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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↗
PubMed1999

Cerebellar lesions and prism adaptation in macaque monkeys.

If a laterally displacing prism is placed in front of one eye of a person or monkey with the other eye occluded, they initially will point to one side of a target that is located directly in front of them. Normally, people and monkeys adapt easily to the displaced vision and correct their aim after a few trials. If the prism then is removed, there is a postadaptation shift in which the subject misses the target and points in the opposite direction for a few trials. We tested five Macaque monkeys for their ability to adapt to a laterally displacing prism and to show the expected postadaptation shift. When tested as normals, all five animals showed the typical pattern of adaptation and postadaptation shift. Like human subjects, the monkeys also showed complete interocular transfer of the adaptation but no transfer of the adaptation between the two arms. When preoperative training and testing was complete, we made lesions of various target areas on the cerebellar cortex. A cerebellar lesion that included the dorsal paraflocculus and uvula abolished completely the normal prism adaptation for the arm ipsilateral to the lesion in one of the five monkeys. The other four animals retained the ability to prism-adapt normally and showed the expected postadaptation shift. In the one case in which the lesion abolished prism adaptation, the damage included Crus I and II, paramedian lobule and the dorsal paraflocculus of the cerebellar hemispheres as well as lobule IX, of the vermis. Thus in this case, the lesion included virtually all the cerebellar cortex that receives mossy-fiber visual information relayed via the pontine nuclei from the cerebral cortex. The other four animals had damage to lobule V, the classical anterior lobe arm area and/or vermian lobules VI/VII, the oculomotor region. When tested postoperatively, some of these animals showed a degree of ataxia equivalent to that of the case in which prism adaptation was affected, but prism adaptation and the postadaptation shift remained normal. We conclude that in addition to its role in long-term motor learning and reflex adaptation, the region of the cerebellum that was ablated also may be a critical site for a short-term motor memory. Prism adaptation seems to involve a region of the cerebellum that receives a mossy-fiber visual error signal and probably a corollary discharge of the movement.

Adaptation, Physiological↗
PubMed2002

Constraints on the source of short-term motion adaptation in macaque area MT. II. tuning of neural circuit mechanisms.

Neurons in area MT, a motion-sensitive area of extrastriate cortex, respond to a step of target velocity with a transient-sustained firing pattern. The transition from a high initial firing rate to a lower sustained rate occurs over a time course of 20-80 ms and is considered a form of short-term adaptation. In the present paper, we compared the tuning of the adaptation to the neuron's tuning to direction and speed. The tuning of adaptation was measured with a condition/test paradigm in which a testing motion of the preferred direction and speed of the neuron under study was preceded by a conditioning motion: the direction and speed of the conditioning motion were varied systematically. The response to the test motion depended strongly on the direction of the conditioning motion. It was suppressed in almost all neurons by conditioning motion in the same direction and could be either suppressed or enhanced by conditioning motion in the opposite direction. Even in neurons that showed suppression for target motion in the nonpreferred direction, the adaptation and response direction tuning were the same. The speed tuning of adaptation was linked much less tightly to the speed tuning of the response of the neuron under study. For just more than 50% of neurons, the preferred speed of adaptation was more than 1 log unit different from the preferred response speed. Many neurons responded best when slow motions were followed by faster motions (acceleration) or vice versa (deceleration), suggesting that MT neurons may encode information about the change of target velocity over time. Finally, adaptation by conditioning motions of different directions, but not different speeds, altered the latency of the response to the test motion. The adaptation of latency recovered with shorter intervals between the conditioning and test motions than did the adaptation of response size, suggesting that latency and amplitude adaptation are mediated by separate mechanisms. Taken together with the companion paper, our data suggest that short-term motion adaptation in MT is a consequence of the neural circuit in MT and is not mediated by either input-specific mechanisms or intrinsic mechanisms related to the spiking of individual neurons. The circuit responsible for adaptation is tuned for both speed and direction and has the same direction tuning as the circuit responsible for the initial response of MT neurons.

