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PubMed2003

Reciprocal interactions between calcium and chloride in rod photoreceptors.

This study used imaging and electrophysiological techniques in salamander retinal slices to correlate Ca2+ and Cl- levels in rods and thus test the hypothesis of a feedback interaction between Ca2+- and Ca2+-activated Cl- channels whereby Cl- efflux through Cl- channels can inhibit Ca2+ channels. Increasing [K+]o levels produced a concentration-dependent depolarization of rods accompanied by increases in [Ca2+]i measured with Fura-2. The voltage dependence of increases in [Ca2+]i was compared with the voltage dependence of the calcium current (ICa). [Cl-]i was measured with the dye, MEQ. Depolarization with high K+ to membrane potentials below -20 mV reduced [Cl-]i; larger depolarizations increased [Cl-]i. The Na/K/Cl cotransport inhibitor, bumetanide, shifted the apparent Cl- equilibrium potential (ECl) to more negative potentials, suggesting that this cotransporter helps establish a relatively depolarized ECl. MEQ fluorescence changes evoked by high K+ were inhibited by niflumic acid (0.1 mM), NPPB (2 microM), or replacement of Ca2+ with Ba2+, suggesting that depolarization-evoked Cl- changes result partly from stimulation of Ca2+-activated Cl- channels. Replacing >/=12 mM [Cl-]o with CH3SO4- produced a significant reduction in [Cl-]i. [Ca2+]i increases evoked by 20 or 50 mM K+ were also significantly inhibited by replacing >/=12 mM [Cl-]o with CH3SO4-. Thus modest depolarization can evoke increases in [Ca2+]i that lead to reductions in [Cl-]i, and conversely, reductions in [Cl-]i inhibit depolarization-evoked [Ca2+]i increases. These findings support the hypothesis that feedback interactions between Ca2+- and Ca2+-activated Cl- channels may contribute to the regulation of presynaptic Ca2+ currents involved in synaptic transmission from rod photoreceptors.

Ambystoma↗
PubMed2003

Properties of exocytotic response in vertebrate photoreceptors.

Synaptic transmission at the photoreceptor synapse is characterized by continuous release of glutamate in darkness. Release is regulated by the intracellular calcium concentration ([Ca2+]i). We here examined the physiological properties of exocytosis in tiger salamander (Ambystoma tigrinum) retinal rods and cones. Patch-clamp capacitance measurements were used to monitor exocytosis elicited by a rapid and uniform increase in [Ca2+]i by photolysis of the caged Ca2+ compound NP-EGTA. The amplitude of flash-induced increases in membrane capacitance (Cm) varied monotonically with [Ca2+]i beyond approximately 15 microM. The following two types of kinetic responses in Cm were recorded in both rods and cones: 1) a single exponential rise (39% of cells) or 2) a double-exponential rise (61%). Average rate constants of rapid and slow exocytotic responses were 420 +/- 168 and 7.85 +/- 5.02 s-1, respectively. The rate constant for the single exponential exocytotic response was 17.5 +/- 12.4 s-1, not significantly different from that of the slow exocytotic response. Beyond the threshold [Ca2+]i of approximately 15 microM, the average amplitude of rapid, slow, and single Cm response were 0.84 +/- 0.35, 0.82 +/- 0.20, and 0.70 +/- 0.23 pF, respectively. Antibodies against synaptotagmin I, a vesicle protein associated with fast exocytosis, strongly stained the synaptic terminal of isolated photoreceptors, suggesting the presence of fusion-competent vesicles. Our results confirm that photoreceptors possess a large rapidly releasable pool activated by a low-affinity Ca2+ sensor whose kinetic and calcium-dependent properties are similar to those reported in retinal bipolar cells and cochlear hair cells.

Animals↗
PubMed2003

Gonadotropin releasing hormone (GnRH) modulates odorant responses in the peripheral olfactory system of axolotls.

