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121.
Kevin A. Mazurek 《Cognitive neuropsychology》2019,36(3-4):103-116
ABSTRACTElectrical stimulation of the nervous system is a powerful tool for localizing and examining the function of numerous brain regions. Delivered to certain regions of the cerebral cortex, electrical stimulation can evoke a variety of first-order effects, including observable movements or an urge to move, or somatosensory, visual, or auditory percepts. In still other regions the subject may be oblivious to the stimulation. Often overlooked, however, is whether the subject is aware of the stimulation, and if so, how the stimulation is experienced by the subject. In this review of how electrical stimulation has been used to study selected aspects of sensorimotor and language function, we raise questions that future studies might address concerning the subjects’ second-order experiences of intention and agency regarding evoked movements, of the naturalness of evoked sensory percepts, and of other qualia that might be evoked in the absence of an overt first-order experience. 相似文献
122.
Jiqing Guo Kyoichi Ono Akinori Noma 《Pflügers Archiv : European journal of physiology》1996,433(1-2):209-211
Under the whole cell clamp, superfusion of the rabbit sinoatrial node cells with a Na+-free solution suppressed the sustained inward current (Ist), and the L-type Ca2+ current (ICa,L) could be recorded on depolarization less negative than –40 mV from the holding potential of –80 mV. On the other hand, replacement
of Ca2+ with Mg2+ in the external solution suppressed inward-going ICa,L and isolated Ist. Under this condition, Ist measured as a nicardipine-sensitive current showed an activation threshold between –60 and –70 mV. The conductance sequence
of Ist for monovalent ions was determined as Na+ > Li+ >> K+ @ Cs+ by replacing the external Na+ with these alkali metal ions. The contribution of Ist to the diastolic depolarization is discussed.
Received: 12 June 1996 / Received after revision: 31 July 1996 / Accepted: 7 August 1996 相似文献
123.
Won -Kyung Ho Hilary F. Brown Denis Noble 《Pflügers Archiv : European journal of physiology》1994,426(1-2):68-74
The ionic selectivity of the hyperpolarizationactivated inward current (i
f) channel to monovalent cations was investigated in single isolated sinoatrial node cells of the rabbit using the whole-cell patch-clamp technique. With a 140 mM K+ pipette, replacement of 90% external Na+ by Li+ caused a –24.5 mV shift of the fully activated current/voltage I/V curve without a significant decrease of the slope conductance. With a 140 mM Cs+ pipette, the i
f current decreased almost proportionally to the decrease in external [Na+]o as Li+ was substituted. These responses are practically the same as those observed with N-methyl glucamine (NMG+) substitution, suggesting that the relative permeability of Li+ compared with Na+ for the i
f channel is as low as that of NMG+. When Cs+ or Rb+ was substituted for internal K+, the fully activated I/V relationship for i
f showed strong inward rectification with a positive reversal potential, indicating low permeability of the i
f channel for Cs+ and Rb+. These results show that the i
f channel is highly selective for Na+ and K+ and will not pass the similar ions Li+ and Rb+. Such a high degree of selectivity is unique and may imply that the structure of the i
f channel differs greatly from that of other Na+ and K+ conducting channels. 相似文献
124.
F. Barros Donato del Camino Luis A. Pardo Teresa Palomero Teresa Giráldez Pilar de la Peña D. del Camino 《Pflügers Archiv : European journal of physiology》1997,435(1):119-129
Reduction of an inwardly rectifying K+ current by thyrotropin-releasing hormone (TRH) and caffeine has been considered to be an important determinant of electrical
activity increases in GH3 rat anterior pituitary cells. However, the existence of an inwardly rectifying K+ current component was recently regarded as a misidentification of an M-like outward current, proposed to be the TRH target
in pituitary cells, including GH3 cells. In this report, an inwardly rectifying component of K+ current is indeed demonstrated in perforated-patch voltage-clamped GH3 cells. The degree of rectification varied from cell to cell, but both TRH and caffeine specifically blocked a fraction of
current with strong rectification in the hyperpolarizing direction. Use of ramp pulses to continuously modify the membrane
potential demonstrated a prominent blockade even in cells with no current reduction at voltages at which M-currents are active.
Depolarization steps to positive voltages at the maximum of the inward current induced a caffeine-sensitive instantaneous
outward current followed by a single exponential decay. The magnitude of this current was modified in a biphasic way according
to the duration of the previous hyperpolarization step. The kinetic characteristics of the current are compatible with the
possibility that removal from inactivation of a fast-inactivating delayed rectifier causes the hyperpolarization-induced current.
Furthermore, the inwardly rectifying current was blocked by astemizole, a potent and selective inhibitor of human ether-á-go-go -related gene (HERG) K+ channels. Along with other pharmacological and kinetic evidence, this indicates that the secretagogue-regulated current is
probably mediated by a HERG-like K+ channel. Addition of astemizole to current-clamped cells induced clear increases in the frequency of action potential production.