Acceleration↗
PubMed2003

Adaptation in pheromone-sensitive trichoid sensilla of the hawkmoth Manduca sexta.

In extracellular tip recordings from long trichoid sensilla of male Manduca sexta moths, we studied dose-response relationships in response to bombykal stimuli of two different durations in the adapted and the non-adapted state. Bombykal-responsive cells could be distinguished from non-bombykal-sensitive cells in each trichoid sensillum because the bombykal-responsive cell always generated the action potentials of larger initial amplitude. The bombykal cell, which was recorded at a defined location within a distal flagellar annulus, can resolve at least four log(10)-units of pheromone concentrations but is apparently unable to encode all stimulus durations tested. Parameters of the amplitude-modulated sensillar potential and the frequency-modulated action potential responses were examined in different states of adaptation. Evidence is presented for the existence of several mechanisms of adaptation, which affect distinct steps of the transduction cascade. After adapting pheromone stimuli, the sensillar potential rises to a lower amplitude and declines faster compared with the non-adapted response. In addition, the frequency of the adapted action potential response is reduced. Only the time of rise of the sensillar potential is differentially affected by adapting pheromone stimuli of different duration. The time of rise does not increase after short, but only after long, adapting stimuli. Both short and long adapting stimuli shift the dose-response curves of the sensillar potential amplitude, as well as the initial slope of its rising phase, to higher stimulus concentrations by approximately one log(10)-unit. The shift in the dose-response curve of the action potential response is larger than for the sensillar potential response, suggesting that an additional adaptation mechanism acts at the level of action potential generation. Furthermore, a faster decline of the sensillar potential after short and long adapting stimuli suggests that the resting potential of the olfactory receptor neuron is stabilized.

Action Potentials↗
PubMed1999

Impaired odor adaptation in olfactory receptor neurons after inhibition of Ca2+/calmodulin kinase II.

Odor adaptation in vertebrate olfactory receptor neurons (ORNs) is commonly attributed to feedback modulation caused by Ca(2+) entry through the transduction channels, but it remains unclear and controversial whether this Ca(2+)-mediated adaptation resides in the cAMP-gated channel alone or whether other molecules of the transduction cascade are modulated as well. Attenuation of adenylyl cyclase activity by Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) has also been proposed as a mechanism for adaptation. To test this in intact ORNs, we have compared the properties of adaptation induced by a sustained (8 sec) or brief (100 msec) odor stimulus. Although adaptation induced by both types of stimuli occurs downstream from the odor receptors and is Ca(2+)-dependent, only adaptation induced by a sustained pulse involves alterations in the odor response kinetics, consistent with a reduction in the rate of adenylyl cyclase activation. By disrupting CaMKII to block adenylyl cyclase attenuation using a specific peptide inhibitor of CaMKII, autocamtide-2-related inhibitory peptide (AIP), we show that this reaction is necessary for odor adaptation in vivo. With CaMKII disrupted, adaptation induced by a sustained stimulus is significantly impaired: the onset rate of adaptation is decreased by threefold, and the recovery rate from adaptation is increased by up to sixfold. In contrast, adaptation induced by a brief odor pulse is unaffected, demonstrating that the effect of AIP must be highly specific. The results indicate that CaMKII controls the temporal response properties of ORNs during odor adaptation. We propose that CaMKII plays a prominent role in odor perception.

Adaptation, Physiological↗
PubMed1991

Visual adaptation and the cone flicker electroretinogram.

This study examined the hypothesis that changes in the response properties of the human cone ERG during light adaptation represent the recovery of cone system responsiveness toward a dark-adapted value after an initial decrease in responsiveness at adapting field onset. The electroretinographic (ERG) responses to 31.1 Hz flicker were obtained under both dark-adapted and light-adapted conditions for stimulus luminances ranging from -1.42(-)+0.82 log cd sec/m2. At low stimulus luminances, flicker ERG amplitudes were larger under dark-adapted than under light-adapted conditions, consistent with the hypothesis. However, at high stimulus luminances, flicker ERG amplitudes obtained under light-adapted conditions were approximately double those recorded from the dark-adapted eye. Therefore, the increase in cone ERG amplitude that occurs during light adaptation at high stimulus luminances does not represent a return toward a dark-adapted level but instead entails a substantial enhancement above the dark-adapted value, by a mechanism that is presently unidentified.

