SEARCH · Search PubMed

Results for “Turtles”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 523 records · Page 29Linked to original sources

PubMed1980

Temperature dependence of blood viscosity in frogs and turtles: effect on heat exchange with environment.

The temperature dependence of the viscosity of blood from frogs and turtles has been assessed for temperatures between 5 and 40 degrees C. Viscosity of turtles' blood was, on average, reduced from 3.50 +/- 0.16 to 2.13 +/- 0.10 cP between 10 and 30 degrees C, a decline of 39%. Even larger changes in viscosity were observed for frogs' blood with viscosity falling from 4.55 +/- 0.32 to 2.55 +/- 0.25 cP over the same temperature range, a change of 44%. Blood viscosity was highly correlated with hematocrit in both species at all temperatures. Viscosity of blood from both frogs and turtles showed a large standard deviation at all temperatures and this was attributed to large individual-to-individual variations in hematocrit. Turtles heat faster than they cool, regardless of whether tests are performed at temperatures above or below the range of thermal preference. The effect of temperature dependence of blood viscosity on heating and cooling rates is demonstrated.

Animals↗

PubMed1985

gamma-Aminobutyric acid concentrations are maintained in anoxic turtle brain.

Changes in gamma-aminobutyric acid (GABA) concentrations in the turtle (Pseudemys scripta elegans) brain were studied in situ during prolonged anoxia. With the onset of anoxia, the well-documented rapid increases in GABA found in mammalian brains were not observed in the turtle brain. Although not statistically significant, mean GABA concentrations in the turtle brain were reduced from anesthetized control values during the first 30 min of anoxia. During this initial period brain glutamate content declined. Even after 2 h of nitrogen respiration, GABA in the turtle brain still did not rise above control levels. By the 4th h of anoxia, however, GABA had increased to 147% of control values.

Adenosine Triphosphate↗

PubMed1987

Effect of parathyroid hormone on transport by toad and turtle bladder.

We recently demonstrated that parathyroid hormone (PTH) inhibited both vasopressin- and cyclic AMP-stimulated water transport in the toad bladder. This was associated with an increase in calcium uptake by isolated epithelial cells. We postulated that PTH exerts its action on H2O transport by directly stimulating calcium uptake. The current study was designed to compare the effects of PTH and the calcium ionophore, A23187, on H2O and Na transport and H+ secretion in toad and turtle bladders. In toad bladder, PTH and A23187 decreased arginine vasopressin (AVP)-stimulated H2O flow and short-circuit current (SCC) after 60 min serosal incubation. In turtle bladder A23187 decreased SCC to 79.3 +/- 3.6% of base line (P less than 0.05), and significantly decreased RSCC as well. PTH had no effect on SCC or H+ secretion in turtle bladders. Both PTH and A23187 increased 45Ca uptake in toad bladder epithelial cells; only A23187 increased 45Ca uptake in the turtle bladder. The different action of PTH in these two membranes, compared with that of the calcium ionophore, illustrates the selectivity of PTH on membrane transport. PTH increases calcium uptake and decreases transport only in a hormone-sensitive epithelium, whereas the ionophore works in virtually all living membranes. The mode of action of these two agents to increase calcium uptake is, therefore, likely different.

Animals↗

PubMed1988

Effect of induced hypercapnia on anaerobic metabolic rate of anoxic musk turtles.

To evaluate the possible effect of induced hypercapnia on anaerobic metabolic rate during anoxia, musk turtles (Sternotherus odoratus) were submerged in N2-equilibrated water at 10 degrees C for 3 days either with (anoxic hypercapnic) or without (anoxic normocapnic) elevated aquatic PCO2 (30-40 Torr). Control animals had access to air at 10 degrees C. Plasma [lactate] was significantly higher (P less than 0.01) in the normocapnic [59.4 +/- 7.4 (SD) mM; n = 22] than in the hypercapnic (47.4 +/- 8.5 mM; n = 19) anoxic turtles, although the hypercapnic turtles had lower blood pH (P less than 0.05). Plasma ion concentrations (Na, K, Cl, Ca, and Mg), however, were no different in the two groups, although all values other than Na were different from control. In some of the animals, [lactate] and [glycogen] (per g wet wt) of skeletal muscle, heart, and liver were measured in addition to blood acid-base values and lactate. Tissue lactates, although significantly elevated from control, and glycogens, although (with the exception of skeletal muscle) significantly reduced from control, were no different in the two anoxic groups. We suggest that these tissue data are more valid indicators of anaerobic metabolic rate than is plasma lactate and therefore conclude that induced hypercapnia does not significantly depress anaerobiosis in musk turtles at 10 degrees C.

