Effects of prolonged light exposure, GABA, and glycine on horizontal cell responses in tiger salamander retina

1989 ◽  
Vol 61 (5) ◽  
pp. 1025-1035 ◽  
Author(s):  
X. L. Yang ◽  
S. M. Wu

1. The effects of prolonged light exposure, gamma-aminobutyric acid (GABA), and glycine on the horizontal cell (HC) light responses were studied in the superfused flat-mounted isolated retinas of the larval tiger salamander. 2. Under prolonged dark-adapted conditions, the time-to-peak of the HC light response was approximately 2-4 s, and after the termination of prolonged (6-8 min) light exposure, the time-to-peak became approximately 0.5-1 s. 3. This prolonged light-induced change in response rise time was not observed in either photoreceptors or bipolar cells, and thus the change in HC response rise time may occur postsynaptically in the HC membrane. 4. Application of 100 microM of GABA mimicked prolonged darkness and reversibly slowed down the HC response rise time, and application of 100 microM bicuculline mimicked prolonged light exposure and reversibly sped up the HC response rise time. 5. Glycine also slowed down the HC response rise course, but its effect was not observable until the concentration was raised to 1-3 mM. Strychnine did not exert any effect on HC responses when applied alone, but it could reverse the glycine actions. 6. The actions of glycine disappeared in the presence of bicuculline, indicating that the GABA and glycine pathways were probably not independent. Application of 5-10 mM glycine produced an increase of flow of preloaded 3H-GABA from the retina. 7. These results indicate that GABA may be the primary modulator that slows down the kinetics of the postsynaptic membrane proteins in the HCs. The extracellular concentration of GABA is probably high in prolonged darkness, and it is low after prolonged light exposure. Glycine, when applied at high dose, results in an increase of GABA release that slows down the HC response time course. 8. Prolonged darkness and light exposure appear to modulate the HC response in the time domain through GABA, and this change in HC response time course is probably responsible for shaping the bipolar cell responses and making the retinal signals more transient under light-adapted conditions.

1999 ◽  
Vol 16 (3) ◽  
pp. 503-511 ◽  
Author(s):  
R.A. SHIELLS ◽  
G. FALK

Simultaneous extracellular ERG and intracellular recordings from horizontal and ON-bipolar cells were obtained from the dark-adapted retina of the dogfish. The light intensity–peak response relation (IR) and time course of on-bipolar cell responses closely resembled that of the ERG b-wave, but only at low light intensities [<10 rhodopsin molecules bleached per rod (Rh*)]. Block of on-bipolar cell responses with 50 μM 2-amino-4-phosphonobutyrate (APB) abolished the b-wave and unmasked a vitreal-negative wave. Subtraction from the control ERG resulted in the isolation of a vitreal-positive ERG with an IR which matched that of on-bipolar cells over the full range of light intensities. The D.C. component of the ERG arises as a result of sustained depolarization of on-bipolar cells in response to long (>0.5 s) dim light stimuli, or following bright light flashes. The IR of horizontal cells and the vitreal-negative wave unmasked by APB could be matched by scaling at low light intensities (<5 Rh*). However, horizontal cell responses saturated at about 30 Rh*, while the vitreal-negative wave continued to increase in amplitude. The time course of horizontal cell membrane current with dim flashes could be matched to the rising phase of the vitreal-negative wave, assuming that the delay in generating the voltage response in horizontal cells is due to their long (100 ms) membrane time constant. Blocking post-photoreceptor activity resulted in a much smaller vitreal-negative wave than that unmasked by APB alone. We conclude that the b-wave arises from on-bipolar cell depolarization, while the leading edge of the a-wave is a composite of the change in extracellular voltage drop across the rod layer and a component (proximal PIII) reflecting a decrease in extracellular K+ as horizontal cell synaptic channels close with light.


2000 ◽  
Vol 17 (1) ◽  
pp. 11-21 ◽  
Author(s):  
HAO WANG ◽  
KELLY M. STANDIFER ◽  
DAVID M. SHERRY

Gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the retina and also appears to act as a trophic factor regulating photoreceptor development and regeneration. Although the tiger salamander is a major model system for the study of retinal circuitry and regeneration, our understanding of GABA receptors in this species is almost exclusively based on the results of physiological studies. Therefore, we have examined the pharmacological binding properties of GABAA receptors and their anatomical localization in the tiger salamander retina. Radioligand-binding studies showed that specific 3H-GABA binding to GABAA receptors was dominated by a single high-affinity binding site (Kd = 15.6 ± 6.9 nM). Specific binding of 3H-GABA was almost completely eliminated by muscimol (Ki = 105 ± 62 nM) and bicuculline (Ki = 14.3 ± 2.2 μM); however, SR-95531 only displaced about 40% of specific 3H-GABA binding (Ki = 35.0 ± 3.8 nM). These data indicate that there are at least two subtypes of GABAA receptors present in the salamander retina that can be distinguished by their antagonist binding properties: one sensitive to both bicuculline and SR-95531, and one sensitive to bicuculline but insensitive to SR-95531. Because localization of GABA receptors in the salamander retina by immunocytochemistry is problematic, GABAA receptors were localized by fluorescent ligand binding combined with immunocytochemical labeling for cell specific markers. Binding of fluorescently labeled muscimol to GABAA receptors was present in both plexiform layers and on photoreceptor cell bodies. GABAA receptors in the outer plexiform layer were localized to both photoreceptor terminals and horizontal cell processes.