Adult↗
PubMed1994

[The repair of UV-induced postreplication DNA gaps in Escherichia coli cells adapted to methylmethane sulfonate and ethylmethane sulfonate].

The survival (only after the adaptation to methylmethane sulfonate, MMS) and repair of DNA postreplication gaps in UV-irradiated Escherichia coli, adapted to MMS (20 mkg/ml for 3 h) and ethylmethane sulfonate (EMS, 100 mkg/ml for 3 h), have been investigated. The survival of MMS-adapted bacteria of wild strains B/r and K12 AB1157 somewhat increased, whereas the survival of AB1886 uvrA mutant, which unlike the wild type bacteria is unable to excise cyclobutane pyrimidine dimers, was seen to decrease. The repair of postreplicative gaps in MMS-adapted bacteria correlates qualitatively with changes in survival: in B/r and AB1157 strains the repair is somewhat more effective (10-15%), while in AB1886 uvrA mutant significantly slower (near 30%) than in non-adapted bacteria. Similar changes of postreplicative repair (PRR) of DNA are observed in AB1157 and AB1886 uvrA strains adapted to EMS. It is suggested that the decreased efficiency of PRR in bacteria AB1886 uvrA, adapted to alkylating agent, may be due to the interference between the two inducible repair processes: adaptive response and SOS response. The latter process is involved in the repair of some part of postreplicative gaps of DNA. Different results of PRR of DNA in bacteria of wild types, adapted to MMS and EMS, may be associated with the intrinsic PRR in uvr+ strains. Due to this process in uvr+ bacteria SOS component of PRR of DNA is not formed. It is suggested that PRR in uvr+ bacteria adapted to alkylating agents is accelerated by enzymes of adaptive response in the absence of antagonism between the SOS response and the adaptive response.

Adaptation, Physiological↗
PubMed2006

Dual adaptation to sensory conflicts during whole-body rotations.

A dual adaptation paradigm was used in order to study the adaptation to two conditions of conflicting visual and kinesthetic and vestibular information. Adaptation was induced in humans by modifying visual information during whole-body rotations with the help of a virtual reality set-up. Real rotations' amplitudes were factored by a gain of 0.5 or 1.5. The two conditions were associated to a visual context cue. The aim of the experiment was to provide support for either the feedback or the feedforward model of adaptive states switch. Results show that subjects could adapt to the two conditions of conflict during whole-body rotations. However, the two conflict situations have been found to differ both in their motor dynamics and in their susceptibility to adaptation, as it seems that the adaptation is more complete in the condition of gain 1.5, i.e., faster and more precise. Subjects could be divided into two groups according to their ability to use contextual information to switch between adaptive gains. The visual cues were sufficient for some subjects to switch adaptive state, which corresponds to a context-dependent dual adaptation, or feedforward model of switching. Other subjects showed a switch cost maintained across the experiment, corresponding with a stimulus-dependent adaptation, or feedback model of switching. We are suggesting that the process enabling switching between adaptive states depends on subjects' abilities to use contextual cues of certain types, and thus on their "perceptive styles". This could explain the variability of results obtained in the literature.

Acclimatization↗
PubMed2001

Inhibition of oxidative DNA repair in cadmium-adapted alveolar epithelial cells and the potential involvement of metallothionein.