Acid-Base Equilibrium↗

PubMed1988

Brain and cerebrospinal fluid ion composition after long-term anoxia in diving turtles.

Prolonged anoxia in turtles is associated with marked disturbances in plasma composition. This study examines brain and cerebrospinal fluid (CSF) ion homeostasis in the freshwater turtle, Chrysemys picta bellii, in response to 8-10 days of submergence anoxia at 10 degrees C. For comparison, it also examines the response to experimental elevation of plasma [K], [Ca], and [Mg] in normoxic turtles. Long-term anoxia resulted in marked changes in brain and CSF composition. These included elevated [K], [Ca], [Mg], and [lactate] and reduced [Cl], and the composition of CSF approached that of plasma. Brain water content increased by 17%, which we suggest was an intracellular edema linked largely to an 11% increase in total brain K. In contrast to the lack of effective homeostasis during anoxia, CSF composition was controlled in normoxic animals. We conclude that there is homeostasis of K, Ca, and Mg in the extracellular fluids of normoxic turtle brain, as in other vertebrates, but that this homeostasis fails during long-term anoxia.

Animals↗

PubMed1988

Suppression of evoked potentials with continued ion transport during anoxia in turtle brain.

A key to turtle brain survival during anoxia is continued ion transport and avoidance of anoxic depolarization. Previous findings that ATP concentration remained constant during prolonged anoxia and calculations that ATP production decreased indicate that compensatory processes, other than consumption of energy stores or increased anaerobic glycolysis, must also contribute to ion homeostasis and brain survival. To determine whether preservation of ion transport is associated with changes in electrophysiology during loss of oxidative metabolism, the brains of pentobarbital sodium-anesthetized turtles were electrically stimulated 1) to provoke measurable increments in extracellular K+ activity (a degrees k) for determination of rates of K+ reaccumulation at the stimulus site and 2) to elicit polysynaptic extracellular field potentials (evoked potentials) recordable in the olfactory bulb. During anoxia, base-line a degrees k rose only a few millimolar, and rates of reaccumulation of K+, incremented by stimulation were slightly but not significantly slowed. In contrast, postsynaptic orthodromic responses of olfactory bulb granule cells were markedly depressed by anoxia. Monosynaptic responses of granule cells to antidromic stimulation of the lateral olfactory tract were less affected, and compound action potentials in the olfactory nerve were unchanged by anoxia. These data suggest that synaptic transmission in turtle brain, as in that of mammal, is highly dependent on oxidative metabolism and that the turtle brain may effectively conserve energy for ion transport during anoxia by depression of electrical activity.

Animals↗

PubMed1988

Orthodromic field potentials and recurrent inhibition during anoxia in turtle brain.

Recent evidence suggests that suppression of electrical activity, with the likely reduction of energy use, provides a necessary strategy for prolonged anoxic tolerance of turtle brain. The present study was aimed toward defining mechanisms underlying anoxia-induced suppression of electrical activity in turtle brain. Goals were to determine whether effects of anoxia were selective to excitatory or inhibitory processes and to test the hypothesis that enhanced inhibition underlies suppression of orthodromic field potentials in olfactory bulb. Amplitudes of "conditioning" and "test" responses, provoked by pairs of stimulus pulses to the olfactory nerve, were evaluated before, during, and after anoxic insults in the brains of turtles anesthetized with pentobarbital sodium. Suppression of conditioning responses was proportionally greater than that of test responses, indicating that inhibition was decreased and that enhanced inhibitory activity is not responsible for suppression of field potentials in turtle olfactory bulb during anoxia. When normoxia was restored, conditioning responses recovered but test responses remained suppressed. These data confirm that the inhibitory effect of a conditioning pulse on responses to a second pulse of stimulation results from a recurrent circuit and suggest that anoxia-induced changes in field potentials are independent of this recurrent circuit. Enhanced inhibition during the early period of recovery after anoxic insults may provide advantages for restoring energy status and cell physiology by suppressing electrical activity and energy use.