Peripheral signal modulation plays an important role in sensory processing. Activity in the vertebrate olfactory epithelium may be modulated by peptides released from the terminal nerve, such as gonadotropin releasing hormone (GnRH). Here, we demonstrate that GnRH modulates odorant responses in aquatic salamanders (axolotls, Ambystoma mexicanum). We recorded electrical field potentials (electro-olfactograms, or EOGs) in response to stimulation with four different amino acid odorants, L-lysine, L-methionine, L-cysteine, and L-glutamic acid. EOG responses were recorded from the main olfactory epithelium before, during, and after application of 10 microM GnRH. This protocol was repeated for a total of three trials with 60-80 min between trials. The effect of GnRH on EOG responses was broadly similar across odorants and across trials. In general, EOG responses were reduced to 79% of the initial magnitude during application of GnRH; in some trials in which glutamic acid served as the odorant, EOG responses were enhanced during the wash period. Although the 4-min inter-stimulus interval did not lead to adaptation of EOG responses during the first trial, we frequently observed evidence of adaptation during the second and third trials. In addition, we found that lower concentrations of GnRH produced a smaller effect. These results demonstrate that GnRH can modulate odorant responses in the peripheral olfactory system.

Ambystoma mexicanum↗
PubMed1981

Neurogenesis in olfactory epithelium: loss and recovery of transepithelial voltage transients following olfactory nerve section.

1. Unilateral olfactory nerve section was performed on the salamander, Ambystoma tigrinum. Physiological recordings and macroscopic observations were made to investigate the physiological correlates of functional recovery in the olfactory epithelium. 2. Slow transepithelial voltage transients, Veog, evoked by several odorous stimuli systematically decreased in amplitude during the initial 7 days and were not recorded at 10 days following nerve section, suggesting retrograde degeneration of receptor neurons. This was true for negative Veog(-), and positive, Veog(+), response components. Responses obtained from the untreated contralateral side of each animal remained similar to nonaxotomized controls. 3. Progressive recovery of the voltage transients was studied at 24, 45, 80, and 100 days following nerve section. At all stages of recovery, the wave form and time course of the responses were characteristic for each stimulus. This suggested that the response properties of the newly differentiated neuronal population were similar to those of the mature population. 4. At 100 days, response amplitudes evoked by all stimuli were similar to control values at all recording sites on the epithelial surface. The simultaneous loss and recovery of positive and negative components of the Veog indicated that the sources of both are dependent on the presence of functionally mature olfactory receptor neurons. 5. Visual inspection indicated that the olfactory nerve was reconstituted and reconnected to the olfactory bulb between 30-60 days following transection. The fact that physiological activity was recorded in the epithelium prior to this event suggests that molecular recognition and sensory transduction are not dependent on connectivity with the olfactory bulb. 6. It is concluded that physiological recovery of the olfactory receptor cell population occurs following axotomy. The time course of recovery was consistent with morphological evidence (see Ref. 57), indicating that newly differentiated receptor neurons are derived from cells in the basal region of the epithelium and replace the population lost through retrograde degeneration.

Ambystoma↗
PubMed1990

Independent influences of rod adaptation on cone-mediated responses to light onset and offset in distal retinal neurons.

1. The influence of rod adaptation on cone-mediated intracellular responses of distal retinal neurons was examined in the larval tiger salamander. Rods were selectively stimulated by the use of 450-520 nm adapting stimuli too dim to appreciably influence cones. Cones were primarily stimulated with the use of deep-red stimuli (maximally sensitive to wavelengths greater than 650 nm). The qualitative properties of rod-cone interaction were assessed with the use of several different photic-stimulus paradigms. 2. Confirming results of prior studies, we showed that rod adaptation changed the time course of cone-mediated responses to the onset of square-wave light flashes in horizontal cells (HCs); rod adaptation had no similar influence in other distal retinal neurons. Rod adaptation also enhanced cone-mediated responses to rapid flicker in cones, hyperpolarizing (HPBCs) and depolarizing (DPBCs) bipolar cells, as well as HCs. 3. We also examined the influence of rod-stimulating background fields on cone-mediated responses to slow (approximately 1-Hz) flicker composed of sawteeth with a rapid onset (ramp offset) or with a rapid offset (ramp onset). Such stimulation maintained a constant state of long-term adaptation while providing cones with transient-ON or transient-OFF stimulation. 4. Rod adaptation speeds up the response of HCs to rapid onset and increases response amplitude. Rod adaptation had no reliable influence on response to rapid onset in cones or bipolar cells. 5. Rod adaptation enhanced the amplitude of responses of HCs to rapid offset without altering response time course. 6. Rod adaptation greatly enhanced the amplitude of DPBC responses to rapid offset having no reliable influence on the time course of the response. 7. Rod adaptation caused responses of HPBCs to rapid offset to become much more transient. Rod backgrounds had a similar but smaller and less reliable influence on the response of cones to rapid offset. 8. The foregoing results indicate that rod adaptation exerts a minimum of two separate influences on cone-mediated responses in distal amphibian retina. Changes at light onset must reflect the operation of a mechanism that alters response kinetics of the HC membrane. Changes at light offset reflect the operation of a separate mechanism or set of mechanisms that must act in part presynaptically to the HCs.