This study evaluated the effects of cadmium (Cd) adaptation in cultured alveolar epithelial cells on oxidant-induced DNA damage and its subsequent repair. Using the comet assay, we determined that lower levels of DNA damage occurred in Cd-adapted cells compared with non-adapted cells following treatment of cells with hydrogen peroxide (H(2)O(2)). This may be a consequence of increased thiol-containing antioxidants that were observed in adapted cells, including metallothionein and glutathione. Cd-adapted cells were, however, less efficient at repairing total oxidative DNA damage compared with non-adapted cells. Subsequently, we investigated the effect of Cd adaptation on the repair of particular oxidized DNA lesions by employing lesion-specific enzymes in the comet assay, namely formamidopyrimidine DNA glycosylase (Fpg), an enzyme that predominantly repairs 8-oxoguanine (8-oxoG), and endonuclease III, that is capable of repairing oxidized pyrimidines. The data demonstrated that adaptation to Cd results in significantly impaired repair of both Fpg- and endonuclease III-sensitive lesions. In addition, in situ detection of 8-oxoG using a recombinant monoclonal antibody showed that Cd-adaptation reduces the repair of this oxidative lesion after exposure of cells to H(2)O(2). Activities of 8-oxoG-DNA glycosylase and endonuclease III were determined in whole cell extracts using 32P-labeled synthetic oligonucleotides containing 8-oxoG and dihydrouracil sites, respectively. Cd adaptation was associated with an inhibition of 8-oxoG-DNA glycosylase and endonuclease III enzyme activity compared with non-adapted cells. In summary, this study has shown that Cd adaptation: (1) reduces oxidant-induced DNA damage; (2) increases the levels of key intracellular antioxidants; (3) inhibits the repair of oxidative DNA damage.

Animals↗
PubMed2003

Flexibility of vestibulo-ocular reflex adaptation to modified visual input in human.

The vestibulo-ocular reflex (VOR) serves to keep images relatively stable on the retina. To maintain appropriate performance and minimize image slip throughout life, VOR is subjected to long-term adaptive regulation by visual input. It has been reported that adaptive changes in VOR gain (eye velocity/head velocity) are evoked either by fitting subjects with magnifying, miniaturizing, or reversing spectacles during normal behavior, or by moving a large visual field in or out of phase relative to the subject's head movement. The changes in VOR gain are frequency selective. Here, we examine the extent of VOR gain flexibility by causing VORs of similar direction to undergo different behavioral gain changes. Nine healthy adults participated in the study, ranging in age from 24 to 38 years (mean: 26 years) and with no history of neurotological symptoms. All subjects were clinically normal according to a screening battery that included combined neurologic and otologic physical examinations. Horizontal and vertical eye positions were recorded by bitemporal DC-coupled electro-oculography (EOG). The subject sat in a rotating chair. The axis of rotation of the body was always earth-vertical, with the interaural axis crossing the axis of rotation of the chair. The head was pointed 20 degrees downwards in all experiments and stabilized in this position using a chin rest. The chair was surrounded by a half-cylindrical optokinetic screen (78 cm in diameter) placed in front of the subject, onto which random dot patterns were projected. Goggles were used to ensure that the subject was in complete darkness during both pre- and postadaptation periods. The chair was rotated sinusoidally at maximum amplitude of 30 degrees or 60 degrees : for 30 degrees the stimulation was at 0.1, 0.2, 0.3, and 0.4 Hz; for 60 degrees it was at 0.1, 0.2, and 0.3 Hz. VOR adaptation was obtained by inducing a retinal slip velocity by short-term alteration of the visual input of the large field; this change was produced by a combination of sinusoidal head rotation and the random dot patterns. In each adaptation session, the sinusoidal head rotation was either at 0.1 or 0.3 Hz and the amplitude was 30 degrees. The random dot pattern was synchronized with sinusoidal head rotation in the same direction (x0 experiment) to make the retinal slip zero, and in the opposite direction to make the retinal slip twofold (x2 experiment). Therefore, a total of four adaptation protocols were tested. The subjects were asked to fixate on a single dot with the eyes straight-ahead in the x0 experiment, and follow it within random dot patterns in the x2 experiment. Each adaptation session lasted for 30 min. Two adaptation experiments were performed on each subject once per day. The averages of VOR gain and phase lag were calculated using Fourier analysis. Seven of the subjects who participated in the x2 adaptation experiment at 0.3 Hz and 30 degrees amplitude showed a steady increase of VOR gain within a couple of trials. One of the remaining two subjects showed a decrease in VOR gain in all the three trials, and the other subject showed a VOR gain increase in three trials and decrease in two trials. In the x2 adaptation experiment at 0.3 Hz and 30 degrees amplitude (peak velocity: 28 degrees /s), the percentage gain change ((post-pre)/pre) was 133% at the same stimulation and 100% at 0.4 Hz (peak velocity: 37 degrees /s). The gain change was 65% at 0.1 Hz and 60 degrees amplitude (peak velocity: 18 degrees /s), and 64% at 0.2 Hz and 60 degrees amplitude (peak velocity: 37 degrees /s). In the x1 adaptation experiment (30 degrees at 0.3 Hz), the percentage gain change was -62% under the same conditions, -50% at 0.1 Hz and 60 degrees amplitude, and -30% at 0.2 Hz and 60 degrees amplitude. No change of VOR gain was observed at other frequencies, and the subject was not adapted at 0.1 Hz and 30 degrees amplitude. The larger VOR gain increase in the x2 adaptation experiment for the faster head angular acceleration leads to the conclusion that the VOR gain mechanism can set vuite similar in terms of the head acceleration.

