Osmotic effects on the CA1 neuronal population in hippocampal slices with special reference to glucose

1991 ◽  
Vol 65 (5) ◽  
pp. 1055-1066 ◽  
Author(s):  
B. A. Ballyk ◽  
S. J. Quackenbush ◽  
R. D. Andrew
Keyword(s):  
Action Potential ◽  
Single Cell ◽  
Epileptiform Activity ◽  
Hippocampal Slices ◽  
Stratum Radiatum ◽  
Resting Potential ◽  
Excitatory Postsynaptic Potential ◽  
Stratum Pyramidale ◽  
Postsynaptic Potential ◽  
Axonal Excitability

1. Lowered osmolality promotes epileptiform activity both clinically and in the hippocampal slice preparation, but it is unclear how neurons are excited. We studied the effects of altered osmolality on the electrophysiological properties of CA1 pyramidal cells in hippocampal slices by the use of field and intracellular recordings. The excitability of these neurons under various osmotic conditions was gauged by population spike (PS) amplitude, single cell properties, and evoked synaptic input. 2. The orthodromic PS recorded in stratum pyramidale and the field excitatory postsynaptic potential (EPSP) in stratum radiatum were inversely proportional in amplitude to the artificial cerebrospinal fluid (ACSF) osmolality over a range of +/- 80 milliosmoles/kgH2O (mosM). The effect was osmotic because changes occurred within the time frame expected for cellular expansion or shrinkage and because permeable substances such as dimethyl sulfoxide or glycerol were without effect. Dilutional changes in ACSF constituents were experimentally ruled out as promoting excitability. 3. To test whether the field data resulted from a change in single-cell excitability, CA1 cells were intracellularly recorded during exposure to +/- 40 mosM ACSF over 15 min. There was no consistent effect upon CA1 resting potential, cell input resistance, or action potential threshold. 4. Osmotic alteration of orthodromic and antidromic field potentials might involve a change in axonal excitability. However, the evoked afferent volley recorded in CA1 stratum pyramidale or radiatum, which represents the compound action potential (CAP) generated in presynaptic axons, remained osmotically unresponsive with regard to amplitude, duration, or latency. This was also characteristic of CAPs evoked in isolated sciatic and vagus nerve preparations exposed to +/- 80 mosM. Therefore axonal excitability and associated extracellular current flow generated periaxonally are not significantly affected by osmotic shifts. 5. The osmotic effect on field potential amplitudes appeared to be independent of synaptic transmission because the inverse relationship with osmolality held for the antidromically evoked PS. Moreover, as recorded with respect to ground, the intracellular EPSP-inhibitory postsynaptic potential (IPSP) sequence (evoked from CA3 stratum radiatum) was not altered by osmolality. 6. The PS could occasionally be recorded intracellularly as a brief negativity interrupting the evoked EPSP. In hyposmotic ACSF, the amplitude increased and action potentials arose from the trough of the negativity as expected for a field effect. This is presumably the result of enhanced intracellular channeling of current caused by the increased extracellular resistance that accompanies cellular swelling.(ABSTRACT TRUNCATED AT 400 WORDS)

CA3 neuron excitation and epileptiform discharge are sensitive to osmolality

1993 ◽  
Vol 69 (6) ◽  
pp. 2200-2208 ◽  
Author(s):  
V. Saly ◽  
R. D. Andrew
Keyword(s):  
Action Potential ◽  
Cortical Neurons ◽  
Hippocampal Slices ◽  
Clinical Signs ◽  
Field Potential ◽  
Mossy Fibers ◽  
Excitatory Postsynaptic Potential ◽  
Epsp Amplitude ◽  
Postsynaptic Potential ◽  
Ca3 Neurons

