Subthreshold frequency selectivity in avian auditory thalamus

1994 ◽  
Vol 71 (4) ◽  
pp. 1361-1372 ◽  
Author(s):  
B. Strohmann ◽  
D. W. Schwarz ◽  
E. Puil
Keyword(s):  
Frequency Selectivity ◽  
Membrane Properties ◽  
Resting Potential ◽  
Resonant Peak ◽  
Auditory Signal ◽  
Voltage Response ◽  
Potential Range ◽  
Na Current ◽  
Frequency Responses ◽  
Low Threshold

1. We studied the frequency responses of neurons in the nucleus ovoidalis (OV), the principal thalamic auditory relay nucleus of the chicken, in the subthreshold range of membrane potentials. The frequency response is the impedance amplitude profile evident in the voltage response to a broadband stimulus. The stimulus was a deterministic periodic current input of small amplitude, sweeping through a specified frequency range. We used whole-cell, tight-seal recording techniques in slices to study the voltage responses and membrane properties in current and voltage clamp. 2. Generally, low-frequency resonant humps with peak impedances of approximately 6 Hz characterized the frequency responses of OV neurons. This resonance was the principal determinant for frequency selectivity in the majority of OV neurons expressing only a tonic mode of firing. 3. The 6-Hz resonance was voltage dependent and most distinct where the activation ranges of a hyperpolarization activated inward current (IH) and a persistent Na+ current tend to overlap. The potential range for optimal resonance often included the resting potential. 4. Application of the Na+ current antagonist, tetrodotoxin, blocked the persistent Na+ current and most of the resonant hump at depolarized levels but did not affect the resonant peak along the frequency axis. Thus the persistent Na+ current may serve to amplify the resonance. 5. Extracellular application of Cs+, but not Ba2+, blocked a voltage sag during pulsed hyperpolarization as well as the IH current. Application of Cs+ also eliminated the 6-Hz resonance. An IH seems, therefore, instrumental for the resonance. 6. A minority of neurons that expressed low-threshold Ca2+ spikes and burst firing at hyperpolarized states displayed voltage oscillations at 2-4 Hz, spontaneously or in response to pulsatile stimuli. Application of Ni2+ blocked the oscillations and the low-threshold spikes, presumably produced by a T-type Ca2+ current. The resonance at 6 Hz, however, was only slightly affected by Ni2+. A T-type current, therefore, is critical for the 2- to 4-Hz oscillations. 7. Membrane resonance may dominate the power spectrum of subthreshold potential fluctuations. The resonance demonstrated in vitro may be stabilized by experimental procedures; its frequency may be different and more variable in vivo. Resonances in thalamic neurons may play a role in auditory signal processing in birds.

Properties of visceral primary afferent neurons in the nodose ganglion of the rabbit

1985 ◽  
Vol 54 (2) ◽  
pp. 245-260 ◽  
Author(s):  
C. E. Stansfeld ◽  
D. I. Wallis
Keyword(s):  
Action Potentials ◽  
Input Resistance ◽  
Nodose Ganglion ◽  
Time Dependent ◽  
Membrane Properties ◽  
Resting Potential ◽  
Inward Rectification ◽  
C Cells ◽  
Axonal Conduction ◽  
A Cells

The active and passive membrane properties of rabbit nodose ganglion cells and their responsiveness to depolarizing agents have been examined in vitro. Neurons with an axonal conduction velocity of less than 3 m/s were classified as C-cells and the remainder as A-cells. Mean axonal conduction velocities of A- and C-cells were 16.4 m/s and 0.99 m/s, respectively. A-cells had action potentials of brief duration (1.16 ms), high rate of rise (385 V/s), an overshoot of 23 mV, and relatively high spike following frequency (SFF). C-cells typically had action potentials with a "humped" configuration (duration 2.51 ms), lower rate of rise (255 V/s), an overshoot of 28.6 mV, an after potential of longer duration than A-cells, and relatively low SFF. Eight of 15 A-cells whose axons conducted at less than 10 m/s had action potentials of longer duration with a humped configuration; these were termed Ah-cells. They formed about 10% of cells whose axons conducted above 2.5 m/s. The soma action potential of A-cells was blocked by tetrodotoxin (TTX), but that of 6/11 C-cells was unaffected by TTX. Typically, A-cells showed strong delayed (outward) rectification on passage of depolarizing current through the soma membrane and time-dependent (inward) rectification on inward current passage. Input resistance was thus highly sensitive to membrane potential close to rest. In C-cells, delayed rectification was not marked, and slight time-dependent rectification occurred in only 3 of 25 cells; I/V curves were normally linear over the range: resting potential to 40 mV more negative. Data on Ah-cells were incomplete, but in our sample of eight cells time-dependent rectification was absent or mild. C-cells had a higher input resistance and a higher neuronal capacitance than A-cells. In a proportion of A-cells, RN was low at resting potential (5 M omega) but increased as the membrane was hyperpolarized by a few millivolts. A-cells were depolarized by GABA but were normally unaffected by 5-HT or DMPP. C-cells were depolarized by GABA in a similar manner to A-cells but also responded strongly to 5-HT; 53/66 gave a depolarizing response, and 3/66, a hyperpolarizing response. Of C-cells, 75% gave a depolarizing response to DMPP.(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of ouabain on background and voltage-dependent currents in canine colonic myocytes

