Both high- and low voltage-activated calcium currents contribute to the light-evoked responses of luminosity horizontal cells in the Xenopus retina (original) (raw)
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Pfl�gers Archiv European Journal of Physiology, 1994
The voltage dependence of ?-aminobutyricacid-and norepinephrine-induced inhibition of N-type calcium current in cultured embryonic chick dorsal-root ganglion neurons was studied with whole-cell voltageclamp recording. The inhibitory action of the neurotransmitters was comprised of at least two distinct modulatory components, which were separable on the basis of their differential voltage dependence. The first component, which we term "kinetic slowing", is associated with a slowing of the activation kinetics -an effect that subsides during a test pulse. The kinetic-slowing component is largely reversed at depolarized voltages (i.e., it is voltage-dependent). The second component, which we term "steady-state inhibition", is by definition not associated with a change in activation kinetics and is present throughout the duration of a test pulse. The steady-state inhibition is not reversed at depolarized voltages (i.e., it is voltage-independent). Although the two components can be separated on the basis of their voltage dependence, they appear to be indistinguishable in their time courses for onset and recovery as well as their rates of desensitization following multiple applications of transmitter. Furthermore, neither component requires cell dialysis, as both are observed using perforatedpatch as well as whole-cell recording configurations. The co-existence in nerve terminals of both voltage-dependent and -independent mechanisms to modulate calcium channel function could offer a means of differentially controlling synaptic transmission under conditions of low-and high-frequency presynaptic discharge.
The spontaneous firing patterns of striatal cholinergic interneurons are sculpted by potassium currents that give rise to prominent afterhyperpolarizations (AHPs). Large-conductance calcium-activated potassium (BK) channel currents contribute to action potential (AP) repolarization; small-conductance calcium-activated potassium channel currents generate an apamin-sensitive medium AHP (mAHP) after each AP; and bursts of APs generate long-lasting slow AHPs (sAHPs) attributable to apamin-insensitive currents. Because all these currents are calcium dependent, we conducted voltage-and current-clamp whole-cell recordings while pharmacologically manipulating calcium channels of the plasma membrane and intracellular stores to determine what sources of calcium activate the currents underlying AP repolarization and the AHPs. The Ca v 2.2 (N-type) blocker -conotoxin GVIA (1 M) was the only blocker that significantly reduced the mAHP, and it induced a transition to rhythmic bursting in one-third of the cells tested. Ca v 1 (L-type) blockers (10 M dihydropyridines) were the only ones that significantly reduced the sAHP. When applied to cells induced to burst with apamin, dihydropyridines reduced the sAHPs and abolished bursting. Depletion of intracellular stores with 10 mM caffeine also significantly reduced the sAHP current and reversibly regularized firing. Application of 1 M -conotoxin MVIIC (a Ca v 2.1/2.2 blocker) broadened APs but had a negligible effect on APs in cells in which BK channels were already blocked by submillimolar tetraethylammonium chloride, indicating that Ca v 2.1 (Q-type) channels provide the calcium to activate BK channels that repolarize the AP. Thus, calcium currents are selectively coupled to the calcium-dependent potassium currents underlying the AHPs, thereby creating mechanisms for control of the spontaneous firing patterns of these neurons.
The Journal of Physiology
1. Using the whole-cell recording mode of the patch-clamp technique, we have investigated kinetic and selectivity properties of a low-voltage-activated (l.v.a.) Ca2+ current in chick and rat dorsal root ganglion (d.r.g.) neurones. 2. L.v.a currents were activated at about-50 mV and reached maximum amplitudes between-30 and-20 mV with averages of-0-16 nA in chick and-03 nA in rat d.r.g. cells with 5 mM-extracellular Ca2+. Between-60 and-20 mV, the time to peak, tp, of this current decreased with increasing membrane depolarizations. An e-fold change of tp required a 14 mV potential change in chick and a 17 mV change in rat d.r.g. cells at 22 'C. 3. Between-50 and + 20 mV inactivation of this current was fast, single exponential and voltage dependent. In rat, the time constant of inactivation, Th, was smaller and less voltage dependent than in chick. 4. The amplitude of these currents increased by a factor of 5-10, when the extracellular Ca2+ concentration was changed from 1 to 95 mm. Amplitudes and kinetic parameters of the currents showed typical shifts along the voltage axis. No correlation between Ca2+ current amplitudes and activation-inactivation kinetics was found, suggesting that the reaction rates which control these processes are not dependent on Ca2+ entry. 5. Recovery from inactivation was voltage dependent and developed with a time constant, Tr' in the order of 1 s. Tr was nearly halved by changing the potential from-80 to-120 mV. 6. Tail currents associated with membrane repolarization were also voltage dependent and developed exponentially. Their time constant decreased by a factor of 3 when the potential was changed from-60 to-100 mV. 7. A second and more prominent Ca2+ current was activated at potentials positive to-20 mV (high-voltage-activated Ca2+ currents, h.v.a.), masking the time course of l.v.a. currents. Between-20 and 0 mV, time to peak of the entire current increased by a factor of 2 but decreased again at higher membrane potentials. Inactivation also became significantly slower in this potential range.