2002 ◽  
Vol 88 (1) ◽  
pp. 422-437 ◽  
Author(s):  
Anne J. Blood ◽  
Nader Pouratian ◽  
Arthur W. Toga

Characterization of neurovascular relationships is critical to accurate interpretation of functional neuroimaging data. We have previously observed spatial uncoupling of optical intrinsic signal imaging (OIS) and evoked potential (EP) responses in rodent barrel cortex following simultaneous whisker and forelimb stimulation, leading to changes in OIS response magnitude. To further test the hypothesis that this uncoupling may have resulted from “passive” overspill of perfusion-related responses between functional regions, we conducted the present study using temporally staggered rather than simultaneous whisker and forelimb stimulation. This paradigm minimized overlap of neural responses in barrel cortex and forelimb primary somatosensory cortex (SI), while maintaining overlap of vascular response time courses between regions. When contrasted with responses to 1.5-s lone-whisker stimulation, staggered whisker and forelimb stimulation resulted in broadening of barrel cortex OIS response time course in the temporal direction of forelimb stimulation. OIS response peaks were also temporally shifted toward the forelimb stimulation period; time-to-peak was shorter (relative to whisker stimulus onset) when forelimb stimulation preceded whisker stimulation and longer when forelimb stimulation followed whisker stimulation. In contrast with OIS and EP magnitude decreases previously observed during simultaneous whisker/forelimb stimulation, barrel cortex OIS response magnitude increased during staggered stimulation and no detectable changes in underlying EP activity were observed. Spatial extent of barrel cortex OIS responses also increased during staggered stimulation. These findings provide further evidence for spatial uncoupling of OIS and EP responses, and emphasize the importance of temporal stimulus properties on the effects of this uncoupling. It is hypothesized that spatial uncoupling is a result of passive overspill of perfusion-related responses into regions distinct from those which are functionally active. It will be important to consider potential influences of this uncoupling when designing and interpreting functional imaging studies that use hemodynamic responses to infer underlying neural activity.


1995 ◽  
Vol 12 (4) ◽  
pp. 611-620 ◽  
Author(s):  
William H. Baldridge ◽  
Reto Weiler ◽  
John E. Dowling

AbstractThe responsiveness of luminosity-type horizontal cells, recorded intracellularly from isolated hybrid bass retinas, decreased after superfusion for 2 h in constant darkness. Responsiveness was subsequently increased (light-sensitized) up to 10-fold after exposure to several short (~0.5 min) periods of continuous illumination. The increase in horizontal cell responsiveness following light-sensitization was due to an increase of peak response amplitude rather than a reduction of peak response time. The increased responsiveness after light-sensitization was intensity-dependent with brighter sensitizing stimuli causing a greater increase than dimmer stimuli. The extent of LHC dark-suppression was affected by the time of day, being greater when induced during the night than during the day. However, there was no significant difference in horizontal cell responsiveness after light-sensitization in retinas studied during the night compared to those studied during the day The responsiveness of light-sensitized horizontal cells from isolated hybrid bass retinas was found to be suppressed by relatively brief periods of darkness. The responsiveness of horizontal cells, that were first light-sensitized, decreased by more than 50% following only 5 min of darkness. Suppression of light-sensitized horizontal cell responsiveness after such a short time in the dark has not been described in other teleost retinas. The suppression of light-sensitized horizontal cell responsiveness in hybrid bass retinas may be rapid in comparison to other teleosts.


1997 ◽  
Vol 83 (6) ◽  
pp. 2131-2138 ◽  
Author(s):  
Deborah D. O’Leary ◽  
Karen Hope ◽  
Digby G. Sale

O’Leary, Deborah D., Karen Hope, and Digby G. Sale.Posttetanic potentiation of human dorsiflexors. J. Appl. Physiol. 83(6): 2131–2138, 1997.—Twitch contractions of the ankle dorsiflexors were evoked before and after applied 7-s tetanic stimulation at 100 Hz in 20 young adults. Torque decreased 15% during the tetanus. At 5 s after tetanus, twitch peak torque had potentiated 45%. Potentiation declined to 28% after 1 min, rose slightly to 33% at 2 min, and declined slowly with potentiation still 25% after 5 min. There was large intersubject variation in the amount of potentiation (5–140%) and its persistence (5 to ≥20 min). The muscle compound action potential (M wave) did not change significantly (from pretetanic value) at 5 s after tetanus but increased sharply (26%) at 2 min and then subsided. Twitch half relaxation time (23%) decreased significantly more than twitch rise time (13%) 5 s after tetanus and recovered more slowly. Twitch rates of torque development (75%) and relaxation (71%) increased similarly 5 s after tetanus and were still elevated (∼25%) at 5 min. The extent of twitch torque potentiation was significantly inversely correlated with pretetanic twitch rise time ( r = −0.69), half relaxation time ( r = −0.61), and twitch-to-tetanus ratio ( r = −0.66). The data indicate that posttetanic potentiation has a greater effect on twitch half relaxation time than on time to peak torque and is more prominent in muscles with a short twitch time course and small twitch-to-tetanus ratio.