1990 ◽  
Vol 259 (3) ◽  
pp. C402-C408 ◽  
Author(s):  
E. P. Burke ◽  
K. M. Sanders
Keyword(s):  
Membrane Potential ◽  
Potential Gradient ◽  
Circular Muscle ◽  
Input Resistance ◽  
Pump Current ◽  
Muscle Layer ◽  
Membrane Properties ◽  
Resting Potential ◽  
Voltage Dependent ◽  
In Cells

Previous studies have suggested that the membrane potential gradient across the circular muscle layer of the canine proximal colon is due to a gradient in the contribution of the Na(+)-K(+)-ATPase. Cells at the submucosal border generate approximately 35 mV of pump potential, whereas at the myenteric border the pump contributes very little to resting potential. Results from experiments in intact muscles in which the pump is blocked are somewhat difficult to interpret because of possible effects of pump inhibitors on membrane conductances. Therefore, we studied isolated colonic myocytes to test the effects of ouabain on passive membrane properties and voltage-dependent currents. Ouabain (10(-5) M) depolarized cells and decreased input resistance from 0.487 +/- 0.060 to 0.292 +/- 0.040 G omega. The decrease in resistance was attributed to an increase in K+ conductance. Studies were also performed to measure the ouabain-dependent current. At 37 degrees C, in cells dialyzed with 19 mM intracellular Na+ concentration [( Na+]i), ouabain caused an inward current averaging 71.06 +/- 7.49 pA, which was attributed to blockade of pump current. At 24 degrees C or in cells dialyzed with low [Na+]i (11 mM), ouabain caused little change in holding current. With the input resistance of colonic cells, pump current appears capable of generating at least 35 mV. Thus an electrogenic Na+ pump could contribute significantly to membrane potential.

Inward rectification in rat nucleus accumbens neurons

1989 ◽  
Vol 62 (6) ◽  
pp. 1280-1286 ◽  
Author(s):  
N. Uchimura ◽  
E. Cherubini ◽  
R. A. North
Keyword(s):  
Steady State ◽  
Nucleus Accumbens ◽  
Time Course ◽  
Potassium Conductance ◽  
Resting Potential ◽  
Inward Rectification ◽  
Resting Membrane Potential ◽  
Potential Range ◽  
Inward Current ◽  
Rat Nucleus Accumbens

1. Intracellular recordings were made from neurons in slices cut from the rat nucleus accumbens septi. Membrane currents were measured with a single-electrode voltage-clamp amplifier in the potential range -50 to -140 mV. 2. In control conditions (2.5 mM potassium), the resting membrane potential of the neurons was -83.4 +/- 1.1 (SE) mV (n = 157). Steady state membrane conductance was voltage dependent, being 34.8 +/- 1.7 nS (n = 25) at -100 mV and 8.0 +/- 0.7 nS (n = 25) at -60 mV. 3. Barium (1 microM) markedly reduced the inward rectification and caused a small inward current (40.6 +/- 8.7 pA, n = 8) at the resting potential. These effects became larger with higher barium concentrations, and, in 100 microM barium, the current-voltage relation was straight. 4. The block of the inward current by barium (at -130 mV) occurred with an exponential time course; the time constant was approximately 1 s at 1 microM barium and less than 90 ms with 100 microM. Strontium had effects similar to those of barium, but 1000-fold higher concentrations were required. Cesium chloride (2 mM) and rubidium chloride (2 mM) also blocked the inward rectification; their action reached steady state within 50 ms. 5. It is concluded that the nucleus accumbens neurons have a potassium conductance with many features of a typical inward rectifier and that this contributes to the potassium conductance at the resting potential.

