Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ADAPTATION”

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.

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

At least 649 records · Page 36Linked to original sources

Adaptation in single units in visual cortex: the tuning of aftereffects in the temporal domain.

Adaptation-induced changes in the temporal-frequency tuning and direction selectivity of cat visual cortical cells were studied. Aftereffects were induced largely independent of direction. Adapting in either direction reduced responses in both directions. Aftereffects in the direction opposite that adapted were only slightly weaker than were aftereffects in the adapted direction. No cell showed any enhancement of responses to drifting test stimuli after adapting with moving gratings. Adapting in a cell's null direction usually had no effect. Dramatic differences between the adaptation characteristics of moving and stationary stimuli were observed, however. Furthermore, aftereffects were temporal frequency specific. Temporal frequency-specific aftereffects were found in both directions: adapting in one direction induced frequency-specific effects in both directions. This bidirectionality of frequency-specific aftereffects applied to the spatial domain as well. Often, aftereffects in the direction opposite that adapted were more narrowly tuned. In general, adaptation could shift a cell's preferred temporal frequency. Aftereffects were most prominent at high temporal frequencies when testing in the adapted direction. Aftereffects seemed to be more closely linked to temporal frequency than to velocity matching. These results constrain models of cortical connectivity. In particular, we argue against schemes by which direction selectivity is generated by inhibiting a cell specifically when stimulated in the nonpreferred direction. Instead, we argue that cells receive bidirectional spatially and temporally tuned inputs, which could combine in spatiotemporal quadrature to produce direction selectivity.

Adaptation, Physiological↗

Orientation-selective adaptation to crowded illusory lines.

Visual adaptation has been successfully used as a psychophysical tool for studying the functional organisation of visual awareness. It has been shown that orientation-selective adaptation to a grating pattern occurs in crowded conditions. In such conditions, simultaneous presentation of flanking distractors pushes the target stimulus out of conscious perception and severely impairs orientation discrimination in the periphery of the visual field. In the present study, orientation-selective adaptation to illusory lines induced by two line gratings abutting each other with a phase shift was examined in crowded and non-crowded conditions. To rule out the effects of lower level adaptations we used an animation paradigm in which the orientations of the two line gratings were altered repeatedly during adaptation phase without any change in the orientation of the resulting illusory line. Although performance of subjects in reporting the orientation of crowded illusory lines was at chance level, orientation-selective adaptation was preserved for crowded as well as non-crowded adapting targets. Two control experiments demonstrated that adaptation to endpoints of real lines at the location of abutting grating lines had minimal effect on the adaptation to illusory lines; and changes in the configuration of endpoints could not be responsible for better performance when adapting and test stimuli were different. We conclude that a crowding effect occurs after illusory lines have been processed in the visual stream. Since illusory lines seem to be represented at relatively early stages of visual processing (e.g. area V2), adaptation to crowded illusory stimuli suggests that neuronal activation in those early stages is not necessarily correlated with conscious perception.

Adaptation, Ocular↗

Two temporal phases of light adaptation in retinal rods.

Vertebrate rod photoreceptors adjust their sensitivity as they adapt during exposure to steady light. Light adaptation prevents the rod from saturating and significantly extends its dynamic range. We examined the time course of the onset of light adaptation in bullfrog rods and compared it with the projected onset of feedback reactions thought to underlie light adaptation on the molecular level. We found that adaptation developed in two distinct temporal phases: (1) a fast phase that operated within seconds after the onset of illumination, which is consistent with most previous reports of a 1-2-s time constant for the onset of adaptation; and (2) a slow phase that engaged over tens of seconds of continuous illumination. The fast phase desensitized the rods as much as 80-fold, and was observed at every light intensity tested. The slow phase was observed only at light intensities that suppressed more than half of the dark current. It provided an additional sensitivity loss of up to 40-fold before the rod saturated. Thus, rods achieved a total degree of adaptation of approximately 3,000-fold. Although the fast adaptation is likely to originate from the well characterized Ca(2+)-dependent feedback mechanisms regulating the activities of several phototransduction cascade components, the molecular mechanism underlying slow adaptation is unclear. We tested the hypothesis that the slow adaptation phase is mediated by cGMP dissociation from noncatalytic binding sites on the cGMP phosphodiesterase, which has been shown to reduce the lifetime of activated phosphodiesterase in vitro. Although cGMP dissociated from the noncatalytic binding sites in intact rods with kinetics approximating that for the slow adaptation phase, this hypothesis was ruled out because the intensity of light required for cGMP dissociation far exceeded that required to evoke the slow phase. Other possible mechanisms are discussed.