Adaptation, Physiological↗
PubMed1991

Depolarizing actions of GABA and glycine on amphibian retinal horizontal cells.

1. The effects of inhibitory amino acid transmitters on horizontal cells in the superfused amphibian retina were studied by the use of conventional intracellular recording techniques. 2. Gamma-aminobutyric acid (GABA) caused a calcium-independent depolarization of horizontal cells in mud puppy and tiger salamander. This action was mimicked by muscimol but not baclofen (BAC) and blocked by bicuculline and picrotoxin (PTX), matching the GABAa receptor profile. 3. The purported GABA uptake inhibitors nipecotate (NPA) and guvacine (GUV) acted as GABAa agonists, having pharmacological properties very similar to GABA itself. These agents also activated receptors of amacrine and ganglion cells, causing membrane polarizations similar to GABA. Concentrations of these analogues that did not activate the GABAa receptor (submillimolar) did not lower the effective dose of GABA, even after prolonged application. 4. Glycine (GLY) also depolarized horizontal cells, but only in approximately 25% of the horizontal cells was the amplitude of the depolarization as great as GABA. The glycine response was blocked by both strychnine (STR, 10 microM) and PTX (100 microM). In contrast, the action of GABA was unaffected by STR. 5. Ion substitution and channel-blocking agents indicated that the effects of applied GABA and GLY were independent of both external sodium and calcium. 6. The results suggest that GABA receptors on horizontal cells may act 1) as a positive feedback system to modulate the light response and 2) as a mechanism for chemical coupling between horizontal cells.

Animals↗
PubMed1991

Electrotonic structure of olfactory sensory neurons analyzed by intracellular and whole cell patch techniques.

1. Experimental studies employing whole cell patch recordings from freshly isolated olfactory sensory neurons of the salamander (Ambystoma tigrinum) yield much higher estimates of specific membrane resistance (Rm) than studies using conventional intracellular recordings from in situ neurons. Because Rm is critical for understanding information transfer in these cells, we have used computational methods to analyze the possible reasons for this difference. 2. Compartmental models were constructed for both the in situ and isolated neurons, using SABER, a general-purpose simulation program. For Rm in the in situ cell, we used a high value of 100,000 omega.cm2, as estimated in the whole cell recordings from isolated cells. A shunt across the cell membrane caused by the penetrating microelectrode was simulated by several types of shunt mechanisms, and its effects on lowering the apparent value of resting membrane potential (MP), input resistance (RN), and membrane time constant (tau m) and increasing the electrotonic length (L) were analyzed. 3. A good approximation of the electrotonic properties recorded intracellularly was obtained in the in situ model with high Rm combined with an electrode shunt consisting of Na and K conductances. A raised K conductance (1-5 nS) helps to maintain the resting MP while contributing to the increased conductance, which lowers RN and shortens the apparent tau m toward the experimental values. 4. Combined shunt resistances of 0.1-0.2 G omega (5-10 nS) gave the best fits with the experimental data. These shunts were two to three orders of magnitude smaller than the values reported from intracellular penetrations in muscle cells and motoneurons. This may be correlated with the smaller electrode tips used in the recordings from these small neurons. We thus confirm the prediction that even small values of electrode shunt have relatively large effects on the recorded electrotonic properties of small neurons, because of their high RN (2-5 G omega). 5. We have further explored the effects on electrotonic structure of a nonuniform Rm by giving higher Rm values to the distally located cilia compared with the proximal soma-dendritic region, as indicated by recent experiments. For the same RN, large increases in ciliary Rm above 100,000 omega.cm2 can be balanced by relatively small decreases below that value in soma-dendritic Rm. A high ciliary Rm appears to be a specialization for transduction of the sensory input, as reported also in photoreceptors and hair cells.