1. The clinical signs of rapidly developing overhydration commonly include generalized tonic-clonic seizure, which can be combatted by raising plasma osmolality. How cortical neurons respond to osmotic imbalance has been addressed only recently. In the CA3 cell region of hippocampal slices, lowered osmolality (-40 mOsm) rapidly swelled cells, increasing field potential amplitude over a period of 8 min and thereby elevating field effects and associated neuronal synchronization. 2. Over a longer time course (10-30 min), spontaneous excitatory postsynaptic potential (EPSP) amplitude gradually increased in 7 of 10 CA3 neurons recorded intracellularly. In nine additional CA3 cells, hyposmolality gradually induced combinations of action potential discharge, endogenous bursting, and increased synchronized synaptic input. All of these effects reversed in normosmotic ACSF. 3. Hyperosmotic artificial cerebrospinal fluid (ACSF) using mannitol reduced field potentials and dramatically lowered CA3 excitability by reducing spontaneous EPSP amplitude and associated bursting. Again, the gradual onset (10-30 min) of changes in spontaneous EPSP amplitude appeared independent of field potential changes, which were already maximal by 8 min. 4. Cutting mossy fibers did not affect the excitability changes induced by osmotic stress noted above. The EPSP/inhibitory postsynaptic potential (IPSP) sequence evoked from mossy fibers or stratum oriens was unaltered by osmotic change and so did not represent osmosensitive afferent input to CA3 neurons. Furthermore, as measured at the soma, resting membrane potential, cell input resistance, and the action potential threshold were unchanged in all cells. It followed that, because the CA3 neurons themselves were not responsive, a recurrent excitatory pathway could not represent the osmosensitive input.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in [K+]o evoked by baclofen in guinea pig hippocampus

1998 ◽  
Vol 76 (2) ◽  
pp. 148-154 ◽  
Author(s):  
G V Obrocea ◽  
Mary E Morris
Keyword(s):  
Guinea Pig ◽  
Epileptiform Activity ◽  
Hippocampal Slices ◽  
Brain Slices ◽  
Field Potential ◽  
Stratum Radiatum ◽  
Extracellular Potassium ◽  
Receptor Subtype ◽  
Field Potentials ◽  
Stratum Pyramidale

K+-sensitive microelectrodes were used to record changes evoked by baclofen in extracellular potassium concentration ([K+]o) and field potentials in the stratum pyramidale (SP) and stratum radiatum (SR) in the CA1b region of guinea pig hippocampal slices in vitro. Bath applications of ( ±)-baclofen (1 µM - 3 mM for approx 5 min) evoked changes in [K+]o, which were in most cases sustained throughout agonist application and reversed during washout. The maximal (Rmax) values for curves fitted to the concentration-response data were for SP and SR, respectively, 0.59 ± 0.03 and 0.65 ± 0.03 mM, and EC50 values were 39.7 and 39.4 µM, respectively. The evoked K+ and field potential changes were significantly correlated and could be blocked by 2-OH-saclofen (50 µM) and CGP 35348 (50 µM). In <= 10% of experiments baclofen (10-50 µM) induced either a decrease or a transient increase ( <= 1 min duration) in [K+]o; in some slices with concentrations >=20 µM an initial decrease preceded a progressive increase. Pressure ejection of baclofen (100 µM for 100-900 ms) evoked increases in [K+]o and field potentials, which were larger in SR than in SP. In <= 10% of slices brief and (or) sustained application of baclofen (by either bath perfusion or pressure ejection) also evoked synchronous, repetitive interictal and ictal discharges at frequencies approx 1/s and 1/12 s, respectively, an observation that affirms a proconvulsant capacity. It is concluded that (i) although increases in [K+]o evoked by baclofen in SR compared with SP are slightly larger, they are not significantly different, (ii) GABAB receptor subtype(s) in SR and SP appear similar, as they have identical affinities, and (iii) [K+]o accumulations evoked by GABA likely include a contribution from a GABAB receptor activated K+ conductance, especially in dendritic regions.Key words: brain slices, stratum pyramidale, stratum radiatum, GABAB receptors, ion-selective microelectrodes, epileptiform activity.

Comparison of changes evoked by GABA (γ-aminobutyric acid) and anoxia in [K+]o, [Cl-]o, and [Na+]o in stratum pyramidale and stratum radiatum of the guinea pig hippocampus

2000 ◽  
Vol 78 (5) ◽  
pp. 378-391 ◽  
Author(s):  
G V Obrocea ◽  
M E Morris
Keyword(s):  
Guinea Pig ◽  
Extracellular Space ◽  
Hippocampal Slices ◽  
Brain Slices ◽  
Receptor Activation ◽  
Ion Concentration ◽  
Aminobutyric Acid ◽  
Stratum Radiatum ◽  
Bicuculline Methiodide ◽  
Stratum Pyramidale