scholarly journals Dopamine Receptor Activation Can Reduce Voltage-Gated Na+ Current by Modulating Both Entry Into and Recovery From Inactivation

2004 ◽  
Vol 92 (5) ◽  
pp. 3134-3141 ◽  
Author(s):  
Yuki Hayashida ◽  
Andrew T. Ishida
Keyword(s):  
Dopamine Receptor ◽  
Ganglion Cells ◽  
Receptor Activation ◽  
Resting Potential ◽  
Retinal Ganglion ◽  
Na Current ◽  
Voltage Gated ◽  
Recovery From Inactivation ◽  
Rate Of Recovery ◽  
Type Receptor

We tested whether dopamine receptor activation modulates the voltage-gated Na+ current of goldfish retinal ganglion cells, using a fast voltage-clamp amplifier, perforated-patch whole cell mode, and a physiological extracellular Na+ concentration. As found in other cells, activators of D1-type dopamine receptors and of protein kinase A reduced the amplitude of current activated by depolarizations from resting potential without altering the current kinetics or activation range. However, D1-type dopamine receptor activation also accelerated the rate of entry into inactivation during subthreshold depolarizations and slowed the rate of recovery from inactivation after single, brief depolarizations. Our results provide the first evidence in any preparation that D1-type receptor activation can produce both of these latter effects.

New growth elicited in adult leech mechanosensory neurones by peripheral axon damage

1989 ◽  
Vol 143 (1) ◽  
pp. 419-434
Author(s):  
B. A. Bannatyne ◽  
S. E. Blackshaw ◽  
M. McGregor
Keyword(s):  
Peripheral Nerve ◽  
Input Resistance ◽  
Resting Potential ◽  
High Threshold ◽  
Noxious Stimulation ◽  
Axon Damage ◽  
The Central Nervous System ◽  
Low Threshold ◽  
Peripheral Axon ◽  
Stimulation Of

1. New growth in cutaneous mechanosensory neurones elicited by axotomy or axon crush was studied using intracellular injection of horseradish peroxidase at different times after the lesion, ranging from a few days to over a year. 2. Cutting or crushing major, large-calibre axon branches of mechanosensory neurones elicits sprouting of new processes, either centrally within the ganglion neuropile or at the site of the lesion in the peripheral nerve. In contrast, cutting or crushing fine-calibre axon branches supplying accessory parts of the receptive field does not elicit sprouting of the main arbor or main axon branches. 3. Different modalities of mechanosensory neurone respond differently to lesions of their axons. Cutting the axons of high-threshold units responding to noxious stimulation of the skin elicits sprouting of additional processes from the axon hillock region within the central nervous system (CNS), whereas cutting or crushing the axons of low-threshold cells responding to light touch of the skin elicits sprouting at the site of the lesion only, and not within the CNS. 4. In addition to the new growth directed into the peripheral nerve, damaged nociceptive neurones also form new processes that wrap the somata of particular cells within the ganglion. 5. Sprouted processes of axotomized neurones are retained for long periods after the lesion (up to 425 days). 6. The electrical properties of touch and nociceptive cells were studied between 1 and 60 days after axotomy, by intracellular recording from the centrally located cell bodies. The amplitude, width and maximum dV/dt of the action potential and after-hyperpolarization, as well as the resting potential and input resistance, did not change significantly after axotomy, despite the considerable process sprouting known to occur during this time.

Morphological and Membrane Properties of Rat Magnocellular Basal Forebrain Neurons Maintained in Culture

1998 ◽  
Vol 80 (4) ◽  
pp. 1653-1669 ◽  
Author(s):  
J. A. Sim ◽  
T.G.J. Allen
Keyword(s):  
Basal Forebrain ◽  
Cell Types ◽  
Membrane Properties ◽  
Resting Potential ◽  
Inward Rectification ◽  
Delayed Rectifier ◽  
Magnocellular Neurons ◽  
Membrane Hyperpolarization ◽  
Cell Excitability ◽  
Forebrain Neurons