Animals↗

PubMed1989

Energy metabolism, ion homeostasis, and evoked potentials in anoxic turtle brain.

Unlike the mammalian brain, the turtle brain maintains ion homeostasis and avoids anoxic depolarization during prolonged anoxia. The mechanisms by which turtle brains avoid and recover from anoxic depolarization were investigated by relating changes in cellular ATP levels to extracellular K+ (K+o) and evoked potential activities after 6 h of anoxia and during anoxic depolarization induced by superfusion of the brain surface with iodoacetate during anoxia. ATP levels were maintained during 6 h of anoxia despite marked decreases in energy production, but ATP was lowered during inhibition of both oxidative phosphorylation and glycolysis. K+o activity was unchanged during 6 h of anoxia but increased when ATP levels decreased. Ion homeostasis in the turtle brain appears to be linked to ATP levels but is unaffected by rate of energy production. In contrast, amplitudes of evoked potentials decreased when ATP levels were maintained, but rate of energy production declined. ATP and K+o levels recovered after anoxic depolarization, but evoked potential activity was not restored. These data suggest that the basic strategy for turtle brain to survive anoxia is to avoid anoxic depolarization by maintaining ATP levels.

Animals↗

PubMed1989

Turtles and rats: a biochemical comparison of anoxia-tolerant and anoxia-sensitive brains.

When temperature differences are taken into account, turtle brains use glucose at one-sixth the rate reported in rat brains. Na+-K+-ATPase activities are 2- to 2.5-fold higher in rat than in turtle brains. Maximal activities of hexokinase and lactate dehydrogenase are similar, whereas citrate synthase activities are two- to threefold higher in rat than turtle brains at the respective biological temperatures. Voltage-dependent Ca2+ channel densities, when compared between the two species, showed no consistent pattern. These data, along with the threefold differences in density of voltage-dependent Na+ channels reported by Lutz et al., are consistent with the idea that lower rates of channel and pump-mediated Na+ and K+ fluxes result in lower rates of aerobic energy metabolism in turtle brains compared with rat brains.

Adaptation, Physiological↗

PubMed1991

Characteristics of the anion transport system in sea turtle erythrocytes.

Erythrocytes of Kemp's ridley sea turtle (Lepidochelys kempi) contain a 100- to 105-kDa protein that is reactive with a monoclonal antibody to the membrane domain of human erythrocyte band 3. Based on inhibition of membrane HCO(3-)-Cl- exchange with 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS), sea turtle erythrocytes were found to contain 4 x 10(6) copies of band 3 per cell. Unidirectional HCO3- transfer, specifically HCO3- out----in-Cl-in----out exchange, where subscript in----out represents transfer from inside to outside and subscript out----in represents transfer from outside to inside, was characterized by a maximal exchange rate of 1.0-1.1 nmol.cm-2.s-1, substrate affinity coefficients of 0.1-0.2 mM for HCO3- and 1.6 mM for Cl-, and an apparent inhibition constant for SITS of 0.6-1.0 microM (10 degrees C, pH 7.6). Under physiological conditions (30 degrees C, pH 7.4), the rate of net HCO3- transfer (i.e., the difference between HCO3- in----out-Cl-out----in and HCO3- out----in-Cl-in----out) was 1.13 nmol. cm-2.s-1 for cells subjected to a 5-mM decrement in CO2 content. This yields a rate coefficient for the "physiological" anion shift in sea turtle blood of 1.7 s-1, indicating that the anion shift may require 2.6 s to reach 99% completion in vivo. The erythrocyte anion shift appears to be a potential rate-limiting step for capillary CO2 exchange in these turtles.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗

PubMed1993

Effect of anoxia on excitatory amino acids in brain slices of rats and turtles: in vitro microdialysis.

