Selective Shunting of the NMDA EPSP Component by the Slow Afterhyperpolarization in Rat CA1 Pyramidal Neurons

2007 ◽  
Vol 97 (5) ◽  
pp. 3242-3255 ◽  
Author(s):  
David Fernández de Sevilla ◽  
Marco Fuenzalida ◽  
Ana B. Porto Pazos ◽  
Washington Buño
Keyword(s):  
Pyramidal Neurons ◽  
Spatial Summation ◽  
Decisive Role ◽  
Perforant Path ◽  
Ca1 Pyramidal Neurons ◽  
Basal Dendrites ◽  
Hippocampal Ca1 ◽  
Dendritic Location ◽  
Conductance Increase

Pyramidal neuron dendrites express voltage-gated conductances that control synaptic integration and plasticity, but the contribution of the Ca2+-activated K+-mediated currents to dendritic function is not well understood. Using dendritic and somatic recordings in rat hippocampal CA1 pyramidal neurons in vitro, we analyzed the changes induced by the slow Ca2+-activated K+-mediated afterhyperpolarization (sAHP) generated by bursts of action potentials on excitatory postsynaptic potentials (EPSPs) evoked at the apical dendrites by perforant path-Schaffer collateral stimulation. Both the amplitude and decay time constants of EPSPs (τEPSP) were reduced by the sAHP in somatic recordings. In contrast, the dendritic EPSP amplitude remained unchanged, whereas τEPSP was reduced. Temporal summation was reduced and spatial summation linearized by the sAHP. The amplitude of the isolated N-methyl-d-aspartate component of EPSPs (EPSPNMDA) was reduced, whereas τNMDA was unaffected by the sAHP. In contrast, the sAHP did not modify the amplitude of the isolated EPSPAMPA but reduced τAMPA both in dendritic and somatic recordings. These changes are attributable to a conductance increase that acted mainly via a selective “shunt” of EPSPNMDA because they were absent under voltage clamp, not present with imposed hyperpolarization simulating the sAHP, missing when the sAHP was inhibited with isoproterenol, and reduced under block of EPSPNMDA. EPSPs generated at the basal dendrites were similarly modified by the sAHP, suggesting both a somatic and apical dendritic location of the sAHP channels. Therefore the sAHP may play a decisive role in the dendrites by regulating synaptic efficacy and temporal and spatial summation.

Activation of electrogenic sodium pump in hippocampal CA1 neurons following glutamate-induced depolarization

1986 ◽  
Vol 56 (2) ◽  
pp. 507-522 ◽  
Author(s):  
S. M. Thompson ◽  
D. A. Prince
Keyword(s):  
Pyramidal Neurons ◽  
Sodium Pump ◽  
Equilibrium Potential ◽  
Ca1 Neurons ◽  
Electrogenic Sodium Pump ◽  
Hippocampal Ca1 ◽  
Voltage Dependent ◽  
Specific Antagonist ◽  
Conductance Increase

Intracellular recordings were obtained from guinea pig hippocampal CA1 pyramidal neurons maintained in vitro. Focal applications of glutamate produced depolarizations followed by prolonged hyperpolarizations. The mechanisms underlying this postglutamate hyperpolarization (PGH) were investigated. PGH did not reverse polarity with hyperpolarization to potentials at or near the presumed K+ equilibrium potential. A transient increase in conductance was associated with the PGH; control values returned well before the termination of PGH. Application of Mn2+, an antagonist of voltage-dependent calcium conductance, blocked synaptic transmission and the afterhyperpolarization (AHP) that follows a directly evoked train of action potentials but did not diminish the PGH or the transient conductance increase. Intracellular application of the calcium chelator ethyleneglycol-bis(beta-aminoethylether)-N,N'-tetraacetic acid blocked AHP but did not affect PGH. Reductions in temperature from 37 to 27-32 degrees C reduced the amplitude of PGH and prolonged its duration but increased the amplitude and duration of AHP. The transient conductance increase associated with PGH was unaffected. Application of strophanthidin, a specific antagonist of Na+-K+-ATPase, reversibly blocked PGH and led to large increases in the amplitude and duration of the AHP. It is concluded that PGH is produced by activation of the electrogenic sodium pump by glutamate-induced excitation. As such, PGH is a useful physiological assay of electrogenic sodium transport. In addition, maintenance of the Na+ gradient by the sodium pump is important for the buffering of Ca2+ influx.

scholarly journals Membrane Dysfunction Induced by In Vitro Ischemia in Rat Hippocampal CA1 Pyramidal Neurons

1999 ◽  
Vol 81 (4) ◽  
pp. 1872-1880 ◽  
Author(s):  
E. Tanaka ◽  
S. Yamamoto ◽  
H. Inokuchi ◽  
T. Isagai ◽  
H. Higashi
Keyword(s):  
Membrane Potential ◽  
Voltage Clamp ◽  
Pyramidal Neurons ◽  
Membrane Surface ◽  
Bathing Medium ◽  
Ca1 Pyramidal Neurons ◽  
In Vitro Ischemia ◽  
Hippocampal Ca1 ◽  
Electrode Voltage

