scholarly journals Light-Induced Changes in Photoreceptor Membrane Resistance and Potential in Gecko Retinas

1974 ◽  
Vol 64 (1) ◽  
pp. 49-69 ◽  
Author(s):  
L. H. Pinto ◽  
W. L. Pak
Keyword(s):  
Time Course ◽  
Receptor Potential ◽  
Membrane Resistance ◽  
Rapid Onset ◽  
Membrane Voltage ◽  
Peripheral Stimulus ◽  
Slow Increase ◽  
Membrane Hyperpolarization ◽  
Resistance Decrease ◽  
Induced Changes

The time-course of light-induced changes in membrane voltage and resistance were measured in single photoreceptors in eyecup preparations of Gekko gekko. A small circular stimulus directed toward the impaled receptor produced membrane hyperpolarization. Application of a steady annular light to the receptor periphery resulted in diminution of the receptor's response to the stimulus. The effects of illumination of the surrounding receptors were isolated by directing a small, steady desensitizing light to the impaled receptor and then applying a peripheral stimulus. Brief stimuli produced a transient decrease in resistance with rapid onset and offset, a time-course similar to that of the response diminution. For some cells a depolarization that coincided with the resistance decrease was seen. During illumination with prolonged stimuli the resistance decrease was followed by a slow increase. After offset resistance rose transiently above the original value and then returned slowly to its original value. The slow resistance changes were not accompanied by changes in membrane voltage. The response diminution, resistance decrease, and depolarization were not observed in retinas treated with aspartate or hypoxia. It is therefore concluded that these effects are mediated by horizontal cells. The diminution is achieved by shunting the receptor potential and may play a role in field adaptation.

scholarly journals Light-Induced Changes in Photoreceptor Membrane Resistance and Potential in Gecko Retinas

1974 ◽  
Vol 64 (1) ◽  
pp. 26-48 ◽  
Author(s):  
L. H. Pinto ◽  
W. L. Pak
Keyword(s):  
Time Course ◽  
Membrane Conductance ◽  
Receptor Potential ◽  
Membrane Resistance ◽  
Photoreceptor Membrane ◽  
Membrane Hyperpolarization ◽  
Direct Measurements ◽  
Isolated Retina ◽  
Time Courses ◽  
Induced Changes

The time-course of the light-induced changes in membrane voltage and resistance were measured for single photoreceptors in the retina of Gekko gekko. In the surgically isolated retina, small stimuli directed toward the impaled receptor produced a membrane hyperpolarization the time-course of which was identical to that of the increase in membrane resistance. In the eyecup preparation nearly identical time-courses were evoked only after perfusion of the vitreous surface with solution having high (Mg++). Disparate time-courses were obtained in (a) the isolated retina when large or displaced stimuli were used, and (b) the eyecup preparation when it was treated normally (see Pinto and Pak. 1974. J. Gen. Physiol. 64:49) and when it was exposed to aspartate ions or hypoxia. These results are consistent with the hypothesis that the receptor potential (elicited in the impaled receptor as a result of quanta only it captures) is generated by a single ionic process that decreases membrane conductance. These measurements provide a means to distinguish the receptor potential from interactions. From direct measurements of membrane time constant and total resistance in darkness, total membrane capacitance was calculated. The mean capacitance was 7.1 x 10-5 µF. This high value is consistent with anatomical observations of membrane infoldings at the base of gecko photoreceptors.

Alpha 1-adrenergic receptor activation depolarizes rat supraoptic neurosecretory neurons in vitro

1986 ◽  
Vol 251 (3) ◽  
pp. R569-R574 ◽  
Author(s):  
J. C. Randle ◽  
C. W. Bourque ◽  
L. P. Renaud
Keyword(s):  
Time Course ◽  
Membrane Resistance ◽  
Receptor Activation ◽  
Membrane Hyperpolarization ◽  
Neurosecretory Neurons ◽  
Consistent Change ◽  
K Current ◽  
Supraoptic Neurons ◽  
A Current

Intracellular data were obtained from 35 supraoptic nucleus neurosecretory neurons maintained in vitro in intra-arterially perfused explants of rat hypothalamus. Addition of norepinephrine, phenylephrine, or methoxamine, but not isoproterenol (30-200 microM), consistently induced membrane depolarization, bursting activity, and an associated prolongation in action potential duration, effects that were reversibly antagonized by the alpha 1-antagonist prazosin. Norepinephrine-evoked depolarizations demonstrated no consistent change in membrane resistance and were reduced both by membrane hyperpolarization and by raising extracellular K+. Norepinephrine shortened the time course of spike hyperpolarizing afterpotentials and increased the magnitude of late depolarizing afterpotentials. It is proposed that one of norepinephrine's actions on supraoptic neurons involves K+ channels, perhaps by modulation of a transient K+ current known as A current.

scholarly journals Sodium transport effects on the basolateral membrane in toad urinary bladder.