1994 ◽  
Vol 72 (1) ◽  
pp. 326-336 ◽  
Author(s):  
M. Andreasen ◽  
J. J. Hablitz

1. Whole-cell patch-clamp recordings were used to study paired-pulse facilitation (PPF) of the lateral perforant path input to the dentate gyrus in thin hippocampal slices. 2. Orthodromic stimulation of the lateral perforant pathway evoked a excitatory postsynaptic current (EPSC) with a latency of 3.3 +/- 0.1 ms (mean +/- SE) that fluctuated in amplitude. The EPSC had a rise time (10-90%) of 2.79 +/- 0.06 ms (n = 35) and decayed with a single exponential time course with a time-constant of 9.14 +/- 0.24 ms (n = 35). No correlation was found between the amplitude of the EPSC and the rise time or decay time-constant. The non-N-methyl-D-aspartate (NMDA) antagonist 6-cyano-7-nitroquinoxaline-2,3-dione completely blocked the EPSC whereas the NMDA antagonist D-aminophosphonovaleric acid (APV) had modest effects. 3. When a test (T-)EPSC was preceded at an interval of 100 ms by a conditioning (C-)EPSC, a significant increase in the amplitude of the T-EPSC was seen in 38 out of 44 trials analyzed from a total of 27 granule cells. The average amount of PPF was 35.7 +/- 2.1%. There was no apparent correlation between the amount of PPF and the stimulation intensity or mean amplitude of the C-EPSC. The time course of the facilitated T-EPSC was not significantly different from that of the C-EPSC. 4. No correlation was found between the amplitude of the C-EPSC and that of the T-EPSC. Estimates of quantal content (mcv) were determined by calculating the ratio of the squared averaged EPSC amplitude (from 48 responses) to the variance of these responses (M2/sigma 2) whereas quantal amplitudes (qcv) were estimated by calculating the ratio of the response variance to average EPSC amplitude (sigma 2/M). PPF was found to be associated with an average increase in mcv of 64.8 +/- 7.2% (n = 38) whereas qcv was decreased by 12.1 +/- 3.8%. 5. The time course of PPF was studied by varying the interval between the C- and T-pulse from 10 to 400 ms while keeping the stimulation intensity constant. Maximal facilitation of the T-EPSC was obtained with interpulse intervals < or = 25 ms where the average facilitation amounted to approximately 70% (n = 6). The decline of facilitation was nearly exponential and was no longer evident with intervals > 350 ms.(ABSTRACT TRUNCATED AT 400 WORDS


1991 ◽  
Vol 97 (2) ◽  
pp. 303-320 ◽  
Author(s):  
A Castellano ◽  
J López-Barneo

Voltage-gated Na+ and Ca2+ conductances of freshly dissociated septal neurons were studied in the whole-cell configuration of the patch-clamp technique. All cells exhibited a large Na+ current with characteristic fast activation and inactivation time courses. Half-time to peak current at -20 mV was 0.44 +/- 0.18 ms and maximal activation of Na+ conductance occurred at 0 mV or more positive membrane potentials. The average value was 91 +/- 32 nS (approximately 11 mS cm-2). At all membrane voltages inactivation was well fitted by a single exponential that had a time constant of 0.44 +/- 0.09 ms at 0 mV. Recovery from inactivation was complete in approximately 900 ms at -80 mV but in only 50 ms at -120 mV. The decay of Na+ tail currents had a single time constant that at -80 mV was faster than 100 microseconds. Depolarization of septal neurons also elicited a Ca2+ current that peaked in approximately 6-8 ms. Maximal peak Ca2+ current was obtained at 20 mV, and with 10 mM external Ca2+ the amplitude was 0.35 +/- 0.22 nA. During a maintained depolarization this current partially inactivated in the course of 200-300 ms. The Ca2+ current was due to the activity of two types of conductances with different deactivation kinetics. At -80 mV the closing time constants of slow (SD) and fast (FD) deactivating channels were, respectively, 1.99 +/- 0.2 and 0.11 +/- 0.03 ms (25 degrees C). The two kinds of channels also differed in their activation voltage, inactivation time course, slope of the conductance-voltage curve, and resistance to intracellular dialysis. The proportion of SD and FD channels varied from cell to cell, which may explain the differential electrophysiological responses of intracellularly recorded septal neurons.


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