Effect of Subthreshold Up and Down States on the Whisker-Evoked Response in Somatosensory Cortex

2004 ◽  
Vol 92 (6) ◽  
pp. 3511-3521 ◽  
Author(s):  
Robert N. S. Sachdev ◽  
Ford F. Ebner ◽  
Charles J. Wilson
Keyword(s):  
Membrane Potential ◽  
Cortical Neurons ◽  
Action Potentials ◽  
Reversal Potential ◽  
State Dependence ◽  
The State ◽  
Sensory Stimuli ◽  
Whisker Stimulation ◽  
Reversal Potentials ◽  
Stimulation Of

Changes in spontaneous activity within the cortex recognized by subthreshold fluctuations of the membrane potential of cortical neurons modified the response of cortical neurons to sensory stimuli. Sensory stimuli occurring in the hyperpolarized “down” state evoked a larger depolarization and were more effective in evoking action potentials than stimuli occurring in the depolarized “up” state. Direct electrical stimulation of the thalamus showed the same dependence on the cell's state at the time of the stimulus, ruling out a strictly thalamic mechanism. Stimuli were more effective at triggering action potentials in the down state even during moderate de- or hyperpolarization of the somatic membrane potential. The postsynaptic potential (PSP) evoked from the down state was larger than the up state PSP but achieved about the same peak membrane potential, which was also near the reversal potential of the PSP (about –51 mV). Chloride loading shifted the reversal potentials of both the up state and the whisker-evoked PSP toward a more depolarized membrane potential. In addition, the threshold for action potentials evoked from the down state was lower than for spikes evoked in the up state. Thus the larger PSP from the down state may be caused by its larger driving force, and the state dependence of action potential generation in response to whisker stimulation may in part be related to a shift in threshold. Different mechanisms are therefore responsible for the state-dependence of PSP amplitude and the spike frequency response to the whisker stimulus.

scholarly journals Cortical Neurons Lacking KCC2 Expression Show Impaired Regulation of Intracellular Chloride

2005 ◽  
Vol 93 (3) ◽  
pp. 1557-1568 ◽  
Author(s):  
Lei Zhu ◽  
David Lovinger ◽  
Eric Delpire
Keyword(s):  
Plasma Membrane ◽  
Membrane Potential ◽  
Strong Evidence ◽  
Cortical Neurons ◽  
Action Potentials ◽  
Reversal Potential ◽  
Excitable Cells ◽  
Low Concentrations ◽  
Pump Activity

As excitable cells, neurons experience constant changes in their membrane potential due to ion flux through plasma membrane channels. They maintain their transmembrane cation concentrations through robust Na+/K+-ATPase pump activity. During synaptic transmission and spread of action potentials, the concentration of the major anion, Cl−, is also under constant challenge from membrane potential changes. Moreover, intracellular Cl− is also affected by ligand-gated Cl− channels such as GABAA and glycine receptors. To regulate intracellular Cl− in an electrically silent manner, neurons couple the movement of Cl− with K+. In this study, we have used gene-targeted KCC2−/− mice to provide strong evidence that KCC2, the neuronal-specific K-Cl co-transporter, drives neuronal Cl− to low concentrations, shifting the GABA reversal potential toward more negative potentials, thus promoting hyperpolarizing GABA responses. Cortical neurons lacking KCC2, not only fail to show a developmental decrease in [Cl−]i, but also are unable to regulate [Cl−]i on Cl− loading or maintain [Cl]i during membrane depolarization. These data are consistent with the central role of KCC2 in promoting inhibition and preventing hyperexcitability.

The generation of electric currents in cardiac fibers by Na/Ca exchange

1979 ◽  
Vol 236 (3) ◽  
pp. C103-C110 ◽  
Author(s):  
L. J. Mullins
Keyword(s):  
Membrane Potential ◽  
Duty Cycle ◽  
Action Potentials ◽  
Reversal Potential ◽  
Resting Membrane Potential ◽  
Electrochemical Gradient ◽  
Ca Current ◽  
Cardiac Action ◽  
Cardiac Fiber ◽  
Cardiac Fibers

The presence of a detectable Ca current during the excitation of a cardiac fiber implies that the Ca lost during the resting interval of the duty cycle must also be detectable. Ca outward movement appears to be effected by Na/Ca exchange when more Na enters than Ca leaves per cycle, thus making the mechanism electrogenic. Since Na/Ca exchange can move Ca either inward or outward depending on the direction of the electrochemical gradient for Na, a potential exists where there is no electric current generated by the Na/Ca exchange mechanism, i.e., a reversal potential ER. Cardiac fibers appear to have a reversal potential that is about midway between their resting membrane potential and their plateau. Carrier currents both inward and outward are therefore generated during cardiac action potentials. The implications of the conditions stated above are explored.