1982 ◽  
Vol 80 (5) ◽  
pp. 733-751 ◽  
Author(s):  
C W Davis ◽  
A L Finn
Keyword(s):  
Urinary Bladder ◽  
Time Course ◽  
Apical Membrane ◽  
Basolateral Membrane ◽  
Membrane Resistance ◽  
Membrane Voltage ◽  
Toad Urinary Bladder ◽  
Na Transport ◽  
Bladder Epithelium ◽  
Current Output

In toad urinary bladder epithelium, inhibition of Na transport with amiloride causes a decrease in the apical (Vmc) and basolateral (Vcs) membrane potentials. In addition to increasing apical membrane resistance (Ra), amiloride also causes an increase in basolateral membrane resistance (Rb), with a time course such that Ra/Rb does not change for 1-2 min. At longer times after amiloride (3-4 min), Ra/Rb rises from its control values to its amiloride steady state values through a secondary decrease in Rb. Analysis of an equivalent electrical circuit of the epithelium shows that the depolarization of Vcs is due to a decrease in basolateral electromotive force (Vb). To see of the changes in Vcs and Rb are correlated with a decrease in Na transport, external current (Ie) was used to clamp Vmc to zero, and the effects of amiloride on the portion of Ie that takes the transcellular pathway were determined. In these studies, Vcs also depolarized, which suggests that the decrease in Vb was due to a decrease in the current output of a rheogenic Na pump. Thus, the basolateral membrane does not behave like an ohmic resistor. In contrast, when transport is inhibited during basolateral membrane voltage clamping, the apical membrane voltage changes are those predicted for a simple, passive (i.e., ohmic) element.

Sensory Mechanisms in Paramecium

1972 ◽  
Vol 56 (3) ◽  
pp. 683-694
Author(s):  
R. ECKERT ◽  
Y. NAITOH ◽  
K. FRIEDMAN
Keyword(s):  
Cell Membrane ◽  
Time Course ◽  
Receptor Potential ◽  
Membrane Resistance ◽  
Direct Response ◽  
Direct Stimulation ◽  
Calcium Response ◽  
Refractory Periods ◽  
Stimulus Transduction ◽  
Stimulation Of

1. Specimens of Paramecium caudatum were stimulated mechanically with a piezoelectrically driven microstylus. Membrane potentials were monitored and intracellular polarizing currents were passed with glass microelectrodes. 2. Mechanical stimulation of the anterior 15% of the cell's length produced depolarizing transients in membrane potential. This ‘anterior response’ was amplitude-graded up to a maximum with stimuli of increasing intensities, and was accompanied by a drop in membrane resistance. 3. The anterior response consists of two components, a receptor potential in direct response to stimulus transduction, and a secondarily evoked regenerative component. Both are graded. With hyperpolarization of the cell membrane the regenerative component was suppressed and the receptor potential alone was seen. With hyperpolarization the size of the receptor potential was increased. 4. The regenerative component is identical with the ‘calcium response’ which is elicited by direct stimulation with injected depolarizing current. This conclusion is supported by similar sensitivity of the overshoot to extracellular concentrations of calcium, similar refractory periods, similar inactivation by depolarization and suppression by hyperpolarization, and similar prolongation of the time course by TEA. 5. It is concluded that local inflow of receptor current through the stimulated membrane of the anterior end depolarizes the cell membrane by electrotonic spread, activating the electrically excited calcium conductance of the membrane, and thereby eliciting the regenerative calcium response.

Acute effects of repetitive depolarization on sodium current in chick myocytes

1991 ◽  
Vol 260 (6) ◽  
pp. H1810-H1818
Author(s):  
M. R. Gold ◽  
G. R. Strichartz
Keyword(s):  
Time Course ◽  
Sodium Current ◽  
Complete Recovery ◽  
Acute Effects ◽  
Na Current ◽  
Patch Clamp Technique ◽  
Membrane Hyperpolarization ◽  
Atrial Cells ◽  
Whole Cell Patch Clamp ◽  
Recovery From Inactivation

Acute effects of repetitive depolarization on the inward Na+ current (INa) of cultured embryonic chick atrial cells were studied using the whole cell patch-clamp technique. Stimulation rates of 1 Hz or greater produced a progressive decrement of peak INa. With depolarizations to 0 mV of 150-ms duration, applied at 2 Hz from a holding potential of -100 mV, the steady-state decrement was approximately 20%. The magnitude of this effect increased with stimulation frequency and with test potential depolarization and decreased with membrane hyperpolarization. Analysis of INa kinetics revealed that reactivation was sufficiently slow to preclude complete recovery from inactivation with interpulse intervals less than 1,000 ms. Moreover, reactivation accelerated markedly with membrane hyperpolarization, in parallel with the response to repetitive stimulation. The multiexponential time course of recovery of peak INa from repetitive depolarization was similar to that observed after single stimuli; however, there was a shift toward a greater proportion of current recovering with the slower of two time constants. It is concluded that incomplete recovery from inactivation is responsible for the decrement in INa observed with short interpulse intervals.

scholarly journals Electrophysiological effects of basolateral [Na+] in Necturus gallbladder epithelium.