Ambystoma↗
PubMed1992

Site of action potential initiation in amphibian retinal ganglion cells.

1. We applied morphological, pharmacological, electrophysiological, and computer simulation techniques to analyze the origin of impulse initiation in amphibian retinal ganglion cells. 2. Morphological studies of retinal ganglion cells in the mudpuppy (Necturus maculosus) and larval tiger salamander (Ambystoma tigrinum) were carried out with the use of either retrograde or intracellular labeling with horseradish peroxidase. These studies identified a characteristic thinning of the axon that begins after the initial segment of axon emerges from the ganglion cell soma or primary dendrite. Morphometric analysis of the thin segment revealed an average length of 74 microns with a standard deviation of 22 microns. For 20 conventionally placed ganglion cells, the length of the thin segment could not be correlated with soma size, initial segment diameter, or distance from the optic disk. There was also little or no correlation for seven displaced ganglion cells. The diameter of the thin segment was below reliable estimation by light microscopy. 3. We studied the possible significance of the thin axonal segment for ganglion cell impulse generation through a combination of electrophysiological recordings (intracellular and whole-cell recordings) together with computer modeling experiments. 4. Electrophysiological experiments are consistent with the idea that the thin segment and cell soma are less excitable than the initial segment region, which appears to be the principal site of initiation of the nerve impulse. The initial segment is that portion of the axon that is bounded by the soma (or proximal dendrite) at its origin and the thin segment at its distal end. 5. Computer simulations of impulse activation were carried out with the use of two different anatomic constraints: one class of simulations did not take into account the thin segment and assumed uniform cylinder conditions, whereas the other class of simulations included a model of the thin axonal segment. These comparative simulations indicate that the thin segment must contain a relatively high density of voltage-gated Na+ channels and support impulse traffic to account for physiological observations on orthodromic and antidromic impulse propagation. In addition, to match the physiological recordings, it is necessary for both the initial segment and the soma compartments to contain moderately high levels of Na+ channels. 6. Our physiological and simulation studies are consistent with the idea that the nerve impulse is normally initiated in the initial segment of axon and then spreads to activate a somatic impulse in the retrograde direction and the axonal impulse in the anterograde direction.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1992

Pharmacological properties of N-methyl-D-aspartate receptors on ganglion cells of an amphibian retina.

1. The pharmacological characteristics of the N-methyl-D-aspartate (NMDA) receptors on amphibian retinal ganglion cells were studied to determine their similarities or differences from NMDA receptors found in mammalian central nervous system (CNS) cells. Cells were tested with a variety of NMDA antagonists acting at sites on the NMDA receptor/ion channel complex. 2. Whole-cell voltage-clamp recordings were obtained from ganglion cells of the larval tiger salamander with a retinal slice preparation. All cells responded with inward currents (Vhold = -70 mV) when exposed to bath applications of NMDA, kainate (KA), and glutamate (GLU). NMDA currents reversed near 0 mV and showed a negative slope conductance region in the presence of external Mg2+. 3. NMDA-evoked inward currents could be blocked by application of 300 microM D-2-amino-7-phosphonoheptanoate (DAP7), 100 microM Zn2+, 25 microM 7-chloro-kynurenate (7-cl-KYN), 1 microM MK-801, and 5 mM Mg2+. These results indicate that like mammalian NMDA receptors the amphibian NMDA receptor possesses binding sites for NMDA, glycine, zinc, dissociative anesthetics, and Mg2+. 4. NMDA responses were evoked in the presence of 1 mM extracellular Mg2+ in 100% of cells tested when held at -70 mV. Furthermore, there was a resting conductance at -70 mV and membrane current noise that could be attenuated by the application of NMDA-specific antagonists suggesting a tonic activation of NMDA receptors for cells at the resting potential.