Sim, J. A. and T.G.J. Allen. Morphological and membrane properties of rat magnocellular basal forebrain neurons maintained in culture. J. Neurophysiol. 80: 1653–1669, 1998. Morphological and electrophysiological characteristics of magnocellular neurons from basal forebrain nuclei of postnatal rats (11–14 days old) were examined in dissociated cell culture. Neurons were maintained in culture for periods of 5–27 days, and 95% of magnocellular (>23 μm diam) neurons stained positive with acetylcholinesterase histochemistry. With the use of phase contrast microscopy, four morphological subtypes of magnocellular neurons could be distinguished according to the shape of their soma and pattern of dendritic branching. Corresponding passive and active membrane properties were investigated with the use of whole cell configuration of the patch-clamp technique. Neurons of all cell types displayed a prominent (6–39 mV; 6.7–50 ms duration) spike afterdepolarization (ADP), which in some cells reached firing threshold. The ADP was voltage dependent, increasing in amplitude and decreasing in duration with membrane hyperpolarization with an apparent reversal potential of −59 ± 2.3 (SE) mV. Elevating [Ca2+]o (2.5–5.0 mM) or prolonging spike repolarization with 10 mM tetraethylammonium (TEA) or 1 mM 4-aminopyridine (4-AP), potentiated the ADP while it was inhibited by reducing [Ca2+]o (2.5–1 mM) or superfusion with Cd2+ (100 μM). The ADP was selectively inhibited by amiloride (0.1–0.3 mM or Ni2+ 10 μM) but unaffected by nifedipine (3 μM), ω-conotoxin GVIA (100 nM) or ω-agatoxin IVA (200 nM), indicating that Ca2+ entry was through T-type Ca2+ channels. After inhibition of the ADP with amiloride (300 μM), depolarization to less than −65 mV revealed a spike afterhyperpolarization (AHP) with both fast and slow components that could be inhibited by 4-AP (1 mM) and Cd2+ (100 μM), respectively. In all cell types, current-voltage relationships exhibited inward rectification at hyperpolarized potentials ≥ E K (approximately −90 mV). Application of Cs+ (0.1–1 mM) or Ba2+ (1–10 μM) selectively inhibited inward rectification but had no effect on resting potential or cell excitability. At higher concentrations, Ba2+ (>10 μM) also inhibited an outward current tonically active at resting potential ( V H −70 mV), which under current-clamp conditions resulted in small membrane depolarization (3–10 mV) and an increase in cell excitability. Depolarizing voltage commands from prepulse potential of −90 mV ( V H −70 mV) in the presence of tetrodotoxin (0.5 μM) and Cd2+ (100 μM) to potentials between −40 and +40 mV cause voltage activation of both transient A-type and sustained delayed rectifier-type outward currents, which could be selectively inhibited by 4-AP (0.3–3 mM) and TEA (1–3 mM), respectively. These results show that, although acetylcholinesterase-positive magnocellular basal forebrain neurons exhibit considerable morphological heterogeneity, they have very similar and characteristic electrophysiological properties.

Nonequivalent cylinder models of neurons: interpretation of voltage transients generated by somatic current injection

1988 ◽  
Vol 60 (1) ◽  
pp. 125-148 ◽  
Author(s):  
P. K. Rose ◽  
A. Dagum
Keyword(s):  
Regional Differences ◽  
Dendritic Tree ◽  
Membrane Properties ◽  
Reliable Estimate ◽  
Voltage Response ◽  
Spinal Motoneurons ◽  
Membrane Resistivity ◽  
Voltage Dependent ◽  
Voltage Transients ◽  
Specific Membrane

1. Numerical methods were used to simulate the voltage responses to an intrasomatic current step of neuronal models that incorporated tapering dendrites, dendrites of unequal electrotonic length, nonlinear membrane properties, and regional differences in specific membrane resistivity (Rm). A "peeling" technique was used to estimate the time constants (tau 0 and tau 1) and coefficients (a0 and a1) of the first two exponential terms of the series of exponential terms whose sum represented the slope of the voltage response. 2. The electrotonic structure of models with a uniform Rm was calculated using equations derived by Rall or Johnston or Brown et al. The adequacy of these methods were tested using a wide variety of models that conformed to the equivalent cylinder approximation of Rall. Johnston's method provided the most reliable estimate of electrotonic length (L) and the ratio of the dendritic conductance to the somatic conductance (rho). However, if L exceeded 2 and rho was eight or larger, the equations derived by Johnston could frequently not be solved due to small errors in the peeled values of tau 0, tau 1, a0, and a1. Although the method suggested by Brown et al. could be applied to all models, this method invariably underestimated L and rho. These errors were particularly large for model neurons with L values of 1.5 or larger and rho values of four or larger. Estimates of L using Rall's method were only reliable if rho was large and L was two or less. 3. Changing the geometry of the dendritic tree (dendritic tapering or dendrites of unequal L) or the addition of a time- and voltage-dependent conductance designed to mimic a sag process commonly seen in spinal motoneurons caused systematic changes in tau 0, tau 1, a0, and a1. The sag process always led to an underestimate of tau 0 even after applying a correction procedure. On the other hand, the ratio, tau 0/tau 1, was not affected by the sag process or dendritic tapering.(ABSTRACT TRUNCATED AT 400 WORDS)