Thus, an inwardly-rectifying K+ current and not an M-like outward current seems to be involved in TRH and caffeine modulation of electrical activity in GH3 cells.
Received: 15 May 1997 / Received after revision and accepted: 24 July 1997 相似文献
125.
在这篇论文中,我们提出了用于选择视觉的数据和智能控制的动态网络系统的神经实现过程。模型由数个相互作用的子系统构成,用于不同的处理。所有的神经子系统与信息和控制流程的倒序和顺序紧密相关。 相似文献
126.
J. R. Elliott D. A. Haydon B. M. Hendry 《Pflügers Archiv : European journal of physiology》1987,409(6):596-600
(1) The effects of benzocaine on the ionic currents in the voltage-clamped squid giant axon have been examined under various conditions; intact axons internally perfused with CsF and axons dialysed with tetraethyl-ammonium ions were used. (2) Both the steady state outward (potassium) current and the early transient (sodium) current were reduced by ca. 50% by benzocaine (1 mM). (3) Plots of the changes produced by benzocaine (1 mM) in the Hodgkin-Huxley parameters for the steady state activation (m), the steady state inactivation (h) and the time constants (m and h) for activation and inactivation of the sodium current are shown. Them andh curves are shifted in positive and negative directions respectively on the voltage axis. The time constants are not greatly affected. (4) In axons in which the sodium current inactivation had been largely removed by treatment with chloramine T, the sodium current was still reduced by ca. 50% by 1 mM benzocaine and the positive shift in activation remained unchanged. (5) The dependence on benzocaine concentration (for2mM) of the peak sodium current reduction and the shift in steady state inactivation have been determined. (6) It is concluded that in the squid axon the effects on inactivation are not the main reason for the reduction of the sodium current by benzocaine and that, in common with many other neutral anaesthetics, there are at least two sites at which benzocaine acts. 相似文献
127.
Roland Domann Thomas Dorn Otto W. Witte 《Pflügers Archiv : European journal of physiology》1991,417(5):469-478
Epileptic discharges were induced by superfusion of rat hippocampal slices with penicillin. Under these conditions the neurons generated paroxysmal depolarization shifts (PDS) after electrical stimulation of Schaffer collaterals. The PDS were followed by large afterhyperpolarizations lasting about 2 s. The mechanisms causing these afterhyperpolarizations were studied in CA1 pyramidal cells. A late component of the after hyperpolarizations, which determined their overall duration, was blocked by intracellular application of EGTA and reduced by superfusion with 8-Br-cAMP. In the same neurons these drugs had a comparable effect on after hyperpolarizations following depolarizing current injections; it was therefore concluded that the late component of the PDS afterhyperpolarizations was caused by a slow Ca2+-activated K+ current. An initial fast component of PDS afterhyperpolarizations, which peaked about 60 ms after PDS onset, was reduced by EGTA but not affected by 8-Br-cAMP suggesting that the fast Ca2+-activated K+ current also contributed to the PDS afterhyperpolarizations. Superfusion of the slice with the -aminobutyric acid B receptor (GABAB) antagonists phaclofen or 5-aminovalerate reduced the amplitude of the afterhyperpolarizations during the first 1000 ms but did not affect the late Ca2+-dependent component, indicating that a GABAB-mediated K+ inhibitory postsynaptic potential (IPSP) contributed to the PDS afterhyperpolarization. Intracellular injection of Cl– revealed that an early part of the afterhyperpolarizations lasting about 500 ms was Cl–-dependent. This component was blocked by superfusion of the slices with bicuculline, suggesting that a GABAA-mediated Cl– IPSP contributed to the PDS afterhyperpolarization. The experiments show that different synaptic and intrinsic components with different time courses participate in the generation of PDS afterpotentials. 相似文献
128.