Adult↗
PubMed1994

The duration of the motion aftereffect following adaptation to first-order and second-order motion.

The magnitude of the motion aftereffect (MAE) obtained following adaptation to first-order or to second-order motion was measured by estimating its duration. The second-order adaptation stimulus was composed of contrast-modulated noise produced by multiplying two-dimensional (2-D) noise by a drifting 1 cycle deg-1 sine grating. The first-order adaptation stimulus was composed of luminance-modulated noise produced by summing, rather than multiplying, the noise and the sine grating. The test stimuli were directionally ambiguous motion patterns composed of either two oppositely drifting sine gratings added to noise or the contrast-modulated equivalent. The adaptation and test stimuli were equated for visibility by presenting them at the same multiple of direction-identification threshold. All possible combinations of first-order and second-order adaptation and test stimuli were examined in order to compare the magnitudes of the MAEs obtained following same adaptation and cross adaptation. After adaptation the test stimuli always appeared to drift coherently in the direction opposite to that of adaptation and the magnitudes of this MAE were very similar for all conditions examined. Statistical analyses of the results showed that there was no significant difference between the durations of the MAEs obtained in the same-adaptation and cross-adaptation conditions. The cross-adaptation effects suggest that either first-order or second-order motion are detected by a common low-level mechanism, or that separate parallel motion-detecting mechanisms exist, for the two types of motion, that interact at some later stage of processing.

Humans↗
PubMed1998

Cross-adaptation and molecular modeling study of receptor mechanisms common to four taste stimuli in humans.

Psychophysical cross-adaptation experiments were performed with two carbohydrates, sucrose (SUC) and fructose (FRU), and two sweeteners, acesulfame-K (MOD) and dulcin (DUL). Seven subjects were asked to match concentrations that elicited the same intensity as a sucrose reference (30 g/l). Cross-adaptation levels were calculated as the ratio of isointense concentrations measured for a given stimulus before and under adaptation. On average, cross-adaptation between SUC and FRU is low and apparently reciprocal. By contrast, cross-adaptation between SUC and MOD is clearly non-reciprocal: SUC adapts MOD significantly (24%, P < 0.005), but MOD fails to adapt SUC (2%, P < 0.79). Significant and reciprocal cross-enhancement is observed between DUL and MOD (approximately -20%, P < 0.03), and also between SUC and DUL (approximately -15%, P < 0.08). In parallel, molecular modeling of the four tastants was performed in order to look for the 12 common binding motifs that were isolated on 14 other tastants in a previous study. SUC and FRU each display 10 out of the 12 binding motifs, whereas DUL and MOD only display four and five distinct motifs respectively and do not have any motif in common. Experimental cross-adaptation levels seem to correlate well with the number of motifs that molecules have in common. FRU and SUC share a majority of binding motifs and correlatively show mutual cross-adaptation. Four motifs of MOD are found among the 10 motifs of SUC, which may explain why SUC cross-adapts MOD but not vice versa. By contrast, DUL and MOD do not share any motif and do not cross-adapt. The various molecular mechanisms that may be responsible for cross-adaptation and/or cross-enhancement are discussed in light of our results.