Using in vitro microdialysis, we tested the hypothesis that anoxia-induced release of excitatory amino acids is greater in adult rat brain than in turtle brain. Ten minutes of anoxia produced significant elevation of glutamate (from 0.39 +/- 0.03 to 0.90 +/- 0.18 microM dialysate, means +/- SE, P < 0.05), aspartate (from 0.28 +/- 0.12 to 1.20 +/- 0.49 microM, P < 0.05), glycine, and alanine in the rat brain slice. During reoxygenation, alanine and glycine returned toward baseline values, whereas aspartate and glutamate remained elevated. In contrast, prolonged anoxia (60 min) in the turtle brain slice resulted in only minimal increase in aspartate (from 0.06 +/- 0.01 to 0.09 +/- 0.02 microM, P < 0.05) and, interestingly, a decrease in glutamate (from 0.50 +/- 0.11 to 0.33 +/- 0.09 microM, P < 0.05). Levels of glycine, alanine, and taurine were unchanged. We conclude that oxygen deprivation causes marked increase in excitatory amino acids in the anoxia-sensitive rat brain slice, while oxygen deprivation for an even longer period of time in the turtle brain slice produces substantially less change. We speculate that the difference in sensitivity to anoxia between rat and turtle is at least partly attributable to the major difference in interstitial levels of excitotoxic amino acids during oxygen deprivation.

Alanine↗

PubMed1998

Reduction of NMDA receptor activity in cerebrocortex of turtles (Chrysemys picta) during 6 wk of anoxia.

Survival of brain anoxia during months of winter dormancy by the Western painted turtle, Chrysemys picta, may rely on inactivation of neuronal ion channels. During 2 h of anoxia, Ca2+ influx via the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor decreases 30-40%, but it is not known if prolonged anoxic dormancy is associated with even more profound downregulation of this important channel. Because ionized Ca2+ in cerebrospinal fluid (CSF) increases five- to sixfold during prolonged anoxia, the potential for uncontrolled Ca2+ influx and neurotoxicity is increased. To study the regulation of NMDA receptor activity, we measured NMDA-mediated changes in intracellular Ca2+ (NMDA-DeltaCa2+) in turtle cerebrocortical sheets with fura 2. Turtles were kept in N2-bubbled aquariums for 2 h to 6 wk at 2-3 degrees C. NMDA-DeltaCa2+ decreased 60 +/- 14% (P < 0.05) after 2 h of anoxia and did not decrease further for 6 wk. Intracellular Ca2+ increased from 135 to 183 nM (P < 0.05) after 3 wk of anoxia and thereafter returned toward preanoxic levels. When NMDA receptor activity was assessed in artificial CSF containing the ions found in anoxic brain CSF (pH 7. 25, 69 mM lactate, 8.4 mM Ca2+, and 5.1 mM Mg2+), NMDA-DeltaCa2+ was twice control initially but was 21% less than in normoxic artificial CSF after the end of 6 wk, suggesting altered sensitivity of the NMDA receptor to ionized Ca2+ during prolonged anoxia. Regulation of NMDA receptor activity in turtle cerebrocortex during 6 wk of anoxia thus results in depression of NMDA receptor Ca2+ flux, despite a sixfold increase in ionized extracellular Ca2+.

Animals↗

PubMed1999

Hypoxic hypometabolism in the anesthetized turtle, Trachemys scripta.

A hypometabolic response during acute exposure to hypoxia has been measured in both endothermic and ectothermic vertebrates. In the turtle, we determined the metabolic response to normocapnic hypoxia and hypercapnic hypoxia. In addition, we tested the hypothesis that hypoxic hypometabolism was a regulated response that did not depend on O(2) availability. Metabolic, cardiovascular, and blood gas measurements were collected in anesthetized turtles under two conditions: during normocapnic hypoxia [fractional inspired O(2) FI(O(2)) = 0.1 and 0.05] and during hypercapnic hypoxia [FI(O(2)) = 0.1 and 0.05 plus fractional inspired CO(2) (FI(CO(2))) = 0.05]. During normoxia, rate of O(2) consumption (VO(2)) was 0.82 ml. min(-1). kg(-1) and was reduced by nearly 30% at the lowest FI(O(2)). Normocapnic hypoxia of FI(O(2)) = 0.1 had no significant effect on VO(2). The addition of 5% CO(2) to the inspired air did not enhance the effects of hypoxia. Injections of 2,4-dinitrophenol increased VO(2) during hypercapnic hypoxia in some animals to levels greater than those measured during normoxia. We conclude that hypoxia produces a hypometabolic state in anesthetized turtles, and the pharmacological stimulation of VO(2) counteracts the effects of hypoxia on metabolism. The hypoxic hypometabolism in turtles most likely represents a regulated response and does not reflect limited O(2) availability at the cellular level. Finally, we hypothesize that hypoxemia induced by the right-to-left cardiac shunt often associated with diving may trigger the development of a hypometabolic state and therefore contribute to the prolongation of aerobic dive times.