Membrane dysfunction induced by in vitro ischemia in rat hippocampal CA1 pyramidal neurons. Intracellular and single-electrode voltage-clamp recordings were made to investigate the process of membrane dysfunction induced by superfusion with oxygen and glucose-deprived (ischemia-simulating) medium in hippocampal CA1 pyramidal neurons of rat tissue slices. To assess correlation between potential change and membrane dysfunction, the recorded neurons were stained intracellularly with biocytin. A rapid depolarization was produced ∼6 min after starting superfusion with ischemia-simulating medium. When oxygen and glucose were reintroduced to the bathing medium immediately after generating the rapid depolarization, the membrane did not repolarize but depolarized further, the potential reaching 0 mV ∼5 min after the reintroduction. In single-electrode voltage-clamp recording, a corresponding rapid inward current was observed when the membrane potential was held at −70 mV. After the reintroduction of oxygen and glucose, the current induced by ischemia-simulating medium partially returned to preexposure levels. These results suggest that the membrane depolarization is involved with the membrane dysfunction. The morphological aspects of biocytin-stained neurons during ischemic exposure were not significantly different from control neurons before the rapid depolarization. On the other hand, small blebs were observed on the surface of the neuron within 0.5 min of generating the rapid depolarization, and blebs increased in size after 1 min. After 3 min, neurons became larger and swollen. The long and transverse axes and area of the cross-sectional cell body were increased significantly 1 and 3 min after the rapid depolarization. When Ca2+-free (0 mM) with Co2+ (2.5 mM)-containing medium including oxygen and glucose was applied within 1 min after the rapid depolarization, the membrane potential was restored completely to the preexposure level in the majority of neurons. In these neurons, the long axis was lengthened without any blebs being apparent on the membrane surface. These results suggest that the membrane dysfunction induced by in vitro ischemia may be due to a Ca2+-dependent process that commences ∼1.5 min after and is completed 3 min after the onset of the rapid depolarization. Because small blebs occurred immediately after the rapid depolarization and large blebs appeared 1.5–3 min after, it is likely that the transformation from small to large blebs may result in the observed irreversible membrane dysfunction.

Neuroprotective mechanisms of lidocaine against in vitro ischemic insult of the rat hippocampal CA1 pyramidal neurons

2005 ◽  
Vol 53 (3) ◽  
pp. 271-278 ◽  
Author(s):  
S. Niiyama ◽  
E. Tanaka ◽  
S. Tsuji ◽  
Y. Murai ◽  
M. Satani ◽  
...  
Keyword(s):  
Pyramidal Neurons ◽  
Ischemic Insult ◽  
Ca1 Pyramidal Neurons ◽  
Hippocampal Ca1

Serotonin Modulates Spike Backpropagation and Associated [Ca2+]i Changes in the Apical Dendrites of Hippocampal CA1 Pyramidal Neurons

1999 ◽  
Vol 81 (1) ◽  
pp. 216-224 ◽  
Author(s):  
Vladislav M. Sandler ◽  
William N. Ross
Keyword(s):  
Action Potentials ◽  
Pyramidal Neurons ◽  
Peak Potential ◽  
Fura 2 ◽  
Ca1 Pyramidal Neurons ◽  
Ca1 Region ◽  
Artificial Cerebrospinal Fluid ◽  
Hippocampal Ca1 ◽  
Conductance Increase ◽  
Apical Dendrites

Sandler, Vladislav M. and William N. Ross. Serotonin modulates spike backpropagation and associated [Ca2+]i changes in the apical dendrites of hippocampal CA1 pyramidal neurons. J. Neurophysiol. 81: 216–224, 1999. The effect of serotonin (5-HT) on somatic and dendritic properties was analyzed in pyramidal neurons from the CA1 region in slices from the rat hippocampus. Bath-applied 5-HT (10 μM) hyperpolarized the soma and apical dendrites and caused a conductance increase at both locations. In the dendrites (200–300 μm from the soma) trains of antidromically activated, backpropagating action potentials had lower peak potentials in 5-HT than in normal artificial cerebrospinal fluid. Spike amplitudes were about the same in the two solutions. Similar results were found when the action potentials were evoked synaptically with stimulation in the stratum oriens. In the soma, spike amplitudes increased in 5-HT, with only a small decrease in the peak potential. Calcium concentration measurements, made with bis-fura-2 injected through patch electrodes, showed that the amplitude of the [Ca2+]i changes was reduced at all locations in 5-HT. The reduction of the [Ca2+]i change in the soma was confirmed in slices where cells were loaded with fura-2-AM. The reduction at the soma in 5-HT, where the spike amplitude increased, suggests that the reduction is due primarily to direct modulation of Ca2+ channels. In the dendrites, the reduction is due to a combination of this channel modulation and the lowering of the peak potential of the action potentials.

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