Female↗
PubMed1976

[The role of ketone bodies in nonshivering thermogenesis in cold-adapted rats (author's transl)].

In spite of the ill fame of useless products of metabolism that only accumulate in the blood under abnormal conditions, ketone bodies (KB) have now regained the fame as an important fuel of respiration for the brain and muscles in prolonged starvation in humans and other animals. In cold-adapted animals, ketosis has been well documented, but little is known about the physiological role of KB in cold adaptation. In this study, role of KB in nonshivering thermogenesis was investigated in warm- and cold-adapted rats with or without norepinephrine (NE) loads, a decisive lipid metabolizing hormone in cold adaptation. First, levels of blood KB and plasma free fatty acid (FFA) and FFA turnover rate were examined along with rectal temperature under continuous infusions of various doses of NE. Good dose-response relationship of rectal temperature was obtained with increasing doses of NE in cold-adapted rats, but not in warm-adapted ones. The levels of blood KB and plasma FFA in cold-adapted rats remained almost unaltered during the observation period of 30 minutes. Infusion of NE, however, greatly enhanced FFA turnover rate in cold-adapted rats as compared with controls. Next, fractional turnover rate and half-life of beta-OH-butyrate were obtained from decay curves of endogenous beta-OH-butyrate, using functionally eviscerated rats in which no KB were produced. Calculated turnover rate of KB was also found significantly increased in cold-adapted rats. Finally, the effect of NE on the production of KB was examined using the liver in situ perfusion technique of Mortimore with minor modifications. Viability of the liver preparation was guaranteed by sufficiently high rates of bile production as well as oxygen consumption. The production rate of KB in the preparation under palmitate loads of physiological medium concentration was significantly higher in cold-adapted rats than in warm-adapted controls. However, no significant effect of NE loaded simultaneously was observed in either group. Quantitative analysis shows that the turnover rate of KB in vivo essentially equals the production rate in the perfused liver when no exogenous NE is added. In contrast NE infusion the turnover rate in vivo was almost doubled that of the perfused liver. All these results indicate KB are used as an important energy source with the significancy of FFA in nonshivering thermogenesis. Moreover, it may be surmised that production of KB in vivo, particulary in the cold-adapted state, is effected by other unknown factors than NE.

Acclimatization↗
PubMed1981

Receptive fields of frog retinal ganglion cells: response formation and light-dark-adaptation.

1. The excitatory and inhibitory receptive field mechanisms of retinal ganglion cells were studied by extracellular recording from the eyecup of Rana temporaria in order to elucidate the nature of adaptational changes in the functioning of the receptive field. 2. The responses to large stimuli were always strongly depressed relative to responses evoked by smaller spots. This was true even in the fully dark-adapted state and at the very lowest stimuli intensities. 3. Threshold measurements confirmed earlier findings, usually revealing the surround only in light-adapted states. However, in more than 10% of fully dark-adapted cells thresholds to large stimuli were significantly elevated. 4. The central summation area of the receptive field was found to shrink with light-adaptation. There was a gradual decrease in diameters, amounting to some 20-30%, from the dark-adapted, rod-determined receptive fields to the cone-determined ones. 5. Adaptation by bleaching and adaptation by backgrounds changed the effects of the surround in different ways. After a rhodopsin bleach the transition from a light-adapted to a dark-adapted situation was seen as an abrupt drop of large-stimulus thresholds at some time during adaptation. Steady backgrounds produced no such dramatic changes, but the increment threshold lines were somewhat steeper with test spots stimulated the surround than with smaller spots. 6. Although the discharge patterns generally show the strength of the surround influence, they underwent no qualitative change at the time of the drop of large-stimulus thresholds after a bleach. 7. It is suggested that the drop does not reflect a sudden reorganization of the receptive field, but is the consequence of the different ways the response to large stimuli are formed in different ranges of stimulus intensity (pre-inhibitory at high intensities, post-inhibitory at low intensities), and of gradual changes in signal dynamics.

