Different Ca2+ channels in soma and dendrites of hippocampal pyramidal neurons mediate spike-induced Ca2+ influx

1995 ◽  
Vol 73 (6) ◽  
pp. 2553-2557 ◽  
Author(s):  
B. R. Christie ◽  
L. S. Eliot ◽  
K. Ito ◽  
H. Miyakawa ◽  
D. Johnston
Keyword(s):  
Pyramidal Cell ◽  
Action Potentials ◽  
Pyramidal Neurons ◽  
High Threshold ◽  
Intracellular Recordings ◽  
Hippocampal Pyramidal Neurons ◽  
Low Threshold ◽  
Dependent Processes ◽  
Cell Somata ◽  
Ca2 Channels

1. Intracellular recordings, in conjunction with fura-2 fluorescence imaging, were used to evaluate the contribution of the different Ca2+ channel subtypes to the Ca2+ influx induced by back-propagating trains of action potentials. High-threshold channels contributed mainly to Ca2+ influx in pyramidal cell somata and proximal dendrites, whereas low-threshold and other Ni(2+)-sensitive channels played a greater role in more distal dendritic signaling. These data suggest that the different Ca2+ channel types participate in distinct physiological functions; low-threshold channels likely play a greater role in dendritic integration, whereas high-threshold channels are more important for somatic Ca(2+)-dependent processes.

Electrophysiology of neurosecretory cells from the pituitary intermediate lobe

1988 ◽  
Vol 139 (1) ◽  
pp. 317-328
Author(s):  
R. N. McBurney ◽  
S. J. Kehl
Keyword(s):  
Cell Cultures ◽  
Calcium Ion ◽  
Action Potentials ◽  
Neurosecretory Cells ◽  
Secretory Process ◽  
High Threshold ◽  
Pars Intermedia ◽  
Low Threshold ◽  
Stimulus Secretion Coupling ◽  
Ca2 Channels

One of the goals in studying the electrical properties of neurosecretory cells is to relate their electrical activity to the process of secretion. A central question in these studies concerns the role of transmembrane calcium ion flux in the initiation of the secretory event. With regard to the secretory process in pituitary cells, several research groups have addressed this question in vitro using mixed primary anterior pituitary cell cultures or clonal cell lines derived from pituitary tumours. Other workers, including ourselves, have used homogeneous cell cultures derived from the pituitary intermediate lobes of rats to examine the characteristics of voltage-dependent conductances, the contribution of these conductances to action potentials and their role in stimulus-secretion coupling. Pars intermedia (PI) cells often fire spontaneous action potentials whose frequency can be modified by the injection of sustained currents through the recording electrode. In quiescent cells action potentials can also be evoked by the injection of depolarizing current stimuli. At around 20 degrees C these action potentials have a duration of about 5 ms. Although most of the inward current during action potentials is carried by sodium ions, a calcium ion component can be demonstrated under abnormal conditions. Voltage-clamp experiments have revealed that the membrane of these cells contains high-threshold, L-type, Ca2+ channels and low-threshold Ca2+ channels. Since hormone release from PI cells appears not to be dependent on action potential activity but does depend on external calcium ions, it is not clear what role these Ca2+ channels play in stimulus-secretion coupling in cells of the pituitary pars intermedia. One possibility is that the low-threshold Ca2+ channels are more important to the secretory process than the high-threshold channels.

Metabotropic glutamate receptor-mediated suppression of L-type calcium current in acutely isolated neocortical neurons

1992 ◽  
Vol 68 (3) ◽  
pp. 833-842 ◽  
Author(s):  
R. J. Sayer ◽  
P. C. Schwindt ◽  
W. E. Crill
Keyword(s):  
Glutamate Receptor ◽  
Pyramidal Neurons ◽  
Metabotropic Glutamate Receptor ◽  
High Threshold ◽  
External Application ◽  
Metabotropic Glutamate ◽  
Neocortical Neurons ◽  
Old Rats ◽  
Low Threshold ◽  
Ca2 Channels