Responsiveness to D-glucose in neurosecretory cells of crustaceans

1993 ◽  
Vol 70 (2) ◽  
pp. 758-764 ◽  
Author(s):  
E. Garcia ◽  
A. Benitez ◽  
C. G. Onetti
Keyword(s):  
Membrane Potential ◽  
Action Potentials ◽  
Electrophysiological Study ◽  
Reversal Potential ◽  
Neurosecretory Cells ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Long Time ◽  
Glucose Sensitivity ◽  
Discharge Patterns

1. An electrophysiological study of the D-glucose sensitivity of X-organ (XO) neurosecretory cell bodies in crayfish was carried out with the use of microelectrodes, perforated, and cell-attached patch-clamp techniques. 2. Glucose depolarizes the membrane potential of XO cells in a concentration-dependent manner. 3. Depolarization produced by glucose initiates a change in the pattern of electrical activity. Silent cells began to discharge action potentials. When bursting cells are depolarized by glucose, their action potentials are no longer grouped in bursts or disappear entirely. 4. Although the membrane potential returns to its initial value after removing glucose from the bath, discharge patterns of the cells may remain different. This suggests that besides the depolarizing effect, once the cells have been exposed to glucose, the sugar switches on a process that is maintained for a long time. 5. Glucose produced a reduction of membrane steady-state conductance, and a shift of reversal potential of membrane currents to a more positive value. 6. Depolarization induced by D-glucose appears to be related with a closure of potassium channels. 7. Glucose effect was thought to be generated by a product of metabolism that would act as intracellular mediator.

Membrane Properties Underlying Patterns of GABA-Dependent Action Potentials in Developing Mouse Hypothalamic Neurons

2001 ◽  
Vol 86 (3) ◽  
pp. 1252-1265 ◽  
Author(s):  
Yu-Feng Wang ◽  
Xiao-Bing Gao ◽  
Anthony N. van den Pol
Keyword(s):  
Membrane Potential ◽  
Action Potentials ◽  
Brain Slices ◽  
Reversal Potential ◽  
Membrane Properties ◽  
Resting Membrane Potential ◽  
Hypothalamic Neurons ◽  
Spike Threshold ◽  
Spike Patterns

Spikes may play an important role in modulating a number of aspects of brain development. In early hypothalamic development, GABA can either evoke action potentials, or it can shunt other excitatory activity. In both slices and cultures of the mouse hypothalamus, we observed a heterogeneity of spike patterns and frequency in response to GABA. To examine the mechanisms underlying patterns and frequency of GABA-evoked spikes, we used conventional whole cell and gramicidin perforation recordings of neurons ( n = 282) in slices and cultures of developing mouse hypothalamus. Recorded with gramicidin pipettes, GABA application evoked action potentials in hypothalamic neurons in brain slices of postnatal day 2–9( P2- 9) mice. With conventional patch pipettes (containing 29 mM Cl−), action potentials were also elicited by GABA from neurons of 2–13 days in vitro (2–13 DIV) embryonic hypothalamic cultures. Depolarizing responses to GABA could be generally classified into three types: depolarization with no spike, a single spike, or complex patterns of multiple spikes. In parallel experiments in slices, electrical stimulation of GABAergic mediobasal hypothalamic neurons in the presence of glutamate receptor antagonists [10 μM 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), 100 μM 2-amino-5-phosphonopentanoic acid (AP5)] resulted in the occurrence of spikes that were blocked by bicuculline (20 μM). Blocking ionotropic glutamate receptors with AP5 and CNQX did not block GABA-mediated multiple spikes. Similarly, when synaptic transmission was blocked with Cd2+ (200 μM) and Ni2+(300 μM), GABA still induced multiple spikes, suggesting that the multiple spikes can be an intrinsic membrane property of GABA excitation and were not based on local interneurons. When the pipette [Cl−] was 29 or 45 mM, GABA evoked multiple spikes. In contrast, spikes were not detected with 2 or 10 mM intracellular [Cl−]. With gramicidin pipettes, we found that the mean reversal potential of GABA-evoked current ( E GABA) was positive to the resting membrane potential, suggesting a high intracellular [Cl−] in developing mouse neurons. Varying the holding potential from −80 to 0 mV revealed an inverted U-shaped effect on spike probability. Blocking voltage-dependent Na+ channels with tetrodotoxin eliminated GABA-evoked spikes, but not the GABA-evoked depolarization. Removing Ca2+ from the extracellular solution did not block spikes, indicating GABA-evoked Na+-based spikes. Although E GABA was more positive within 2–5 days in culture, the probability of GABA-evoked spikes was greater in 6- to 9-day cells. Mechanistically, this appears to be due to a greater Na+ current found in the older cells during a period when the E GABA is still positive to the resting membrane potential. GABA evoked similar spike patterns in HEPES and bicarbonate buffers, suggesting that Cl−, not bicarbonate, was primarily responsible for generatingmultiple spikes. GABA evoked either single or multiple spikes; neurons with multiple spikes had a greater Na+ current, a lower conductance, a more negative spike threshold, and a greater difference between the peak of depolarization and the spike threshold. Taken together, the present results indicate that the patterns of multiple action potentials evoked by GABA are an inherent property of the developing hypothalamic neuron.