2,4-Dinitrophenol↗

PubMed1977

Swimming movements elicited by electrical stimulation of turtle spinal cord. I. Low-spinal and intact preparations.

1. Electrical stimulation applied within the dorsolateral funiculus of the spinal cord of an intact, unanesthetized turtle can elicit rhythmic limb movements similar to those observed during swimming. 2. A spontaneous display of hindlimb swimming movements is not observed in adult turtles whose spinal cord is transected at D2. Such swimming movements are observed in these "low-spinal" turtles in response to electrical stimulation applied within the dorsolateral funiculus caudad to the transection. 3. The repetition rate of these swimming movements can be altered by changing stimulus parameters, such as the frequency of electrical pulses. 4. The present results indicate that, in the turtle, a neural pattern generator contributing to the production of hindlimb movements during swimming is located mainly in structures caudad to the cervical enlargement of the spinal cord. These data support the hypothesis that a pattern generator for locomotion is largely resident within the spinal cord.

Animals↗

PubMed1985

Three forms of the scratch reflex in the spinal turtle: central generation of motor patterns.

A turtle with a complete transection of the spinal cord, termed a spinal turtle, exhibits three types or "forms" of the scratch reflex: the rostral scratch, pocket scratch, and caudal scratch (21). Each scratch form is elicited by tactile stimulation of a site on the body surface innervated by afferents entering the spinal cord caudal to the transection. We recorded electromyographic (EMG) potentials from the hindlimb during each of the three forms of the scratch in the spinal turtle (see Fig. 1). Common to all scratch forms is the rhythmic alternation of the activity of the hip protractor muscle (VP-HP) and hip retractor muscle (HR-KF). Each form of the scratch displays a characteristic timing of the activity of the knee extensor muscle (FT-KE) with respect to the cycle of activity of the hip muscles VP-HP and HR-KF. In a rostral scratch, activation of FT-KE occurs during the latter portion of VP-HP activation. In a pocket scratch, activation of FT-KE occurs during HR-KF activation. In a caudal scratch, activation of FT-KE occurs after the cessation of HR-KF activation. The timing characteristics of these muscle activity patterns correspond to the timing characteristics of changes in the angles of the knee joint and the hip joint obtained with movement analyses (21). We recorded electroneurographic (ENG) potentials from peripheral nerves of the hindlimb during each of the three forms of the "fictive" scratch in the spinal turtle immobilized with neuromuscular blockade (see Fig. 4). Common to all forms of the fictive scratch is the rhythmic alternation of the activity of hip protractor motor neurons (VP-HP) and hip retractor motor neurons (HR-KF). Each form displays a characteristic timing of the activity of knee extensor motor neurons (FT-KE) with respect to the cycle of VP-HP and HR-KF motor neuron activity. The timing characteristics of these motor neuron activity patterns are similar to the timing characteristics of the muscle activity patterns obtained in the preparation with movement (cf. Figs. 1 and 4). The motor pattern for each scratch form is generated centrally within the spinal cord. In the spinal immobilized preparation, neuromuscular blockade prevents both limb movement and phasic sensory input, and complete spinal transection isolates the cord from supraspinal input.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1985

Electron microscopy of Golgi-impregnated photoreceptors reveals connections between red and green cones in the turtle retina.