2-Amino-5-phosphonovalerate↗
PubMed1992

Contribution of Ca and Ca-activated Cl channels to regenerative depolarization and membrane bistability of cone photoreceptors.

1. Cone photoreceptors in several vertebrate species generate Ca-dependent regenerative depolarizations (e.g., Ca spikes lasting up to 2 s) in response to current injection or surround illumination and may remain in a state of prolonged depolarization (e.g., a permanent plateau near 0 mV) after these stimuli. This paper, while confirming the role of Ca channels in the regenerative depolarization, demonstrates that Ca-activated Cl channels either enhance or hinder prolonged depolarization, depending on the value of the chloride equilibrium potential (ECl). 2. Current- and voltage-clamp recordings obtained with the whole-cell patch-clamp technique were compared in 158 isolated tiger salamander cones to determine the contribution of specific ion channel types to the two forms of depolarizing response. Cones dialyzed with CsCl or KCl intracellular solution (such that ECl = 0 mV) that had sustained negative slope regions in their current-voltage (I-V) relations recorded under voltage clamp, were, under current clamp, bistable with respect to their resting potential. Injection of approximately 20-pA steps of depolarizing current resulted in transitions from the negative stable membrane potential (near -50 mV) to a long lasting plateau around 0 mV. Injection of 200-300 pA of hyperpolarizing current could then force a return to the negative stable resting potential, although once repolarization occurred, current injection had to be reduced or terminated to prevent damaging hyperpolarization of the cell. 3. The inward currents accounting for the negative slope region of the I-V relation were carried in Ca and Ca-activated Cl channels. Specific block of Ca-activated Cl current (ICl(Ca)) by 100 microM niflumic acid (NFA) eliminated the prolonged depolarization, even though the negative slope conductance region in the I-V persisted and the cone could still produce the briefer Ca-dependent regenerative depolarizations. Application of 100 microM Cd2+ blocked both forms of depolarization. 4. Substitution of Ba2+, which among other actions did not activate ICl(Ca), usually supported regenerative depolarizations of shortened duration, demonstrating the role of Ca channels in the initial phase of these responses. 5. A difference was observed in the regenerative depolarization when ECl was shifted away from 0 mV, where it had been in the experiments described above. With ECl set to -40 or -60 mV by reduction of [Cl-] in the pipette, steady-state membrane bistability was eliminated and prolonged depolarization did not occur. Under these conditions, application of the Cl channel blocker NFA showed that ICl(Ca) contributes to membrane hyperpolarization.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Divalent cations block the cyclic nucleotide-gated channel of olfactory receptor neurons.

1. The effects of external divalent cations on odor-dependent, cyclic AMP-activated single-channel currents from olfactory receptor neurons of the tiger salamander (Ambystoma tigrinum) were studied in inside-out membrane patches taken from dendritic regions of freshly isolated sensory cells. 2. Channels were reversibly activated by 100 microM cyclic AMP. In the absence of divalent cations, the channel had a linear current-voltage relation giving a conductance of 45 pS. With increasing concentrations of either Ca2+ or Mg2+ in the external solution, the channel displayed a rapid flickering behavior. At higher concentrations of divalent cations, the transitions were too rapid to be fully resolved and appeared as a reduction in mean unitary single-channel current amplitude. 3. This effect was voltage dependent, and on analysis was shown to be due to an open channel block by divalent ions. In the case of Mg2+, the block increased steadily with hyperpolarization. In contrast, for Ca2+ the block first increased with hyperpolarization and then decreased with further hyperpolarization beyond -70 mV, providing evidence for Ca2+ permeation of this channel. 4. This block is similar to that seen in voltage-gated calcium channels. Additionally, the cyclic nucleotide-gated channel shows some pharmacological similarities with L-type calcium channels, including a novel block of the cyclic nucleotide channel by nifedipine (50 microM). 5. Our results indicate that the sensory generator current simultaneously depends on the presence of the second messenger and on the membrane potential of the olfactory neuron.

Ambystoma↗
PubMed1994

Ionic conductances of monkey solitary cone inner segments.