Tong Mook Kang Insuk So Ki Whan Kim 《Pflügers Archiv : European journal of physiology》1995,431(1):91-100
In the present experiment, we characterized the intracellular Ca2+ oscillations induced by caffeine (1 mM) or histamine (1–3 M) in voltage-clamped single smooth muscle cells of rabbit cerebral (basilar) artery. Superfusion of caffeine or histamine induced periodic oscillations of large whole-cell K+ current with fairly uniform amplitudes and intervals. The oscillatory K+ current was abolished by inclusion of ethylenebis(oxonitrilo)tetraacetate (EGTA, 5 mM) in the pipette solution. Caffeine- and histamine-induced periodic activation of the large-conductance Ca2+-activated K+ [K(Ca)] channel was recorded in the cell-attached patch mode. These results suggest that the oscillations of K+ current are carried by the K(Ca) channel and reflect the oscillations of intracellular Ca2+ concentration ([Ca2+]i). Ryanodine (1–10 M) abolished both caffeine- and histamine-induced oscillations. Caffeine- induced oscillations were abolished by the sarcoplasmic reticulum Ca2+-adenosine 5-triphosphatase (Ca2+-ATPase) inhibitor, cyclopiazonic acid (10 M), and a high concentration of caffeine (10 mM). Inclusion of heparin (3 mg/ml) in the pipette solution blocked histamine-induced oscillations, but did not block caffeine-induced oscillations. By the removal of extracellular Ca2+, but not by the addition of verapamil and Cd2+, the caffeine-induced oscillations were abolished. Increasing Ca2+ influx rate increased the frequencies of caffeine-induced oscillations. Spontaneous oscillations were also observed in cells that were not superfused with agonists, and had similar characteristics to the caffeine-induced oscillations. From the above results, it is concluded, that in smooth muscle cells of the rabbit cerebral (basilar) artery, ryanodine-sensitive Ca2+-induced Ca2+ release pools play key roles in the generation of caffeine- and histamine-induced intracellular Ca2+ oscillations. 相似文献
129.
The influence of internal Ca2+ ions has been investigated during intracellular perfusion of isolated neurones from pedal ganglia of Helix pomatia in which serotonin (5-HT) induces a cyclic-adenosine-monophosphate-(cAMP)-dependent enhancement of high-threshold Ca2+ current (I
Ca). Internal free Ca2+ ([Ca2+]i) was varied between 0.01 and 10 M by addition of Ca2+-EGTA [ethylenebis(oxonitrilo)tetraacetate] buffer. Elevation of [Ca2+]i depressed the 5-HT effect. The dose/ effect curve for the Ca2+ blockade had a biphasic character and could be described by the sum of two Langmuir's isotherms for tetramolecular binding with dissociation constants K
d1=0.063 M and K
d2=1 M. Addition of calmodulin (CM) antagonists (50 M trifluoperazine or 50 M chlorpromazine), phosphodiesterase (PDE) antagonists [100 M isobutylmethylxanthine (IBMX) or 5 mM theophylline] and protein phosphatase antagonists [2 M okadaic acid (OA)] in the perfusion solution caused anticalcium action and modified the Ca2+ binding isotherm. Using the effect of OA and IBMX, two components of the total Ca2+ inhibition were separated and evaluated. In the presence of one of these blockers tetramolecular curves with K
d1=0.04 M and K
d2=0.69 M were obtained describing the activation of the retained unblocked enzyme — PDE or calcineurin (CN) correspondingly. The sum of these isotherms gave a biphasic curve similar to that in control. Leupeptin (100 M), a blocker of Ca2+-dependent proteases did not influence the amplitude of 5-HT effect, indicating that channel proteolysis is not involved in the depression. Our findings show that the molecular mechanism of Ca2+-induced suppression of the cAMP-dependent upregulation of Ca2+ channels is due to involvement of two Ca2+-CM-dependent enzymes: PDE reducing the cAMP level, and CN causing channel dephosphorylation. No other processes are involved in the investigated phenomenon at a Ca2+ concentration of less than or equal to 10 M. 相似文献
130.
Among other characteristics, the steady-state current-voltage relationship of patch-clamped single atrial myocytes from guinea-pig hearts is defined by an outward current hump in the potential region –15 to +40mV. This hump was reversibly suppressed by Co2+ (3 mM) or nitrendipine (5 M) and enhanced by Bay K 8644 (5 M). The maintained outward current component suppressed by Co2+ extended between –15.2±1.9 mV and +39.5 ±1.7 mV (mean±SEM of 14 cells) and has an amplitude of 95.7±9.4 pA at +10 mV. In isochronal I-V curves, the hump was already visible at 400 ms with essentially the same amplitude as at 1500 ms. The Co2+ -sensitive outward current underlying the hump was poorly time-dependent during 1.5 s voltage pulses but slowly relaxed upon repolarization. Tail currents reversed near the K+ equilibrium potential under our experimental conditions. The current hump of the steady-state I-V curve was also abolished by caffeine (10 mM) or ryanodine (3 M), both drugs that interfere with sarcoplasmic reticulum function. Apamin (1 M) or quinine (100 M) but not TEA (5–50 mM) markedly reduced its amplitude. However, at similar concentrations as required to inhibit the hump, both apamin and quinine appeared to be poorly specific for Ca2+ -activated K+ currents in heart cells since they also inhibited the L-Type Ca2+ current. It is concluded that a long lasting Ca2+ -activated outward current, probably mainly carried by K+ ions but not sensitive to TEA, exists in atrial myocytes which is responsible for the current hump of the background I-V curve. 相似文献