Ion-selective microelectrode recordings were made to assess a possible contribution of extracellular γ-aminobutyric acid (GABA) accumulation to early responses evoked in the brain by anoxia and ischemia. Changes evoked by GABA or N2 in [K+]o, [Cl-]o, [Na+]o, and [TMA+]o were recorded in the cell body and dendritic regions of the stratum pyramidale (SP) and stratum radiatum (SR), respectively, of pyramidal neurons in CA1 of guinea pig hippocampal slices. Bath application of GABA (1-10 mM) for approximately 5 min evoked changes in [K+]o and [Cl-]o with respective EC50 levels of 3.8 and 4.1 mM in SP, and 4.7 and 5.6 mM in SR. In SP 5 mM GABA reversibly increased [K+]o and [Cl-]o and decreased [Na+]o; replacement of 95% O2 -5% CO2 by 95% N2 -5% CO2 for a similar period of time evoked changes which were for each ion in the same direction as those with GABA. In SR both GABA and N2 caused increases in [K+]o and decreases in [Cl-]o and [Na+]o. The reduction of extracellular space, estimated from levels of [TMA+]o during exposures to GABA and N2, was 5-6% and insufficient to cause the observed changes in ion concentration. Ion changes induced by GABA and N2 were reversibly attenuated by the GABAA receptor antagonist bicuculline methiodide (BMI, 100 µM). GABA-evoked changes in [K+]o in SP and SR and [Cl-]o in SP were depressed by >=90%, and of [Cl-]o in SR by 50%; N2-evoked changes in [K+]o in SP and SR were decreased by 70% and those of [Cl-]o by 50%. BMI blocked Δ [Na+]o with both GABA and N2 by 20-30%. It is concluded that during early anoxia: (i) accumulation of GABA and activation of GABAA receptors may contribute to the ion changes and play a significant role, and (ii) responses in the dendritic (SR) regions are greater than and (or) differ from those in the somal (SP) layers. A large component of the [K+]o increase may involve a GABA-evoked Ca2+-activated gk, secondary to [Ca2+]i increase. A major part of [Cl-]o changes may arise from GABA-induced gCl and glial efflux, with strong stimulation of active outward transport and anion exchange at SP, and inward Na+/K+/2Cl- co-transport at SR. Na+ influx is attributable mainly to Na+-dependent transmitter uptake, with only a small amount related to GABAA receptor activation. Although the release and (or) accumulation of GABA during anoxia might be viewed as potentially protectant, the ultimate role may more likely be an important contribution to toxicity and delayed neuronal death. Key words: brain slices, ion-selective microelectrodes, stratum pyramidale, stratum radiatum, bicuculline methiodide, extracellular space shrinkage.

Nonsynaptic epileptogenesis in the mammalian hippocampus in vitro. I. Development of seizurelike activity in low extracellular calcium

1986 ◽  
Vol 56 (2) ◽  
pp. 409-423 ◽  
Author(s):  
A. Konnerth ◽  
U. Heinemann ◽  
Y. Yaari
Keyword(s):  
Epileptiform Activity ◽  
Large Population ◽  
Hippocampal Slices ◽  
Field Potential ◽  
Pyramidal Cells ◽  
Discharge Zone ◽  
Critical Threshold ◽  
Mean Velocity ◽  
Stratum Pyramidale ◽  
Ca1 Area