Membrane properties and synaptic responses of the guinea pig nucleus accumbens neurons in vitro

1989 ◽  
Vol 61 (4) ◽  
pp. 769-779 ◽  
Author(s):  
N. Uchimura ◽  
H. Higashi ◽  
S. Nishi
Keyword(s):  
Membrane Potential ◽  
Nucleus Accumbens ◽  
Guinea Pig ◽  
Action Potential ◽  
Action Potentials ◽  
Reversal Potential ◽  
Membrane Properties ◽  
Current Pulses ◽  
Synaptic Responses

1. The membrane properties and synaptic responses of guinea pig nucleus accumbens neurons in vitro were studied with intracellular recording methods. 2. The population of neurons could be divided into groups of low (20-60 M omega, average 46.5 M omega) and high (60-180 M omega, average 96.5 M omega) input resistance. The resting membrane potential in both groups was approximately -70 mV. 3. Other membrane properties were quite similar in both groups. Inward rectification occurred at potentials more negative than -80 mV; this was blocked by Cs+ (2 mM). Membrane potential oscillations were observed at potentials between -65 and -55 mV; these were blocked by tetrodotoxin (TTX, 0.5 microM). Outward rectification occurred at potentials less negative than -45 mV; this was depressed by tetraethylammonium (TEA, 10 mM). 4. Action potentials elicited by small depolarizing current pulses (2-5 ms, 0.3-0.5 nA) were approximately 95 mV in amplitude and 1.0 ms in duration. The afterhyperpolarization following each action potential was less than 30 ms in duration, and no accommodation of action-potential discharge was seen at frequencies up to 40 Hz. The action potentials were reversibly blocked by TTX (0.3 microM). In addition, TTX-insensitive, Ca2+-dependent spikes were evoked by passing larger and more prolonged current pulses (greater than 40 ms, greater than 0.5 nA) across the membrane. 5. Focal electrical stimulation of the slice surface with low intensity (1 ms, less than 10 V) elicited excitatory postsynaptic potentials (EPSPs) in neurons of both high- and low-resistance groups. The reversal potential (+10.2 mV) for the EPSPs was close to the reversal potential (+7.7 mV) of the responses to glutamate applied in the superfusing solution. The N-methyl-D-aspartic acid (NMDA) receptor antagonists, D-alpha-aminoadipic acid (1 mM) and DL-2-amino-5-phosphonovaleric acid (DL-APV, 250 microM), reversibly depressed the EPSP; the glutamate uptake inhibitor, L-aspartic acid-beta-hydroxamate (50 microM), or removal of Mg2+ from the superfusate, augmented the EPSP. 6. When the intensity of the focal stimulus was increased (1 ms, greater than or equal to 10 V), a second larger depolarizing response (duration, 800 ms to 2 s) could be evoked in addition to the smoothly graded EPSP. This was seen only in cells of the high-resistance group (90-130 M omega).(ABSTRACT TRUNCATED AT 400 WORDS)

Monitoring the excitability of neocortical efferent neurons to direct activation by extracellular current pulses

1992 ◽  
Vol 68 (2) ◽  
pp. 605-619 ◽  
Author(s):  
H. A. Swadlow
Keyword(s):  
Cortical Neurons ◽  
Action Potentials ◽  
Short Latency ◽  
Gamma Aminobutyric Acid ◽  
Afferent Pathways ◽  
Synaptic Inputs ◽  
Direct Activation ◽  
Current Pulses ◽  
Efferent Neurons ◽  
Stimulation Of