1. The effects of metabotropic glutamate receptor (mGluR) stimulation on whole-cell Ca2+ currents were studied in pyramidal neurons isolated from the dorsal frontoparietal neocortex of rat. The selective mGluR agonist cis-(+/-)-1-aminocyclopentane-1,3-dicarboxylic acid [trans-ACPD (100 microM)] suppressed the peak high-threshold Ca2+ current by 21 +/- 1.7% (mean +/- SE) in 40 of 43 cells from 10- to 21-day-old rats. Consistent with previous findings for mGluR, glutamate, quisqualate, and ibotenate [but not alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)] reduced the Ca2+ currents, and the responses were not blocked by the ionotropic glutamate receptor antagonists 6-cyano-7-nitro-quinoxaline-2,3-dione (CNQX) and DL-2-amino-5-phosphonovaleric acid (APV). EC50S for Ca2+ current suppression were 29 nM for quisqualate, 2.3 microM for glutamate, and 13 microM for trans-ACPD. 2. The low-threshold Ca2+ current was not modulated by trans-ACPD. The component of the high-threshold CA2+ current suppressed by mGluR was determined by pharmacology; the responses were not affected by omega-conotoxin GVIA but were occluded by the dihydropyridine Ca2+ antagonist nifedipine. Ca2+ tail currents prolonged by the dihydropyridine Ca2+ agonist (+)-SDZ 202-79] were suppressed by mGluR stimulation in parallel with the peak current. These findings strongly suggest that L-type Ca2+ channels are modulated by mGluR. 3. In neurons dialyzed with 100 microM guanosine 5'-(gamma-thio)triphosphate (GTP-gamma-S), Ca2+ current suppression was elicited by the first application of trans-ACPD (in 5 of 6 cells), but not by subsequent applications. Responses in neurons dialyzed with 2 mM guanosine 5'-(beta-thio)diphosphate (GDP-beta-S) were significantly smaller than controls. The results are consistent with mGluR acting via linkage to a G protein. 4. The responses to mGluR agonists were smaller when the external Ca2+ was replaced by Ba2+, indicating that some part of the mechanism underlying the current suppression is Ca2+ dependent. Because mGluR stimulates phosphoinositide turnover and release of Ca2+ from intracellular stores in other types of neurons, the possibility of released Ca2+ mediating inactivation of Ca2+ channels was considered. However, the Ca2+ current suppression was not attenuated by strong intracellular Ca2+ buffering [20 mM bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic acid (BAPTA)], by dialysis with 100 microM inositol-1,4,5-triphosphate (IP3), or by external application of 1 microM thapsigargin. 5. We conclude that in neocortical neurons, one action of mGluR is to suppress the component of high-threshold Ca2+ current conducted by L-type Ca2+ channels.(ABSTRACT TRUNCATED AT 400 WORDS)

A model for dendritic Ca2+ accumulation in hippocampal pyramidal neurons based on fluorescence imaging measurements

1994 ◽  
Vol 71 (3) ◽  
pp. 1065-1077 ◽  
Author(s):  
D. B. Jaffe ◽  
W. N. Ross ◽  
J. E. Lisman ◽  
N. Lasser-Ross ◽  
H. Miyakawa ◽  
...  
Keyword(s):  
Fluorescence Imaging ◽  
Action Potentials ◽  
Hippocampal Neurons ◽  
Pyramidal Neurons ◽  
Na Channels ◽  
Hippocampal Pyramidal Neurons ◽  
K Channels ◽  
Voltage Gated ◽  
Synaptic Potentials ◽  
Ca2 Channels

1. High-speed fluorescence imaging was used to measure intracellular Ca2+ concentration ([Ca2+]i) changes in hippocampal neurons injected with the Ca(2+)-sensitive indicator fura-2 during intrasomatic and synaptic stimulation. The results of these experiments were used to construct a biophysical model of [Ca2+]i dynamics in hippocampal neurons. 2. A compartmental model of a pyramidal neuron was constructed incorporating published passive membrane properties of these cells, three types of voltage-gated Ca2+ channels characterized from adult hippocampal neurons, voltage-gated Na+ and K+ currents, and mechanisms for Ca2+ buffering and extrusion. 3. In hippocampal pyramidal neurons imaging of Na+ entry during electrical activity suggests that Na+ channels, at least in sufficient density to sustain action potentials, are localized in the soma and the proximal part of the apical dendritic tree. The model, which incorporates this distribution, demonstrates that action potentials attenuate steeply in passive distal dendritic compartments or distal dendritic compartments containing Ca2+ and K+ channels. This attenuation was affected by intracellular resistivity but not membrane resistivity. 4. Consistent with fluorescence imaging experiments, a non-uniform distribution of Ca2+ accumulation was generated by Ca2+ entry through voltage-gated Ca2+ channels opened by decrementally propagating Na+ action potentials. Consequently, the largest increases in [C2+]i were produced in the proximal dendrites. Distal voltage-gated Ca2+ currents were activated by broad, almost isopotential action potentials produced by reducing the overall density of K+ channels. 5. Simulations of subthreshold synaptic stimulation produced dendritic Ca2+ entry by the activation of voltage-gated Ca2+ channels. In the model these Ca2+ signals were localized near the site of synaptic input because of the attenuation of synaptic potentials with distance from the site of origin and the steep voltage-dependence of Ca2+ channel activation. 6. These simulations support the hypotheses generated from experimental evidence regarding the differential distribution of voltage-gated Ca2+ and Na+ channels in hippocampal neurons and the resulting voltage-gated Ca2+ accumulation from action and synaptic potentials.