Ionic Mechanisms Underlying Depolarizing Responses of an Identified Insect Motor Neuron to Short Periods of Hypoxia

1999 ◽  
Vol 81 (1) ◽  
pp. 307-318 ◽  
Author(s):  
Hervé Le Corronc ◽  
Bernard Hue ◽  
Robert M. Pitman
Keyword(s):  
Motor Neuron ◽  
Periplaneta Americana ◽  
Membrane Properties ◽  
Resting Potential ◽  
Induced Response ◽  
Long Term Effects ◽  
Sodium Influx ◽  
Hypoxia Response ◽  
Initial Transient ◽  
Ionic Mechanisms

Le Corronc, Hervé, Bernard Hue, and Robert M. Pitman. Ionic mechanisms underlying depolarizing responses of an identified insect motor neuron to short periods of hypoxia. J. Neurophysiol. 81: 307–318, 1999. Hypoxia can dramatically disrupt neural processing because energy-dependent homeostatic mechanisms are necessary to support normal neuronal function. In a human context, the long-term effects of such disruption may become all too apparent after a “stroke,” in which blood-flow to part of the brain is compromised. We used an insect preparation to investigate the effects of hypoxia on neuron membrane properties. The preparation is particularly suitable for such studies because insects respond rapidly to hypoxia, but can recover when they are restored to normoxic conditions, whereas many of their neurons are large, identifiable, and robust. Experiments were performed on the “fast” coxal depressor motoneuron (Df) of cockroach ( Periplaneta americana). Five-minute periods of hypoxia caused reversible multiphasic depolarizations (10–25 mV; n = 88), consisting of an initial transient depolarization followed by a partial repolarization and then a slower phase of further depolarization. During the initial depolarizing phase, spontaneous plateau potentials normally occurred, and inhibitory postsynaptic potential frequency increased considerably; 2–3 min after the onset of hypoxia all electrical activity ceased and membrane resistance was depressed. On reoxygenation, the membrane potential began to repolarize almost immediately, becoming briefly more negative than the normal resting potential. All phases of the hypoxia response declined with repeated periods of hypoxia. Blockade of ATP-dependent Na/K pump by 30 μM ouabain suppressed only the initial transient depolarization and the reoxygenation-induced hyperpolarization. Reduction of aerobic metabolism between hypoxic periods (produced by bubbling air through the chamber instead of oxygen) had a similar effect to that of ouabain. Although the depolarization seen during hypoxia was not reduced by tetrodotoxin (TTX; 2 μM), lowering extracellular Na+ concentration or addition of 500 μM Cd2+ greatly reduced all phases of the hypoxia-induced response, suggesting that Na influx occurs through a TTX-insensitive Cd2+-sensitive channel. Exposure to 20 mM tetraethylammonium and 1 mM 3,4-diaminopyridine increased the amplitude of the hypoxia-induced depolarization, suggesting that activation of K channels may normally limit the amplitude of the hypoxia response. In conclusion we suggest that the slow hypoxia-induced depolarization on motoneuron Df is mainly carried by a TTX-resistant, Cd2+-sensitive sodium influx. Ca2+ entry may also make a direct or indirect contribution to the hypoxia response. The fast transient depolarization appears to result from block of the Na/K pump, whereas the reoxygenation-induced hyperpolarization is largely caused by its subsequent reactivation.