1. Extracellular action potentials were recorded from antidromically activated efferent neurons in visual, somatosensory, and motor cortex of the awake rabbit using low-impedance metal microelectrodes. Efferent neurons were also activated by current pulses delivered near the soma [juxtasomal current pulses (JSCPs)] through the recording microelectrode. Action potentials generated by JSCPs were not directly observed (because of the stimulus artifact), but were inferred with the use of a collision paradigm. Efferent populations studied include callosal neurons [CC (n = 80)], ipsilateral corticocortical neurons [C-IC (n = 21)], corticothalamic neurons of layer 6 [CF-6 (n = 57)], and descending corticofugal neurons of layer 5 [CF-5, corticotectal neurons of the visual cortex (n = 48)]. 2. Most CC neurons (45/46) and all C-IC (8/8) and CF-6 neurons (39/39) were directly activated by JSCPs at near-threshold intensities. Some CF-5 neurons (9/38), however, showed evidence of indirect activation. All efferent classes had similar current thresholds (means 1.85-2.10 microA) to direct activation by JSCPs, and thresholds were inversely related to extracellular spike amplitude. For each neuron, the range of JSCP intensities that generated response probabilities of between 0.2 and 0.8 was measured, and this "range of uncertainty" was significantly greater in CF-5 neurons (mean 32.7% of threshold) than in CC (mean 19.0%) or CF-6 (mean 20.4%) neurons. 3. Several factors indicate that the threshold of efferent neurons to JSCPs is very sensitive to excitatory and inhibitory synaptic inputs. Iontophoretic applications of gamma-aminobutyric acid (GABA) increased the threshold to JSCPs, and glutamate reduced the threshold. Electrical stimulation of afferent pathways at intensities just below threshold for eliciting action potentials resulted in a dramatic decrease in JSCP threshold. This initial short-latency threshold decrease was specific to stimulation of particular afferent pathways and is thought to reflect excitability changes associated with EPSPs. Examination of such subliminal responses revealed subthreshold synaptic inputs that were not revealed by examination of all-or-none action potentials. In contrast to the specificity of the short-latency threshold decrease, a long-lasting increase in JSCP threshold was seen in virtually all neurons after stimulation of each of the afferent pathways tested. This increase in threshold usually began 20-40 ms after stimulation, lasted for 100-200 ms, and is thought to reflect excitability changes associated with a long-lasting inhibitory postsynaptic potential (IPSP) seen in many cortical neurons. 4. Many neurons in primary somatosensory cortex of rat, cat, and rabbit have no demonstrable receptive fields.(ABSTRACT TRUNCATED AT 400 WORDS)

Mechanism of long-lasting synaptic inhibition in Aplysia neuron R15

1980 ◽  
Vol 44 (6) ◽  
pp. 1148-1160 ◽  
Author(s):  
W. B. Adams ◽  
I. Parnas ◽  
I. B. Levitan
Keyword(s):  
Action Potentials ◽  
Potassium Conductance ◽  
Reversal Potential ◽  
Short Exposure ◽  
Ion Conductance ◽  
Current Voltage ◽  
Voltage Dependent ◽  
Aplysia Neuron ◽  
Reversible Component ◽  
Stimulation Of

1. Long-lasting inhibition is a synaptically mediated response found in certain molluscan nerve cells that fire action potentials in bursts. It is elicited by repetitive stimulation of a presynaptic nerve and may last for minutes or hours after stimulation. 2. Voltage-clamp techniques were employed to measure the voltage dependence of the synaptically elicited current. Current-voltage curves were obtained by stepping or sweeping the voltage over the range -40 to -120 mV. 3. Long-lasting inhibition was found to be mediated by two separate conductance mechanisms. A component that reverses near -80 mV is most prominent at times up to 5 min following stimulation. A component with no reversal potential between -40 and -120 mV predominates at later times. 4. The reversible component is attenuated by reducing the intensity of stimulation of the presynaptic nerve, by injection of TEA into the postsynaptic cell, or by activation of a potassium conductance with serotonin prior to stimulation of the nerve. Thus, the reversible component appears to be mediated by an increase in potassium conductance. 5. The effects of the nonreversible component measured in the soma appear to be too large to attribute it to a conductance change that is electrically "distant" from the soma. It is attenuated by turning off a resting inward ion conductance with dopamine prior to stimulation of the nerve. It is not affected by short exposure to ouabain, but is attenuated by longer exposures that reduce the sodium and calcium gradients. Thus, the nonreversible component may be mediated by a decrease in voltage-dependent inward current flow carried by sodium or calcium.