Epileptiform activity induced in rat hippocampal slices by lowering extracellular Ca2+ concentration ([Ca2+]o) was studied with extracellular and intracellular recordings. Perfusing the slices with low Ca2+ (less than or equal to 0.2 mM) or EGTA-containing solutions blocked the synaptic responses of hippocampal pyramidal cells (HPCs). Despite the block, spontaneous paroxysms, termed seizurelike events (SLEs), appeared in the CA1 area and then recurred regularly at a stable frequency. Transient hypoxia accelerated their development and increased their frequency. When [Ca2+]o was raised in a stepwise manner, the SLEs disappeared at 0.3 mM. With extracellular recording from the CA1 stratum pyramidale, a SLE was characterized by a large negative shift in the field potential, which lasted for several seconds. During this period a large population of CA1 neurons discharged intensely and often in synchrony, as concluded from the frequent appearance of population spikes. Synchronization, however, was not a necessary precursor for the development of paroxysmal activity, but seemed to be the end result of massive neuronal excitation. The cellular counterpart of a SLE, as revealed by intracellular recording from HPCs in the discharge zone of the paroxysms, was a long-lasting depolarization shift (LDS) of up to 20 mV. This was accompanied by accelerated firing of the neuron. A prolonged after-hyperpolarization succeeded each LDS and arrested cell firing. Brief (approximately 50 ms) bursts were commonly observed before LDS onset. Single electrical stimuli applied focally to the stratum pyramidale or alveus evoked paroxysms identical to the spontaneous SLEs, provided they surpassed a critical threshold intensity. Subthreshold stimuli elicited only small local responses, whereas stimuli of varied suprathreshold intensities evoked the same maximal SLEs. Thus the buildup of a SLE is an all or nothing or a regenerative process, which mobilizes the majority, if not all, of the local neuronal population. Each SLE was followed by absolute and relative refractory periods during which focal stimulation was, respectively, ineffective and less effective in evoking a maximal SLE. In most slices the spontaneous SLEs commenced at a "focus" located in the CA1a subarea (near the subiculum). SLEs evoked by focal stimulation arose near the stimulating electrode. From their site of origin the paroxysmal discharges spread transversely through the entire CA1 area at a mean velocity of 1.74 mm/s. Consequently, the discharge zone of a SLE could encompass for several seconds the entire CA1 area.(ABSTRACT TRUNCATED AT 400 WORDS)

Persistent hyperexcitability in isolated hippocampal CA1 of kainate-lesioned rats

1992 ◽  
Vol 68 (6) ◽  
pp. 2120-2127 ◽  
Author(s):  
C. L. Meier ◽  
A. Obenaus ◽  
F. E. Dudek
Keyword(s):  
Pyramidal Neurons ◽  
Hippocampal Sclerosis ◽  
Mean Amplitude ◽  
Cell Loss ◽  
Stratum Radiatum ◽  
Excitatory Postsynaptic Potential ◽  
Population Spikes ◽  
Acute Seizures ◽  
Postsynaptic Potential ◽  
Area Ca1

1. Subcutaneous kainate injection in rats evoked acute seizures and led to cell loss in the hilus and areas CA1 and CA3, which resembled the pattern of hippocampal sclerosis often associated with temporal lobe epilepsy in humans. 2. Simultaneous intra- and extracellular recordings were performed in the stratum pyramidale of area CA1 while stimulating in the stratum radiatum close to the recording electrodes. Responses from control slices consisted of a brief excitatory postsynaptic potential (EPSP) with only one action potential, corresponding to a single extracellular population spike, followed by a clear biphasic inhibitory postsynaptic potential (IPSP). In slices from kainate-treated animals, however, stimulation evoked a prolonged EPSP, which often triggered multiple action potentials corresponding to multiple extracellular population spikes. 3. In slices from kainate-treated animals, the mean amplitude but not the duration of the stimulation-evoked IPSP was reduced. The extent of the kainate-induced loss of inhibition in area CA1 was highly variable. 4. Low concentrations of bicuculline in control slices led to a moderate hyperexcitability, which consisted of multiple population spikes and mirrored the responses observed in slices from kainate-treated animals in normal ACSF. Prolonged application of 10-30 microM bicuculline for > or = 30 min led to a much higher level of hyperexcitability, which was similar in slices from controls and kainate-treated rats. These findings are consistent with the hypothesis that the hyperexcitability of CA1 pyramidal neurons following kainate treatment is mainly due to decreased GABAA-receptor-mediated inhibition and that the loss of inhibition is only partial.(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanisms of Neuronal Hyperexcitability Caused by Partial Inhibition of Na+-K+-ATPases in the Rat CA1 Hippocampal Region

2002 ◽  
Vol 88 (6) ◽  
pp. 2963-2978 ◽  
Author(s):  
Cyrille Vaillend ◽  
Susanne E. Mason ◽  
Matthew F. Cuttle ◽  
Bradley E. Alger
Keyword(s):  
Hippocampal Slices ◽  
Pyramidal Cells ◽  
Burst Firing ◽  
Membrane Properties ◽  
Initial Slope ◽  
Excitatory Postsynaptic Potential ◽  
Neuronal Hyperexcitability ◽  
Partial Inhibition ◽  
Postsynaptic Potential ◽  
Bursting Activity