Ca2+ Channels Involved in the Generation of the Slow Afterhyperpolarization in Cultured Rat Hippocampal Pyramidal Neurons

2000 ◽  
Vol 83 (5) ◽  
pp. 2554-2561 ◽  
Author(s):  
M. Shah ◽  
D. G. Haylett
Keyword(s):  
Calcium Channels ◽  
Action Potentials ◽  
Calcium Release ◽  
Pyramidal Neurons ◽  
Pyramidal Cells ◽  
Isolated Cells ◽  
Hippocampal Pyramidal Neurons ◽  
Calcium Induced Calcium Release ◽  
Ca2 Channels ◽  
Hippocampal Pyramidal Cells

The advantages of using isolated cells have led us to develop short-term cultures of hippocampal pyramidal cells, which retain many of the properties of cells in acute preparations and in particular the ability to generate afterhyperpolarizations after a train of action potentials. Using perforated-patch recordings, both medium and slow afterhyperpolarization currents (m I AHP and s I AHP, respectively) could be obtained from pyramidal cells that were cultured for 8–15 days. The s I AHP demonstrated the kinetics and pharmacologic characteristics reported for pyramidal cells in slices. In addition to confirming the insensitivity to 100 nM apamin and 1 mM TEA, we have shown that the s I AHP is also insensitive to 100 nM charybdotoxin but is inhibited by 100 μMd-tubocurarine. Concentrations of nifedipine (10 μM) and nimodipine (3 μM) that maximally inhibit L-type calcium channels reduced the s I AHP by 30 and 50%, respectively. However, higher concentrations of nimodipine (10 μM) abolished the s I AHP, which can be partially explained by an effect on action potentials. Both nifedipine and nimodipine at maximal concentrations were found to reduce the HVA calcium current in freshly dissociated neurons to the same extent. The N-type calcium channel inhibitor, ω-conotoxin GVIA (100 nM), irreversibly inhibited the s I AHP by 37%. Together, ω-conotoxin (100 nM) and nifedipine (10 μM) inhibited the s I AHP by 70%. 10 μM ryanodine also reduced the s I AHP by 30%, suggesting a role for calcium-induced calcium release. It is concluded that activation of the s I AHP in cultured hippocampal pyramidal cells is mediated by a rise in intracellular calcium involving multiple pathways and not just entry via L-type calcium channels.

Interaction of opioids and membrane potential to modulate Ca2+ channels in rat dorsal root ganglion neurons

1995 ◽  
Vol 73 (5) ◽  
pp. 1793-1798 ◽  
Author(s):  
M. D. Womack ◽  
E. W. McCleskey
Keyword(s):  
Dorsal Root Ganglion ◽  
Sensory Neurons ◽  
Action Potentials ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
High Threshold ◽  
Partial Recovery ◽  
Drg Neurons ◽  
Ganglion Neurons ◽  
Ca2 Channels

1. Using patch-clamp methods, we show that brief prepulses to very positive voltages increase (facilitate) the amplitude of current through Ca2+ channels during a subsequent test pulse in some, but not all, dorsal root ganglion (DRG) sensory neurons. The amplitude of this facilitated current generally increases when the Ca2+ channels are inhibited by activation of the mu-opioid receptor. 2. The facilitated current is blocked by omega-conotoxin GVIA, activates in the range of high-threshold Ca2+ channels, and inactivates at relatively negative holding voltages. Thus facilitated current passes through N-type Ca2+ channels, the same channels that are inhibited by opioids and control neurotransmitter release in sensory neurons. 3. Although maximal facilitation occurs only at unphysiologically high membrane potentials (above +100 mV), some facilitation is seen after prepulses to voltages reached during action potentials. After return to the holding potential, facilitation persists for hundreds of milliseconds, considerably longer than in other neurons. Brief trains of pulses designed to mimic action potentials caused small facilitation (19% of maximal) in a fraction (8 of 24) of opioid-inhibited neurons. 4. We conclude that 1) prepulses to extremely positive voltages can cause partial recovery of Ca2+ channels inhibited by opioids; and 2) small, but detectable, facilitation is also seen after physiological stimulation in some DRG neurons. Facilitation, largely considered a biophysical epiphenomenon because of the extreme voltages used to induce it, appears to be physiologically relevant during opioid inhibition of Ca2+ channels in DRG neurons.