COMPARISON BETWEEN THERMORECEPTOR AND MECHANORECEPTOR CURRENTS IN PARAMECIUM CAUDATUM

1994 ◽  
Vol 189 (1) ◽  
pp. 117-131 ◽  
Author(s):  
T Tominaga ◽  
Y Naitoh
Keyword(s):  
Membrane Potential ◽  
Reversal Potential ◽  
Mechanical Stimulus ◽  
Membrane Current ◽  
Resting Potential ◽  
Sign Reversal ◽  
Positive Direction ◽  
Algebraic Summation ◽  
Stimulation Of ◽  
External K

1. A voltage-clamped Paramecium produced an inward membrane current upon thermal or mechanical stimulation of its anterior region, whereas it produced an outward membrane current upon similar stimulation of its posterior region. 2. Anterior thermo- and mechanoreceptor currents decreased when the membrane potential was shifted in a positive direction, showing sign reversal at a positive membrane potential, whereas posterior thermo- and mechanoreceptor currents decreased when the membrane potential was shifted in a negative direction, showing sign reversal at a membrane potential more negative than the resting potential. 3. The reversal potential for both anterior receptor currents shifted in a positive direction when external [Ca2+] was increased, whereas those for both posterior receptor currents shifted in a positive direction when external [K+] was increased. 4. External [Mg2+], [Mn2+], [Na+], [Rb+] and [TEA+] had similar effects on the thermo- and mechanoreceptor currents. 5. Thermoreceptor currents decreased whereas mechanoreceptor currents increased as the ambient temperature was raised. 6. When a mechanical stimulus was applied to the membrane where a thermoreceptor current was being produced, an algebraic summation of these receptor currents occurred. 7. It is concluded that thermoreceptor currents are dependent on ion channels different from those responsible for the mechanoreceptor currents, although the ionic pores for the channels are similar to each other in various respects. 8. A possibility that a thermoreceptor mechanism exclusively shares a Ca2+ pore in the anterior membrane, or a K+ pore in the posterior membrane, with a mechanoreceptor mechanism is discussed.

scholarly journals VAGAL AND SYMPATHETIC EFFECTS ON THE PACEMAKER FIBERS IN THE SINUS VENOSUS OF THE HEART

1956 ◽  
Vol 39 (5) ◽  
pp. 715-733 ◽  
Author(s):  
Otto F. Hutter ◽  
Wolfgang Trautwein
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Action Potentials ◽  
Vagal Stimulation ◽  
Sinus Venosus ◽  
Sympathetic Stimulation ◽  
Pacemaker Potential ◽  
Pacemaker Potentials ◽  
Different Parts ◽  
Stimulation Of

1. Action potentials from sinus venosus and auricle fibers of spontaneously beating frog hearts have been recorded with intracellular electrodes. 2. Sinus fibers show a slow depolarization, the pacemaker potential, during diastole. The amplitude of this potential varies in different parts of the sinus. In some fibers the membrane potential falls by 11 to 15 mv. during diastole and the transition to the upstroke of the action potential is comparatively gradual. In other regions the depolarization develops more slowly and the action potential takes off more abruptly from a higher membrane potential. It is proposed that the fibers showing the largest fall in membrane potential during diastole are the pacemaker fibers of the heart, and that the rest of the preparation is excited by conduction. In auricle fibers the membrane potential is constant during diastole. 3. The maximum diastolic membrane potential and the overshoot of the action potential vary inversely with the amplitude of the pacemaker potential. The highest values were measured in auricle fibers. 4. Stimulation of vagi suppresses the pacemaker potentials. While the heart is arrested the membrane potential of the sinus fibers rises to a level above the maximum diastolic value reached in previous beats. In 28 experiments vagal stimulation increased the membrane potential from an average maximal diastolic value of 55 mv. to a "resting" level of 65.4 mv. The biggest vagal polarization was 23 mv. 5. In contrast to the sinus fibers vagal inhibition does not change the diastolic membrane potential of frog auricle fibers. 6. Vagal stimulation greatly accelerates the repolarization of the action potential and reduces its amplitude. These changes were seen both in the sinus and in auricle fibers stimulated by direct shocks during vagal arrest. 7. The conduction velocity in the sinus venosus of the tortoise is reduced by vagal stimulation. Block of conduction often occurs. 8. In the frog sinus venosus sympathetic stimulation increases the rate of rise of the pacemaker potential, accelerating the beat. The threshold remains unchanged. The rate of rise of the upstroke and the amplitude of the overshoot are increased. 9. The analogies between the vagal inhibition of the heart and the nervous inhibition of other preparations are discussed.

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