Action Potentials↗
PubMed2025

Genome-wide Parallelism Underlies Rapid Freshwater Adaptation Fueled by Standing Genetic Variation in a Wild Fish.

A fundamental focus of ecological and evolutionary biology is determining how natural populations adapt to environmental changes. Rapid parallel phenotypic evolution can be leveraged to uncover the genetics of adaptation. Using population genomic approaches, we investigated the genetic architecture underlying rapid parallel freshwater adaptation of Neosalanx brevirostris by comparing four freshwater-resident populations with their common ancestral anadromous population. We demonstrated that the rapid parallel adaptation to freshwater followed a complex polygenic architecture and was characterized by genomic-level parallelism, which proceeded predominantly through repeated selection on the preexisting standing genetic variations. Frequencies of the genome-wide adaptive standing variations were moderate in the ancestral anadromous population, which had pre-adapted to fluctuating salinities. Relatively large allele frequency shifts were observed at some adaptive single-nucleotide polymorphisms (SNPs) during parallel adaptation to freshwater environments, with a large fraction of freshwater-favored alleles being fixed or nearly fixed. These adaptive SNPs were involved in multiple biological functions associated with osmoregulation, immunoregulation, locomotion, metabolism, etc., which were highly consistent with the polygenic architecture of adaptive divergence between the two ecotypes involving multiple complex physiological and behavioral traits. This work provides insight into the mechanisms by which natural populations rapidly evolve to changes in the environment and highlights the importance of standing genetic variation for the evolutionary potential of populations facing global environmental changes.

Animals↗
PubMed1992

Adaptive response of Vibrio cholerae and Escherichia coli to nitrofurantoin.

Pretreatment with sublethal doses of nitrofurantoin induced adaptive response in both Vibrio cholerae and Escherichia coli cells as indicated by their greater resistance to the subsequent challenging doses of the same drug. Adaptive response was maximum corresponding to pretreatment drug concentrations of 0.40 microgram/ml and 0.015 microgram/ml respectively for V. cholerae OGAWA 154 (wild type) and E. coli K-12 AB 2463 (recA-) cells. Adaptive response was inhibited by chloramphenicol (100 micrograms/ml) indicating the need of concomitant protein synthesis. Induction of adaptive response in recA deficient E. coli cells indicated that it was different from the conventional "SOS" response. Melting temperature of DNA of V. cholerae cells subjected to adaptive (0.4 microgram/ml for 1 hr) and challenging (120 micrograms/ml for 1 hr) doses of nitrofurantoin (76 degrees C) was closer to that of native DNA (75 degrees C) vis-a-vis DNA isolated from nonadapted and drug treated cells (77.5 degrees C). Also, DNA isolated from V. cholerae cells subjected to adaptive and challenging doses of the drug revealed the presence of fewer interstrand cross-links (16% reversible DNA) vis-a-vis DNA from nonadapted but drug treated cells (55% reversible DNA). Photomicrographic studies revealed that V. cholerae cells that were nonadapted but drug treated grew into long filamentous forms (4.25 +/- 2.97 micron) whereas those subjected to both adaptive and challenge doses of the drug exhibited much less filamentation (2.08 +/- 0.84 micron) vis-a-vis native cells (1.42 +/- 0.5 micron). Similar results on DNA melting temperature, cross-links in DNA, and filamentation of cells were obtained for E. coli AB 2463 (recA-) cells subjected to adaptive and challenging treatments with nitrofurantoin. Almost equal degree of resistance against nitrofurantoin could be induced in both V. cholerae OGAWA 154 (wild type) and E. coli strain PJ3 (AB 1157 ada-) when these cells were pretreated with nontoxic doses of hydrogen peroxide or nitrofurantoin. Evidence obtained in this work on the nature of the nitrofuratoin induced adaptive response with particular references to the oxidative and/or alkylating DNA damages were discussed. Nitrofuratoin induced adaptive response appeared similar to that elicited by furazolidone in V. cholerae cells and appeared to be directed towards oxidative and not alkylating adaptive repair pathway.