1. The membrane properties of cone inner segments dissociated enzymatically from monkey retina were studied under voltage-clamp conditions using patch pipettes in the whole-cell clamp configuration. 2. A noninactivating, voltage-gated calcium current was evoked at potentials positive to -60 mV and peaked between -30 and -20 mV when barium was substituted for calcium. Cadmium (50 microM) but not nickel (50 microM) blocked the current. 3. A large calcium-activated anion current (IAn) was observed when the membrane potential was set to a level between -60 and 30 mV. The reversal potential of IAn was 0 mV with chloride as the sole anion and about -30 and -40 mV when methanesulfonate and D-aspartate, respectively, replaced intracellular chloride to set the equilibrium potential for chloride at -50 mV. IAn inactivated and oscillated when the membrane potential was maintained at depolarized levels, contrary to calcium-activated anionic currents seen in photoreceptors of other species. 4. A sustained-type potassium current was activated by depolarizations positive to -50 mV. The time course of activation and deactivation were voltage dependent. This potassium current was partially blocked by 20 mM tetraethylammonium ions. 5. A transient potassium current was activated by depolarizations positive to -20 mV. This current was blocked by 4-aminopyridine (2 mM) and inactivated with a time constant of approximately 500 ms. The amplitude in response to voltage steps to 45 mV was decreased by prepulses to voltages more positive than -30 mV. 6. Hyperpolarization negative to -65 mV activated an inward current that was completely blocked by external cesium (10 mM). The reversal potential suggested a conductance mechanism permeable to both sodium and potassium ions. 7. A calcium-activated potassium current, which was found in salamander photoreceptors, was not detected. 8. The presence of these conductances is expected to influence the membrane potential and the time course of the light response in monkey cones.

Animals↗
PubMed1994

Intracellular pH changes produced by glutamate uptake in rat hippocampal slices.

1. The mean intracellular pH in area CA1 of rat hippocampal slices was monitored fluorescently after loading the cells with the dye BCECF-AM. 2. Including L-glutamate in the solution superfusing the slice led to the intracellular pH becoming more acid. This acidification had a roughly Michaelis-Menten dependence on the superfused glutamate concentration with a half-maximal dose around 200 microM: this value must overestimate the glutamate concentration at most of the cells, which will be reduced by uptake. 3. The glutamate-evoked acidification was not significantly reduced by blockers of glutamate-gated ion channels [6-cyano-7-nitroquinoxaline-2,3- dione (CNQX) and D-aminophosphonovalerate (APV)] nor by blockers of gamma-aminobutyric acid (GABA)- and glycine-gated channels (picrotoxin and strychnine), and so was not produced by H+ entry through alpha-amino-3-hydroxy-5-methyl-4- isoxazolepropionic acid (AMPA) or N-methyl-D-aspartate (NMDA) receptor channels nor by HCO3- exit through the chloride channels controlled by GABA or glycine. 4. The glutamate-evoked acidification was not reduced by tetrodotoxin (TTX), ruling out the possibility of it being generated by action potentials. It was also unaffected by saturation of presynaptic L-amino-4-phosphonobutanoate (AP4) receptors with AP4. 5. In the presence of blockers of glutamate-, GABA-, and glycine-gated channels, the acidification showed the pharmacology of glutamate uptake and was reduced by a glutamate uptake blocker. 6. The glutamate-evoked acidification showed an ion dependence similar to that of glutamate uptake. It was abolished by removal of extracellular sodium and was reduced by raising the extracellular potassium concentration. It was unaffected by blockers of Na+/H+ exchange (amiloride) and Na+/HCO3- cotransport [4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS)] and so was not produced by the Na+ influx accompanying glutamate uptake changing the activity of these carriers. 7. These data show that the glutamate uptake carrier acidifies hippocampal cells, possibly because it transports a pH-changing anion out of the cell as in salamander glial cells. Glutamate uptake may thus contribute to activity-induced pH changes in the nervous system.

Acid-Base Equilibrium↗
PubMed1995

Interaction of anionic and cationic currents leads to a voltage dependence in the odor response of olfactory receptor neurons.