Extra- and intracellular records were made from rat acute hippocampal slices to examine the effects of partial inhibition of Na+-K+-ATPases (Na+-K+pumps) on neuronal hyperexcitability. Bath application of the low-affinity cardiac glycoside, dihydroouabain (DHO), reversibly induced interictal-like epileptiform bursting activity in the CA1 region. Burst-firing was correlated with inhibition of the pumps, which was assayed by changes in [K+]ouptake rates measured with K+-ion-sensitive microelectrodes. Large increases in resting [K+]odid not occur. DHO induced a transient depolarization (5–6 mV) followed by a long-lasting hyperpolarization (∼6 mV) in CA1 pyramidal neurons, which was accompanied by a 30% decrease in resting input resistance. Block of an electrogenic pump current could explain the depolarization but not the hyperpolarization of the membrane. Increasing [K+]ofrom 3 to 5.5 mM minimized these transient shifts in passive membrane properties without preventing DHO-induced hyperexcitability. DHO decreased synaptic transmission, but increased the coupling between excitatory postsynaptic potentials and spike firing (E-S coupling). Monosynaptic inhibitory postsynaptic potential (IPSP) amplitudes declined to ∼25% of control at the peak of bursting activity; however, miniature TTX-resistant inhibitory postsynaptic current amplitudes were unaffected. DHO also reduced the initial slope of the intracellular excitatory postsynaptic potential (EPSP) to ∼40% of control. The conductances of pharmacologically isolated IPSPs and EPSPs in high-Ca/high-Mg-containing saline were also reduced by DHO by ∼50%. The extracellular fiber volley amplitude was reduced by 15–20%, suggesting that the decrease in neurotransmission was partly due to a reduction in presynaptic fiber excitability. DHO enhanced a late depolarizing potential that was superimposed on the EPSP and could obscure it. This potential was not blocked by antagonists of NMDA receptors, and blockade of NMDA, mGlu, or GABAAreceptors did not affect burst firing. The late depolarizing component enabled the pyramidal cells to reach spike threshold without changing the actual voltage threshold for firing. We conclude that reduced GABAergic potentials and enhanced E-S coupling are the primary mechanisms underlying the hyperexcitability associated with impaired Na+-K+pump activity.

Extracellular Magnesium Ion Modifies the Actions of Volatile Anesthetics in Area CA1 of Rat Hippocampus In Vitro 

2002 ◽  
Vol 96 (3) ◽  
pp. 681-687 ◽  
Author(s):  
Rika Sasaki ◽  
Koki Hirota ◽  
Sheldon H. Roth ◽  
Mitsuaki Yamazaki
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Hippocampal Slices ◽  
Volatile Anesthetics ◽  
Population Spike ◽  
Magnesium Ion ◽  
Excitatory Postsynaptic Potential ◽  
Aspartate Receptor ◽  
Postsynaptic Potential

Background Magnesium ion (Mg2+) is involved in important processes as modulation of ion channels, receptors, neurotransmitter release, and cell excitability in the central nervous system. Although extracellular Mg2+ concentration ([Mg2+]o) can be altered during general anesthesia, there has been no evidence for [Mg2+]o-dependent modification of anesthetic actions on neural excitability in central nervous system preparations. The purpose of current study was to determine whether the effects of volatile anesthetics are [Mg2+]o-dependent in mammalian central nervous system. Methods Extracellular electrophysiologic recordings from CA1 neurons in rat hippocampal slices were used to investigate the effects of [Mg2+]o and anesthetics on population spike amplitude and excitatory postsynaptic potential slope. Results The depression of population spike amplitudes and excitatory postsynaptic potential slopes by volatile anesthetics were significantly dependent on [Mg2+]o. The effects were attenuated in the presence of a constant [Mg2+]o/extracellular Ca2+ concentration ratio. However, neither N-methyl-d-aspartate receptor antagonists nor a non-N-methyl-d-aspartate receptor antagonist altered the [Mg2+]o-dependent anesthetic-induced depression of population spikes. Volatile anesthetics produced minimal effects on input-output (excitatory postsynaptic potential-population spike) relations or the threshold for population spike generation. The effects were not modified by changes in [Mg2+]o. In addition, the population spike amplitudes, elicited via antidromic (nonsynaptic) stimulation, were not influenced by [Mg2+]o in the presence of volatile anesthetics. Conclusions These results provide support that alteration of [Mg2+]o modifies the actions of volatile anesthetics on synaptic transmission and that the effects could be, at least in part, a result of presynaptic Ca2+ channel-related mechanisms.