1992 ◽  
Vol 99 (2) ◽  
pp. 241-262 ◽  
Author(s):  
G A Altenberg ◽  
J S Stoddard ◽  
L Reuss
Keyword(s):  
Apical Membrane ◽  
Basolateral Membrane ◽  
Membrane Resistance ◽  
Membrane Voltage ◽  
Gallbladder Epithelium ◽  
K Channels ◽  
Necturus Gallbladder ◽  
Electrophysiological Effects ◽  
Paracellular Diffusion ◽  
Cl Conductance

In Necturus gallbladder epithelium, lowering serosal [Na+] ([Na+]s) reversibly hyperpolarized the basolateral cell membrane voltage (Vcs) and reduced the fractional resistance of the apical membrane (fRa). Previous results have suggested that there is no sizable basolateral Na+ conductance and that there are apical Ca(2+)-activated K+ channels. Here, we studied the mechanisms of the electrophysiological effects of lowering [Na+]s, in particular the possibility that an elevation in intracellular free [Ca2+] hyperpolarizes Vcs by increasing gK+. When [Na+]s was reduced from 100.5 to 10.5 mM (tetramethylammonium substitution), Vcs hyperpolarized from -68 +/- 2 to a peak value of -82 +/- 2 mV (P less than 0.001), and fRa decreased from 0.84 +/- 0.02 to 0.62 +/- 0.02 (P less than 0.001). Addition of 5 mM tetraethylammonium (TEA+) to the mucosal solution reduced both the hyperpolarization of Vcs and the change in fRa, whereas serosal addition of TEA+ had no effect. Ouabain (10(-4) M, serosal side) produced a small depolarization of Vcs and reduced the hyperpolarization upon lowering [Na+]s, without affecting the decrease in fRa. The effects of mucosal TEA+ and serosal ouabain were additive. Neither amiloride (10(-5) or 10(-3) M) nor tetrodotoxin (10(-6) M) had any effects on Vcs or fRa or on their responses to lowering [Na+]s, suggesting that basolateral Na+ channels do not contribute to the control membrane voltage or to the hyperpolarization upon lowering [Na+]s. The basolateral membrane depolarization upon elevating [K+]s was increased transiently during the hyperpolarization of Vcs upon lowering [Na+]s. Since cable analysis experiments show that basolateral membrane resistance increased, a decrease in basolateral Cl- conductance (gCl-) is the main cause of the increased K+ selectivity. Lowering [Na+]s increases intracellular free [Ca2+], which may be responsible for the increase in the apical membrane TEA(+)-sensitive gK+. We conclude that the decrease in fRa by lowering [Na+]s is mainly caused by an increase in intracellular free [Ca2+], which activates TEA(+)-sensitive maxi K+ channels at the apical membrane and decreases apical membrane resistance. The hyperpolarization of Vcs is due to increase in: (a) apical membrane gK+, (b) the contribution of the Na+ pump to Vcs, (c) basolateral membrane K+ selectivity (decreased gCl-), and (d) intraepithelial current flow brought about by a paracellular diffusion potential.

scholarly journals Chronic Stress-Induced Changes in Pro-Inflammatory Cytokines and Spinal Glia Markers in the Rat: A Time Course Study

2012 ◽  
Vol 19 (6) ◽  
pp. 367-376 ◽  
Author(s):  
Viktoriya Golovatscka ◽  
Helena Ennes ◽  
Emeran A. Mayer ◽  
Sylvie Bradesi
Keyword(s):  
Chronic Stress ◽  
Inflammatory Cytokines ◽  
Time Course ◽  
Time Course Study ◽  
Induced Changes ◽  
Pro Inflammatory Cytokines

Limb weakness

2015 ◽  
Author(s):  
Hugo Farne ◽  
Edward Norris-Cervetto ◽  
James Warbrick-Smith
Keyword(s):  
Motor Neurons ◽  
Time Course ◽  
Internal Capsule ◽  
Time Frame ◽  
Rapid Onset ◽  
Sudden Onset ◽  
Limb Weakness ◽  
Ischaemic Attack ◽  
Definition Of ◽  
Slow Growing