1. We recorded odor-induced currents from isolated olfactory receptor neurons of the land phase tiger salamander (Ambystoma tigrinum) with the whole cell patch clamp. 2. In a subset of cells the current-voltage relation for the odor-induced current showed a strong rectification with, in some cells, a negative resistance slope between about -45 and -25 mV. In these cells there was little or no odor-induced current at -55 mV, the average resting potential of olfactory neurons. 3. Depolarizing the membrane to +20 mV revealed a large outward current, and on repolarizing the membrane to -55 mV we could observe a large inward current. This current was not observed in the absence of the depolarizing step or in the absence of odor stimuli. 4. This odor-induced tail current was dependent on extracellular Ca2+ and voltage, activating with increased depolarization. The reversal potential was sensitive to the chloride equilibrium potential and it could be significantly blocked by niflumic acid, a blocker of calcium-activated chloride currents. The voltage dependence could result from either the voltage-dependent block of adenosine 3',5'-cyclic monophosphate-gated cation channels known to be activated by odorants and permeable to Ca2+, or from an inherent voltage dependence in the chloride channel gating. 5. The current appears to function as a regenerative mechanism that might increase the amplitude and duration of the odor-induced current, especially to low concentrations of stimulus.

Ambystoma↗
PubMed1995

Regulation of cyclic nucleotide-gated channels and membrane excitability in olfactory receptor cells by carbon monoxide.

1. The effect of the putative neural messenger carbon monoxide (CO) and the role of the cGMP second-messenger system for olfactory signal generation was examined in isolated olfactory receptor neurons (ORNs) of the tiger salamander. 2. With the use of whole cell voltage-clamp recordings in combination with a series of ionic and pharmological tests, it is demonstrated that exogenously applied CO is a potent activator (K1/2 = 2.9 microM) of cyclic nucleotide-gated (CNG) channels previously described to mediate odor transduction. 3. Several lines of evidence suggest that CO mediates its effect through stimulation of a soluble guanylyl cyclase (sGC) leading to formation of the second-messenger cGMP. This conclusion is based on the findings that CO responses show an absolute requirement for guanosine 5'-triphosphate (GTP) in the internal solution, that no direct effect of CO on CNG currents in the absence of GTP is detectable, and that a blocker of sGC activation, LY85383 (10 microM), completely inhibits the CO response. 4. The dose-response curve for cGMP at CNG channels is used as a calibration to provide a quantitative estimate of the CO-stimulated cGMP formation. This analysis implies that CO is a potent activator of olfactory sGC. 5. Perforated patch recordings using amphotericin B demonstrate that low micromolar doses of CO effectively depolarize the membrane potential of ORNs through tonic activation of CNG channels. This effect in turn regulates excitable and adaptive properties of ORNs and modulates neuronal responsiveness. 6. These data argue for an important role of the cGMP pathway in olfactory signaling and support the idea that CO may function as a diffusible messenger in the olfactory system.

Adaptation, Physiological↗
PubMed1997

Decoding visual information from a population of retinal ganglion cells.

Decoding visual information from a population of retinal ganglion cells. J. Neurophysiol. 78: 2336-2350, 1997. This work investigates how a time-dependent visual stimulus is encoded by the collective activity of many retinal ganglion cells. Multiple ganglion cell spike trains were recorded simultaneously from the isolated retina of the tiger salamander using a multielectrode array. The stimulus consisted of photopic, spatially uniform, temporally broadband flicker. From the recorded spike trains, an estimate was obtained of the stimulus intensity as a function of time. This was compared with the actual stimulus to assess the quality and quantity of visual information conveyed by the ganglion cell population. Two algorithms were used to decode the spike trains: an optimized linear filter in which each action potential made an additive contribution to the stimulus estimate and an artificial neural network trained by back-propagation to match spike trains with stimuli. The two methods performed indistinguishably, suggesting that most of the information about this stimulus can be extracted by linear operations on the spike trains. Individual ganglion cells conveyed information at a rate of 3.2 +/- 1.7 bits/s (mean +/- SD), with an average information content per spike of 1.6 bits. The maximal possible rate of information transmission compatible with the measured spiking statistics was 13.9 +/- 6.3 bits/s. On average, ganglion cells used 22% of this capacity to encode visual information. When a decoder received two spike trains of the same response type, the reconstruction improved only marginally over that obtained from a single cell. However, a decoder using an ON and an OFF cell extracted as much information as the sum of that obtained from each cell alone.Thus cells of opposite response type encode different and nonoverlapping features of the stimulus. As more spike trains were provided to the decoder, the total information rate rapidly saturated, with 79% of the maximal value obtained from a local cluster of just four neurons of different functional types. The decoding filter applied to a given neuron's spikes within such a multiunit decoder differed substantially from the filter applied to that same neuron in a single-unit decoder. This shows that the optimal interpretation of a ganglion cell's action potential depends strongly on the simultaneous activity of other nearby cells. The quality of the stimulus reconstruction varied greatly with frequency: flicker components below 1 Hz and above 10 Hz were reconstructed poorly, and the performance was optimal near 2.5 Hz. Further analysis suggests that temporal encoding by ganglion cell spike trains is limited by slow phototransduction in the cone photoreceptors and a corrupting noise source proximal to the cones.