Altered excitability of goldfish mauthner cell following axotomy. I. Characterization and correlations with somatic and axonal morphological reactions

1986 ◽  
Vol 55 (6) ◽  
pp. 1424-1439 ◽  
Author(s):  
M. J. Titmus ◽  
D. S. Faber ◽  
S. J. Zottoli
Keyword(s):  
Cell Body ◽  
Initial Segment ◽  
Membrane Properties ◽  
Resting Potential ◽  
M Cells ◽  
M Cell ◽  
Spike Amplitude ◽  
Axon Hillock ◽  
The Mean ◽  
Lateral Dendrite

Axonal transection 7-10 mm distal to the cell body of the goldfish Mauthner (M) cell induced alterations in its excitability; namely, the antidromic spike recorded in the soma was converted from a single-component axon-hillock response to a larger amplitude, two-component impulse. The mean spike amplitude of the axotomized cells was approximately 50% greater (59.6 +/- 15.1 mV, n = 94) than that in controls (39.4 +/- 6.3 mV, n = 73). The onset of the induced increase in spike amplitude occurs at approximately 20 days postaxotomy, and the transition to a reactive spike is complete by approximately 30-35 days. Eighty-three percent of the M-cells axotomized for more than 30 days were physiologically reactive as judged by their large spike amplitudes and/or the presence of an additional spike component. Concomitant with the enhanced spike amplitudes, there was a depression of excitability in the initial segment-axon hillock region of the axotomized cells. This depression was suggested by a decrease in the initial segment (IS) spike height (from 39.4 +/- 6.3 mV, n = 73, in controls to 27.5 +/- 5.6 mV, n = 13, in axotomized cells), a decrease in its maximum rate of rise (from 153.6 +/- 24 V/s, n = 15, to 112.5 +/- 30 V/s, n = 29), and frequent failure of antidromic invasion into the initial segment and axon hillock. These changes in excitability could not be attributed to alterations in passive membrane properties, since the mean resting potential (77.8 +/- 5.2 mV, n = 37, control; 76.9 +/- 7.8 mV, n = 87, axotomized) and input resistance (170 +/- 21.3 K omega, n = 13, control; 176 +/- 26.6 K omega, n = 21, axotomized) were not altered significantly by axotomy. Threshold voltage was also unaffected (13.4 +/- 3.2 mV, n = 11, control; 11.9 +/- 2.5 mV, n = 11, axotomized). Sequential recordings of spike amplitudes from the axon hillock, soma, and lateral dendrite suggest that the generator of the axotomy-induced component is localized to the normally passive soma and proximal dendrite. In addition, the presumed soma-dendritic In addition, the presumed soma-dendritic component contributes very little if anything to the action potentials recorded in the axon. The onset and occurrence of alterations in excitability and cell body morphology (chromatolysis and nuclear associated changes) were compared in different M-cell populations and in the same identified M-cells. The comparisons suggested that these two events tend to occur in parallel.(ABSTRACT TRUNCATED AT 400 WORDS)

Membrane Properties of Chick Semicircular Canal Hair Cells In Situ During Embryonic Development

2000 ◽  
Vol 83 (5) ◽  
pp. 2740-2756 ◽  
Author(s):  
S. Masetto ◽  
P. Perin ◽  
A. Malusà ◽  
G. Zucca ◽  
P. Valli
Keyword(s):  
Hair Cell ◽  
Hair Cells ◽  
Central Zone ◽  
Cell Voltage ◽  
Peripheral Zone ◽  
Membrane Properties ◽  
Voltage Response ◽  
Type I ◽  
Electrophysiological Properties ◽  
Different Types

The electrophysiological properties of developing vestibular hair cells have been investigated in a chick crista slice preparation, from embryonic day 10 ( E10) to E21 (when hatching would occur). Patch-clamp whole-cell experiments showed that different types of ion channels are sequentially expressed during development. An inward Ca2+ current and a slow outward rectifying K+current ( I K(V)) are acquired first, at or before E10, followed by a rapid transient K+current ( I K(A)) at E12, and by a small Ca-dependent K+ current ( I KCa) at E14. Hair cell maturation then proceeds with the expression of hyperpolarization-activated currents: a slow I h appears first, around E16, followed by the fast inward rectifier I K1around E19. From the time of its first appearance, I K(A) is preferentially expressed in peripheral ( zone 1) hair cells, whereas inward rectifying currents are preferentially expressed in intermediate ( zone 2) and central ( zone 3) hair cells. Each conductance conferred distinctive properties on hair cell voltage response. Starting from E15, some hair cells, preferentially located at the intermediate region, showed the amphora shape typical of type I hair cells. From E17 (a time when the afferent calyx is completed) these cells expressed I K, L, the signature current of mature type I hair cells. Close to hatching, hair cell complements and regional organization of ion currents appeared similar to those reported for the mature avian crista. By the progressive acquisition of different types of inward and outward rectifying currents, hair cell repolarization after both positive- and negative-current injections is greatly strengthened and speeded up.

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