The definition of weakness is important, because many patients who self-describe a ‘weak limb’ will actually have a clumsy limb (ataxia), a numb limb (reduced sensation), or a limb that is too painful to move. The time course of the onset of the symptoms in general reflects the time course of the underlying pathology: • Sudden onset (seconds to minutes) usually implies either trauma (e.g. displaced vertebral fractures due to major trauma) or certain vascular insults (e.g. stroke, transient ischaemic attack (TIA)). • Subacute onset (hours to days) suggests a progressive demyelination (e.g. Guillain–Barre syndrome, multiple sclerosis) or a slowly expanding haematoma (e.g. subdural haematoma). • Chronic onset (weeks to months), is consistent with pathologies such as a slow-growing tumour or motor neuron disease (progressive degeneration of motor neurons). As only acute and subacute limb weakness will present acutely to generalists in hospital (chronic onset cases will most likely be referred to neurology from primary care), we have limited the chapter to these cases. Limb movement requires an intact pathway from the cerebral cortex, down the corona radiata, internal capsule, and pons, along the corticospinal tract of the spinal cord, out along a nerve root, and down a peripheral nerve to the neuromuscular junction and muscle itself. If a patient has limb weakness, there must be a lesion somewhere in this pathway. Figure 26.2 gives the differential diagnosis for limb weakness. Mr Walker has presented with rapid onset of left-sided arm weakness. Key clues in the history to elicit include: • Exact time of onset? This is critical in suspected strokes because the window of time in which to confirm the diagnosis and administer thrombolysis (if appropriate) is only 4.5 hours from onset of symptoms (after that, you risk doing more harm than good to the patient). If you suspect a stroke in a patient within that time frame, call the thrombolysis team immediately. In this case, all we can say is that the onset was at some point in the 7 hours between 11 p.m. (when he went to sleep) and 6 a.m. (when he woke up), so we cannot confidently say the onset was within 4.5 hours.

Conductance changes underlying a late synaptic hyperpolarization in hippocampal CA3 neurons

1987 ◽  
Vol 58 (1) ◽  
pp. 160-179 ◽  
Author(s):  
J. J. Hablitz ◽  
R. H. Thalmann
Keyword(s):  
Membrane Potential ◽  
Voltage Clamp ◽  
Time Course ◽  
Membrane Potentials ◽  
Resting Membrane Potential ◽  
Extracellular Potassium ◽  
Voltage Sensitivity ◽  
Base Line ◽  
Membrane Hyperpolarization ◽  
Ca3 Neurons

1. Single-electrode current- and voltage-clamp techniques were employed to study properties of the conductance underlying an orthodromically evoked late synaptic hyperpolarization or late inhibitory postsynaptic potential (IPSP) in CA3 pyramidal neurons in the rat hippocampal slice preparation. 2. Late IPSPs could occur without preceding excitatory postsynaptic potentials at the resting membrane potential and were graded according to the strength of the orthodromic stimulus. The membrane hyperpolarization associated with the late IPSP peaked within 140-200 ms after orthodromic stimulation of mossy fiber afferents. The late IPSP returned to base line with a half-decay time of approximately 200 ms. 3. As determined from constant-amplitude hyperpolarizing-current pulses, the membrane conductance increase during the late IPSP, and the time course of its decay, were similar whether measurements were made near the resting membrane potential or when the cell was hyperpolarized by approximately 35 mV. 4. When 1 mM cesium was added to the extracellular medium to reduce inward rectification, late IPSPs could be examined over a range of membrane potentials from -60 to -140 mV. For any given neuron, the late IPSP amplitude-membrane potential relationship was linear over the same range of membrane potentials for which the slope input resistance was constant. The late IPSP reversed symmetrically near -95 mV. 5. Intracellular injection of ethyleneglycol-bis-(beta-aminoethylether)-N,N'-tetraacetic acid or extracellular application of forskolin, procedures known to reduce or block certain calcium-dependent potassium conductances in CA3 neurons, had no significant effect on the late IPSP. 6. Single-electrode voltage-clamp techniques were used to analyze the time course and voltage sensitivity of the current underlying the late IPSP. This current [the late inhibitory postsynaptic current (IPSC)] began as early as 25 ms after orthodromic stimulation and reached a peak 120-150 ms following stimulation. 7. The late IPSC decayed with a single exponential time course (tau = 185 ms). 8. A clear reversal of the late IPSC at approximately -99 mV was observed in a physiological concentration of extracellular potassium (3.5 mM).(ABSTRACT TRUNCATED AT 400 WORDS)

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