage‐activated Ca2+ currents. We named this blocke...
The Journal of physiology, 1992
1. Current or voltage clamp recordings from CA3 neurones of the adult rat hippocampal slice were performed to study the inactivation properties of a slow outward K+ current identified as the delayed rectifier (IK). 2. In current clamp experiments, burst firing evoked from resting membrane potential by intracellular current injection was reduced or blocked by conditioning hyperpolarizing pre-pulses of 20-40 mV amplitude. This effect was inhibited by tetraethylammonium (TEA; 20 mM) but was unaffected by Cs+ (3 mM), 4-aminopyridine (4-AP; 2 mM), carbachol (30-50 microM), mast cell degranulating peptide (MCDP; 300 nM), thyrotrophin releasing hormone (TRH; 1 microM) or by a Ca(2+)-free solution containing Mn2+ or Co2+ (2 mM). 3. Single-electrode voltage clamp experiments were carried out on neurones superfused with Ca(2+)-free solution, containing tetrodotoxin (TTX; 1 microM), Mn2+ or Co2+ (2 mM), 4-AP (2 mM), Cs+ (3 mM) and carbachol (30 microM). Step depolarizations from a holding pote...