Facilitation of L-type Calcium Current in Thalamic Neurons
Journal of Neurophysiology, 1998
Kammermeier, Paul J. and Stephen W. Jones. Facilitation of L-type calcium current in thalamic neurons. J. Neurophysiol. 79: 410–417, 1998. We have studied facilitation of the L-type calcium current in neurons acutely isolated from the ventrobasal nucleus of the rat thalamus. Currents were recorded after pretreatment with 1 μM ω-conotoxin GVIA and 5 μM ω-conotoxin MVIIC, to better isolate L-current. Long, strong depolarizations induced slow tail currents at negative voltages, but did not affect currents at voltages where channels were strongly activated. The initial peak tail current was not measurably increased. The time course of recovery from facilitation paralleled the time course of the tail current, indicating that facilitation does not outlast channel closing. The kinase inhibitors staurosporine and H-7 and the phosphatase inhibitor okadaic acid had no significant effect on L-current facilitation compared with control, but facilitation was greater with H-7 than with okadaic ac...
European Journal of Neuroscience, 1992
Action potentials generated by voltagedependent Ca2+ conductances were studied at 25OC with the perforatedpatch technique, in freshly dispersed adult rat sensory neurons perfused with Na-free solutions containing tetraethylammonium. Brief depolarizing currents from membrane potentials negative to -75 mV always elicited long (> 100 ms) plateau spikes which had different thresholds in different neurons: a low threshold around -601-50 mV and a high-threshold at -301 -20 mV. Stimulations from potentials positive to -55 mV, on the contrary, elicited spikes originating only in the high threshold region and sensitive to 25 pM Cd2+, designated high-threshold spikes. In neurons which showed spikes with low threshold, addition of 25 pM Cd2+ disclosed a smaller and shorter regenerative response, the low-threshold spike. Moreover, the classical 'anodebreak' stimulation from -50/ -60 mV uncovered isolated low-threshold spikes, indicating a time-and voltagedependent de-inactivating process. From the properties of the low (LVA) and high (HVA) voltage-activated Ca2+ currents, recorded under the same extracellular conditions, a Hodgkin -Huxley model was derived and used to reconstruct all the features of the recorded spikes. The model was also able to simulate experimental blocking of LVA channels by amiloride, modulation of HVA channels by baclofen and induced oscillatory firing. This agreement between the behaviour of recorded spikes and their mathematical description led us to conclude that the LVA and HVA Ca2+ currents underlie the low-and high-threshold Ca2+ spikes, respectively. Furthermore, our data suggest that complex behaviour known to be typical of central nervous system neurons is also present in sensory peripheral neurons.
Modulation of bursts and high-threshold calcium spikes in neurons of rat auditory thalamus
Neuroscience, 1998
Neurons in the ventral partition of the medial geniculate body are able to fire high-threshold Ca2+-spikes. The neurons normally discharge such spikes on low-threshold Ca2+-spikes after the action potentials of a burst. We studied membrane mechanisms that regulate the discharge of high-threshold Ca2+-spikes, using whole-cell recording techniques in a slice preparation of rat thalamus. A subthreshold (persistent) Na+-conductance amplified depolarizing inputs, enhancing membrane excitability in the tonic firing mode and amplifying the low-threshold CaZ+-spike in the burst firing mode. Application of tetrodotoxin blocked the amplification and high-threshold CaZ+-spike firing. A slowly inactivating K + conductance, sensitive to blockade with 4-aminopyridine (50-100 gM), but not tetraethylammonium (2-10mM), appeared to suppress excitability and high-threshold CaZ+-spike firing. Application of 4-aminopyridine increased the low-threshold CaZ+-spike and the number of action potentials in the burst, and led to a conversion of the superimposed high-threshold Ca2+-spike into a plateau potential. Application of the Ca2+-channel blocker Cd 2+ (50 gM), reduced or eliminated this plateau potential. The tetrodotoxin sensitive, persistent Na+-conductance also sustained plateau potentials, triggered after 4-aminopyridine application on depolarization by current pulses. Our results suggest that high-threshold CaZ+-spike firing, and a short-term influx of Ca 2+, are regulated by a balance of voltage-dependent conductances. Normally, a slowly inactivating A-type K+-conductance may reduce high-threshold Ca2+-spike firing and shorten high-threshold Ca2+-spike duration. A persistent Na+-conductance promotes coupling of the low-threshold Ca2+-spike to a high-threshold Ca2+-spike. Thus, the activation of both voltage-dependent conductances would affect Ca 2+ influx into ventral medial geniculate neurons. This would alter the quality of the different signals transmitted in the thalamocortical system during wakefulness, sleep and pathological states..~; 1998 IBRO. Published by Elsevier Science Ltd.