Adaptation, Physiological↗
PubMed1996

Adaptation to ozone in rats and its association with ascorbic acid in the lung.

Ozone (O3) adaptation is a well-known, but poorly understood phenomenon that has been demonstrated in humans and laboratory animals. This study examined pulmonary function and bronchoalveolar lavage fluid (BALF) parameters in O3-adapted F-344 rats to explore possible mechanisms of adaptation. Of particular interest was ascorbic acid (AA), an antioxidant reported to be protective against O3 injury and found to be increased in O3-adapted rats. Adaptation was induced by exposure to 0.25 ppm O3, 12 hr/day for 6 or 14 weeks and evaluated with a challenge test, one that reexposed rats to 1.0 ppm O3 and measured attenuation in the O3 effect on frequency of breathing. Pulmonary function was assessed 1 day postexposure and adaptation and BALF were evaluated 1, 3, and 7 days postexposure. Results showed that forced vital capacity increased over time but decreased due to exposure and that the 14-week, O3-exposed rats had an increase in forced expiratory flow rate. All of the O3-exposed rats that were tested demonstrated adaptation on Postexposure Days 1, 3, and 7, but it was diminished on Day 7. Adaptation was also more pronounced in rats exposed for 14 weeks. Except for AA, BALF levels of total protein, potassium, lysozyme, uric acid, and alpha-tocopherol were unaffected by O3 exposure. Lactic acid dehydrogenase, alkaline phosphatase, glucose-6-phosphate dehydrogenase, and total glutathione were also assayed but were always below detectable limits. Ascorbic acid concentrations were elevated on Days 1, 3, and 7, showing postexposure patterns similar to those found for adaptation. Significant correlation was found between AA concentration and the magnitude of adaptation (r = 0.91, p < 0.002). We conclude that AA may play an important role in mechanisms associated with O3 adaptation in rats.

Adaptation, Physiological↗
PubMed1998

Context-specific short-term adaptation of the phase of the vestibulo-ocular reflex.

The phase of the angular vestibulo-ocular reflex (VOR) is subject to adaptive control. We had previously found that adapting the phase of the VOR also produced changes in drift on eccentric gaze-holding, implying a change in the time constant of the velocity-to-position neural integrator. Here we attempted to dissociate changes in gaze-holding drift from changes in the phase of the VOR. In normal human subjects, for 2 h, we alternated 5 min of VOR phase adaptation (sinusoids, 0.2 Hz) with 5 min of making saccades in the light with the head stationary. Afterwards, changes in VOR phase were the same (32% of requested) as those obtained with 1 h of phase adaptation alone, but changes in drift following saccades were much smaller than those found after phase adaptation alone (0.8 degrees/s compared with 5 degrees/s). When measuring drift after VOR steps, however, the changes were closer to those found after phase adaptation alone (3.8 degrees/s). To test the relationship between gaze-holding drift after VOR steps and adaptive changes in VOR phase, we alternated sinusoidal VOR phase adaptation with normal VOR steps in the light. In this paradigm, the adaptive change in VOR phase was about the same as with phase-adaptation alone (35%), but there was now little drift after saccades (1.9 degrees/s) or after VOR steps (0.7 degrees/s). We conclude that the state of the velocity-to-position neural integrator can be altered selectively and rapidly depending upon the task required. Such context-specific adaptation is advantageous, because it allows adjustment of the phase of the VOR without degrading the ability to hold eccentric fixation.

Adaptation, Physiological↗