Red and green cones of two turtle species (Pseudemys scripta elegans and Chelydra serpentina) retina have been stained with Golgi procedures and examined by light microscopy of whole-mount tissue and by electron microscopy of serial thin sections. By light microscopy, red and green single cones appear indistinguishable, but double cones can be readily identified. All Golgi-stained photoreceptors in turtle retina have a spray of telodendria radiating from their synaptic pedicles. The telodendria of single cones are 10-20 micron long and end in clusters of terminals, whereas double cones have 30- to 50-micron long telodendria in addition to a very short bush of telodendria arising from one side of the pedicle. Electron microscopy of the Golgi-stained cones allows them to be distinguished into red or green spectral types by the appearance of their oil droplets. Furthermore, the spectral identity of cones contacted by the telodendria of identified Golgi-stained cones can similarly be determined. Red single cones make telodendrial contacts with other red singles, both members of the double cones, and with green single cones. Green single cones likewise connect to many surrounding red cones, both single and double types, and a few other green singles. Both members of the double cone connect to neighboring red and green singles and occasionally to double cones. The telodendria of stained cones end on spectrally homologous or heterologous cone types at basal junctions, central elements of ribbon synapses or, sometimes, as lateral elements of ribbon synapses. However, all these synaptic contacts appear to be of the same type, i.e., narrow-cleft basal junctions. Small gap junctions occur between neighboring cone pedicles, regardless of spectral type, in the visual streak area of the retina. Large gap junctions occur between unidentified cone telodendria in the neuropil of the outer plexiform layer. The telodendrial connections between red and green cones in the turtle retina have the appearance of chemical synapses and suggest an anatomical pathway responsible for the mixing of red and green signals in red or green cones of the turtle retina as reported in the accompanying physiological paper by Normann, Perlman, and Daly (27).

Animals↗

PubMed1991

Analysis of vertebrate eye movements following intravitreal drug injections. IV. Drug-induced eye movements are unyoked in the turtle.

1. Eye movements of awake turtles were measured from both eyes simultaneously using two search-coil contact lenses. Optokinetic nystagmus (OKN) was evoked by full field patterns moving horizontally at different stimulus velocities. Intravitreal injections of either bicuculline or 2-amino-4-phosphonobutyrate (APB) were then made into one eye, after which eye movements were again recorded under similar stimulus conditions. Several days later, eye movements were again recorded and recovery was observed. 2. The effects of these two synaptic drugs on the optokinetic responses of the injected eye were similar to those previously reported in turtles, rabbits, and decorticate cats. APB, which blocks the retinal ON pathways, completely blocked visually evoked responses to any stimulus direction or velocity presented to the injected eye. On the other hand, the uninjected eye was still responsive to optokinetic stimuli. This difference between the eyes is consistent with the nonconjugate nature of OKN in the turtle. 3. After bicuclline application, the injected eye displayed a spontaneous nystagmus with its slow phase in the temporal-to-nasal direction. The movements of the injected eye were independent of stimulus direction or a range of stimulus velocities. During that effect, the eye contralateral to the injection still responded to visual stimuli in a direction- and velocity-dependent manner. For example, if the uninjected eye was exposed to optokinetic stimuli moving temporal-to-nasal, both eyes would then move in their respective temporal-to-nasal directions. This nonconjugate ocular behavior is similar to that seen when each eye of a normal turtle was exposed to its temporal-to-nasal stimulus.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminobutyrates↗

PubMed1994

Calcium currents in turtle retinal ganglion cells. I. The properties of T- and L-type currents.

1. Voltage-activated calcium currents from single, isolated turtle retinal ganglion cells were characterized with standard whole cell patch clamp techniques. Calcium current amplitude was increased with the use of 10 mM extracellular Ca2+, whereas sodium and potassium currents were pharmacologically suppressed. 2. A transient component, expressed in approximately 39% of the cells recorded from, closely resembled the T-type calcium current described previously in other tissues. This component activated at low voltages (around -50 mV from a holding potential of -70 mV) and inactivated with a time constant 10-30 ms at -20 mV; the inactivation was strongly voltage dependent. Substitution of Ca2+ with Ba2+ reduced this current in most cases or had no effect in some instances. Surprisingly, the transient calcium current was potentiated by Bay-K 8644 and inhibited by nifedipine in some of the ganglion cells tested. 3. A sustained component, which activated at between -20 and -10 mV from a holding potential of -70 mV, was found in all ganglion cells from which we recorded. This component was substantially larger when equimolar Ba2+ replaced Ca2+ as the charge carrier, and was sensitive to the dihydropyridine agonist Bay-K 8644 and the antagonist nifedipine. Thus the sustained current in turtle retinal ganglion cells was similar to the L-type calcium current described in chick DRG neurons. However, unlike the typical L-type current, this component in turtle ganglion cells showed an inactivation that was highly dependent on the intracellular free Ca2+ concentration but not the membrane potential. 4. Synthetic omega-conotoxin MVIIC selectively blocked the sustained calcium current while sparing the transient component. It could completely block the sustained current that was resistant to nifedipine in some cells. Thus there may exist several different high voltage-activated calcium channels in turtle retinal ganglion cells.

Animals↗