Action Potentials↗
PubMed1998

Calcium-sensitive calcium influx in photoreceptor inner segments.

The effect of external calcium concentration ([Ca2+]o) on membrane potential-dependent calcium signals in isolated tiger salamander rod and cone photoreceptor inner segments was investigated with patch-clamp and calcium imaging techniques. Mild depolarizations led to increases in intracellular Ca2+ levels ([Ca2+]i) that were smaller when [Ca2+]o was elevated to 10 mM than when it was 3 mM, even though maximum Ca2+ conductance increased 30% with the increase in [Ca2+]o. When external calcium was lowered to 1 mM [Ca2+]o, maximum Ca2+ conductance was reduced, as expected, but the mild depolarization-induced increase in [Ca2+]i was larger than in 3 mM [Ca2+]o. In contrast, when photoreceptors were strongly depolarized, the increase in [Ca2+]i was less when [Ca2+]o was reduced. An explanation for these observations comes from an assessment of Ca2+ channel gating in voltage-clamped photoreceptors under changing conditions of [Ca2+]o. Although Ca2+ conductance increased with increasing [Ca2+]o, surface charge effects dictated large shifts in the voltage dependence of Ca2+ channel gating. Relative to the control condition (3 mM [Ca2+]o), 10 mM [Ca2+]o shifted Ca2+ channel activation 8 mV positive, reducing channel open probability over a broad range of potentials. Reducing [Ca2+]o to 1 mM reduced Ca2+ conductance but shifted Ca2+ channel activation negative by 6 mV. Thus the intracellular calcium signals reflect a balance between competing changes in gating and permeation of Ca2+ channels mediated by [Ca2+]o. In mildly depolarized cells, the [Ca2+]o-induced changes in Ca2+ channel activation proved stronger than the [Ca2+]o-induced changes in conductance. In response to the larger depolarizations caused by 80 mM [K+]o, the opposite is true, with conductance changes dominating the effects on channel activation.

Ambystoma↗
PubMed1998

Spatiotemporal patterns at the retinal output.

Edge enhancement in the retina is thought to be mediated by classical center-surround antagonism, first encountered as the interactions between horizontal cells and cones. But in the salamander retina these interactions do little to enhance edges. Instead, a robust dynamic interaction between amacrine and bipolar cells appears to be responsible for a sharp edge enhancement. To demonstrate this we recorded extracellularly from a single ganglion cell and moved a flashed square, 300 micro(m) on a side, over a 1.5 x 1.0 mm2 grid at 25-micro(m) increments. Playing back all of these recordings simultaneously simulated the pattern of responses that would have been measured from an array of ganglion cells. The emerging pattern of ganglion cell activity first faithfully represented the flashed square, but after approximately 60 ms the center of the representation collapsed, leaving a representation of only the edges. We inferred that the feedback synapse from amacrine to bipolar cells at gamma-aminobutyric acid-C (GABAC) receptors mediated this effect: bicuculline and strychnine were ineffective in altering the response pattern, but in picrotoxin the center of the representation did not collapse. The GABAergic amacrine cells thought to mediate this effect have quite narrow spread of processes, so the existence of this edge-enhancing effect suggests a mechanism quite different from classical lateral inhibition, namely the delayed inhibition of a spatially expanding input pattern.

Ambystoma↗

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