Invertebrate Neuroscience, 2017
In the present study, cytosolic calcium concentration changes were recorded in response to various forms of excitations, using the fluorescent calcium indicator dye OG-BAPTA1 together with the current or voltage clamp methods in stretch receptor neurons of crayfish. A single action potential evoked a rise in the resting calcium level in the axon and axonal hillock, whereas an impulse train or a large saturating current injection would be required to evoke an equivalent response in the dendrite region. Under voltage clamp conditions, amplitude differences between axon and dendrite responses vanished completely. The fast activation time and the modulation of the response by extracellular calcium concentration changes indicated that the evoked calcium transients might be mediated by calcium entry into the cytosol through a voltage-gated calcium channel. The decay of the responses was slow and sensitive to extracellular sodium and calcium concentrations as well as exposure to 1-10 mM NiCl 2 and 10-500 lM lanthanum. Thus, a sodium calcium exchanger and a calcium ATPase might be responsible for calcium extrusion from the cytosol. Present results indicate that the calcium indicator OG-BAPTA1 might be an efficient but indirect way of monitoring regional membrane potential differences in a single neuron. Keywords Crayfish Á Stretch receptor neuron Á Action potential Á Calcium transients Á OG-BAPTA1
The Journal of Physiology, 1999
Voltage-activated calcium currents (VACCs) have a primary role in regulating membrane electrophysiological behaviour, intercellular communication and other non-membranal cell functions in neurones (Llin as, 1988; Berridge, 1998). VACCs can influence neuronal electroresponsiveness both directly, by sustaining inward currents that promote depolarizing responses, and indirectly, by recruiting calcium-dependent currents. The kinetic properties and the voltage range of activation of the underlying calcium conductances are key elements in determining the specific contribution of the various VACC types in neuronal functions. For instance, a calcium current activated at more negative voltage levels than another one of similar size will have a stronger depolarizing effect on neuronal membrane: at relatively negative voltage levels, indeed, a higher membrane input resistance and a lesser weight of repolarizing potassium currents due to a smaller driving force for potassium ions are to be expected. The characterization of the calcium currents expressed by a given neuronal type can therefore be relevant to the understanding of its specific functional behaviour.
Intracellular Calcium and Control of Burst Generation in Neurons of Guinea-Pig Neocortex in Vitro
European Journal of Neuroscience, 1989
Response properties of neurons in brain slices of guinea pig parietal neocortex were examined following intracellular injection of the Ca2+ chelators, EGTA and BAPTA. Although chelator injection did not cause any consistent change in passive membrane properties, it did induce 81% of neurons encountered at all sub-pial depths to become 'bursters', in that just-threshold depolarizing current pulses triggered all-or-none bursts of 2-5 fast action potentials. Transition to 'burstiness' was associated with disappearance of an AHP and appearance of a DAP. Although chelator caused a slight increase in steady-state firing rate, marked accommodation persisted. Extracellular Co2+ or Mn2+ had an effect on steady-state firing rate similar to that of the intracellular chelators; however, exposure to these Ca2+ channel blockers also caused steady state depolarization, increased resting input resistance and time constant, and profound spike broadening. This treatment never induced transition to 'burstiness'. Chelator-injected neurons ceased to generate bursts when Ca2+ was replaced by Mn2+ in the Ringer's solution. During exposure to 50-200 msec Ca2+ spikes followed brief depolarizing pulses. As chelator was injected into the cell, there was progressive prolongation of the Ca2' plateaus, which was associated with slowing of the rate at which membrane resistance gradually recovered following the initial increase in conductance. activate processes which prevent most neocortical neurons from being bursters. These processes probably include Ca2+-dependent K + currents, and Ca2+-dependent Ca2+ channel inactivation. M TTX and 20 mM TEA, These findings indicate that under normal conditions, activity-related increases in intracellular Ca2' Correspondence to; M. J. Gutnick, as above