Role of norepinephrine in seizurelike activity of hippocampal pyramidal cells maintained in vitro: alteration by 6-hydroxydopamine lesions of norepinephrine-containing systems

1983 ◽  
Vol 61 (8) ◽  
pp. 841-846 ◽  
Author(s):  
I. Mody ◽  
P. Leung ◽  
J. J. Miller
Keyword(s):  
Epileptiform Activity ◽  
Pyramidal Cells ◽  
Population Spike ◽  
Stratum Radiatum ◽  
Excitatory Postsynaptic Potential ◽  
Ca1 Pyramidal Cells ◽  
Ca1 Region ◽  
Population Spike Amplitude ◽  
6 Hydroxydopamine

Perfusion of 50 μM norepinephrine (NE) produced a marked, reversible decrease (range 20–28%) of the extracellular population spike and excitatory postsynaptic potential (EPSP) responses of the CA1 region evoked by stratum radiatum stimulation in the rat hippocampal slice preparation. The effects of NE were dramatically altered in slices obtained from animals which were previously treated with intracerebral or intraventricular injections of 6-hydroxydopamine (6-OHDA) to destroy forebrain catecholamine systems. In the latter preparations NE produced a reduction in the inhibition of the EPSP (50%), enhancement of the population spike amplitude, and multiple spike discharges characteristic of ongoing epileptiform activity. The reversal of NE-induced inhibition and the generation of seizurelike activity in 6-OHDA-treated animals suggests that NE may, in part, act upon interneurons to produce a disinhibition of CA1 pyramidal cells.

Mechanisms of depolarizing inhibition at the crayfish giant motor synapse. II. Quantitative reconstruction

1990 ◽  
Vol 64 (2) ◽  
pp. 541-550 ◽  
Author(s):  
D. H. Edwards
Keyword(s):  
Potassium Current ◽  
Sodium Current ◽  
Outward Current ◽  
Resting Potential ◽  
Excitatory Postsynaptic Potential ◽  
Inhibitory Effects ◽  
Inward Current ◽  
Postsynaptic Potential ◽  
Parameter Values ◽  
Outward Potassium Current

1. The relative strengths of four mechanisms of depolarizing synaptic inhibition described in the previous paper were evaluated with an electrical model of the giant motor synapse (GMS) and postsynaptic region of the motor giant motoneuron (MoG). 2. The model consists of one compartment that represents the presynaptic region of the medial giant (MG) interneuron and three compartments that represent the postsynaptic region and proximal axon of the MoG. The presynaptic MG compartment is linked to a postsynaptic MoG compartment by a rectifying conductance that represents the GMS. Each compartment consists of parallel paths to ground for active and/or passive membrane currents. 3. Parameter values of the model were set so the MG compartment would replicate an MG impulse and the MoG compartments would replicate the current-clamp, voltage-clamp, and synaptic responses of a single MoG neuron described in the previous paper. The Hodgkin-Huxley equations described voltage-sensitive sodium and potassium currents. 4. Comparison of the MoG compartment currents that mediate an inhibited excitatory postsynaptic potential (EPSP) [triggered during a depolarizing inhibitory postsynaptic potential (d-IPSP)] with those of an uninhibited EPSP indicate that all four mechanisms have significant inhibitory effects. Reverse bias of the GMS by the d-IPSP reduced the GMS current by 65 nA (12%). The remaining inward current was further reduced by a 243-nA outward current through the inhibitory postsynaptic conductance. The d-IPSP inactivated sodium conductance so the inward sodium current evoked by the EPSP was reduced by 319 nA (-68%). The d-IPSP reduced the latency for potassium activation by the EPSP so that the outward potassium current coincided with the inward sodium current and reduced the net inward current by 100 nA. Together, these mechanisms reduced the EPSP amplitude by 69%. 5. The resting potential of MoG is normally 15 mV more positive than MG rest potential, but in some preparations this difference may be as much as 25 mV or as little as 0 mV. Corresponding differences in the rest potentials of the MoG and MG models have little effect on the amplitude of the model MoG EPSP because changes in the inward synaptic and sodium currents are balanced by corresponding changes in the outward potassium current.

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