scholarly journals Biophysical Factors that Promote Mechanically-Induced Action Potentials in Neocortical and Hippocampal Pyramidal Neurons

2016 ◽  
Vol 110 (3) ◽  
pp. 349a ◽  
Author(s):  
Yury A. Nikolaev ◽  
Peter J. Dosen ◽  
Derek R. Laver ◽  
Dirk F. Van Helden ◽  
Owen P. Hamill
Keyword(s):  
Action Potentials ◽  
Pyramidal Neurons ◽  
Hippocampal Pyramidal Neurons ◽  
Biophysical Factors

Calcium currents of cardiovascular neurons isolated from adult guinea pigs

1987 ◽  
Vol 252 (4) ◽  
pp. H867-H871
Author(s):  
D. L. Kunze
Keyword(s):  
Guinea Pigs ◽  
Action Potentials ◽  
Calcium Current ◽  
Threshold Current ◽  
Bipolar Cells ◽  
Calcium Currents ◽  
High Threshold ◽  
Calcium Dependent ◽  
Low Threshold ◽  
Patch Technique

A preparation of cells isolated from the medial and dorsal nuclei of the solitary tract of the medulla of adult guinea pigs was developed to examine the electrical properties of neurons isolated from an area of the central nervous system which is involved in the control of arterial pressure and heart rate. Bipolar cells of approximately 10 microns diameter were obtained on enzymatic dispersion. The cells were studied with the use of the patch technique for whole cell recording. Action potentials were elicited by depolarizing pulses in the presence of 10(-5) M tetrodotoxin which blocked a sodium-dependent current. These action potentials were calcium dependent and were eliminated by adding 1 mM Cd to the bath. In all cells studied, two voltage-dependent components to the calcium current were identified. In 10 mM Ca a high-threshold component activated at approximately -20 mV from holding potentials of -30 mV. A second lower threshold component was activated at -40 mV from more negative holding potentials of -80 mV. The low-threshold component was rapidly inactivating, whereas the high-threshold current slowly inactivated. The peak amplitudes of the two components were similar. Both components were blocked by 1 mM Cd. A role for the low-threshold calcium current in generating repetitive activity is postulated.

Calcium currents in acutely isolated human neocortical neurons

1993 ◽  
Vol 69 (5) ◽  
pp. 1596-1606 ◽  
Author(s):  
R. J. Sayer ◽  
A. M. Brown ◽  
P. C. Schwindt ◽  
W. E. Crill
Keyword(s):  
Pyramidal Neurons ◽  
Intractable Epilepsy ◽  
Pyramidal Cells ◽  
Cell Voltage ◽  
Threshold Current ◽  
Calcium Currents ◽  
High Threshold ◽  
Peak Current ◽  
Neocortical Neurons ◽  
Low Threshold

1. Ca2+ currents were investigated in neurons acutely isolated from adult human temporal neocortex. The aim was to compare the basic characteristics of the currents with those previously described in animals and to examine the effects of dihydropyridine Ca2+ antagonists and antiepileptic drugs. The tissue, obtained from patients undergoing temporal lobe surgery for medically intractable epilepsy, was sliced, incubated in papain, and triturated. 2. Most of the isolated neurons (34 of 36) were judged to be pyramidal cells by their morphology. Whole-cell voltage-clamp recordings revealed two components of Ca2+ current: 1) a low-threshold (T-type) current that was transient, small in amplitude, and required hyperpolarization more negative than -70 mV for removal of inactivation and 2) a high-threshold current that was slowly inactivating and was available for activation from more positive potentials. The characteristics of the Ca2+ currents were very similar to those in the neocortical neurons of young rats, although the low-threshold current was less prominent in the human cells. 3. Subcomponents of the high-threshold current were identified by pharmacology. About 20% of the peak current was blocked by omega-conotoxin GVIA (presumed N current) and 40-50% of the peak current was blocked by micromolar concentrations of the dihydropyridine Ca2+ antagonists nifedipine and nimodipine (presumed L current). In two neurons tested with a range of nimodipine concentrations, the threshold for suppression of the high-threshold current was approximately 10 nM. 4. The antiepileptic agents ethosuximide, carbamazepine, and valproate did not affect the Ca2+ currents at therapeutically relevant concentrations. Phenytoin marginally reduced the low- and high-threshold Ca2+ currents at 8 microM (a concentration corresponding to the upper therapeutic range). The results do not support the hypothesis that inhibition of Ca2+ currents in neocortical pyramidal neurons is a major action of these drugs.

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