3',5'-Cyclic-GMP Phosphodiesterases↗

An essential role of the antioxidant gene Bcl-2 in myocardial adaptation to ischemia: an insight with antisense Bcl-2 therapy.

Reperfusion of ischemic myocardium results in apoptotic cell death, which can be blocked by adapting the heart to ischemic stress induced by cyclic episodes of brief periods of ischemia and reperfusion. In concert, the antiapoptotic gene bcl-2 is decreased by ischemia/reperfusion, but increased in the ischemically adapted myocardium. To examine if bcl-2 plays a crucial role in cardioprotection, adaptive cardioprotection was further examined in the hearts treated with antisense bcl-2 oligodeoxynucleotides (ODN). Isolated Langendorff-perfused rat hearts were divided into three groups: control (perfused with Krebs-Henseleit bicarbonate buffer for 210 min); 30-min ischemia followed by 2-h reperfusion; ischemic adaptation followed by 30-min ischemia and 2-h reperfusion. The last (adapted heart) group was subdivided into another two groups: one was transfected 48 h earlier with antisense bcl-2 ODN, whereas the other group was transfected with sense bcl-2 ODN. Cardioprotection was examined by determining cardiomyocyte death due to necrosis and apoptosis. Antisense gene therapy almost completely abolished bcl-2 protein expression in the hearts. Bcl-2 mRNA was down-regulated in the ischemic/reperfused heart, but up-regulated in the adapted myocardium. Adapted myocardium showed decreased infarct size and reduced number of apoptotic cardiomyocytes. Ischemia/reperfusion resulted in increased oxidative stress as evidenced by increased malonaldehyde formation. Adapted myocardium had a reduced amount of malonaldehyde. Antisense bcl-2 ODN completely abolished the cardioprotective effects of adaptation by eliminating the antideath signal of bcl-2. In concert, reduced oxidative stress in the adapted myocardium no longer persisted. The results suggest an antioxidant role of bcl-2 that appeared to be essential for the cardioprotection achieved by ischemic adaptation.

Adaptation, Physiological↗

Divergent evolution during an experimental adaptive radiation.

How repeatable a process is evolution? Comparative studies of multicellular eukaryotes and experimental studies with unicellular prokaryotes document the repeated evolution of adaptive phenotypes during similar adaptive radiations, suggesting that the outcome of adaptive radiation is broadly reproducible. The goal of this study was to test this hypothesis by using phenotypic traits to infer the genetic basis of adaptation to simple carbon-limited environments in an extensive adaptive radiation. We used a clone of the bacterium Pseudomonas fluorescens to found two sets of experimental lines. The first set of lines was allowed to adapt to one of 23 novel environments for 1100 generations while the second set of lines was allowed to accumulate mutations by drift for 2000 generations. All lines were then assayed in the 95 environments provided by Biolog microplates to determine the phenotypic consequences of selection and drift. Replicate selection lines propagated in a common environment evolved similar adaptive components of their phenotype but showed extensive variation in non-adaptive phenotypic traits. This variation in non-adaptive phenotypic traits primarily resulted from the ascendance of different beneficial mutations in different lines. We argue that these results reconcile experimental and comparative approaches to studying adaptation by demonstrating that the convergent phenotypic evolution that occurs during adaptive radiation may be associated with radically different sets of beneficial mutations.

Adaptation, Biological↗

Long-lasting modifications of saccadic eye movements following adaptation induced in the double-step target paradigm.

The adaptation of saccadic eye movements to environmental changes occurring throughout life is a good model of motor learning and motor memory. Numerous studies have analyzed the behavioral properties and neural substrate of oculomotor learning in short-term saccadic adaptation protocols, but to our knowledge, none have tested the persistence of the oculomotor memory. In the present study, the double-step target protocol was used in five human subjects to adaptively decrease the amplitude of reactive saccades triggered by a horizontally-stepping visual target. We tested the amplitude of visually guided saccades just before and at different times (up to 19 days) after the adaptation session. The results revealed that immediately after the adaptation session, saccade amplitude was significantly reduced by 22% on average. Although progressively recovering over days, this change in saccade gain was still statistically significant on days 1 and 5, with an average retention rate of 36% and 19%, respectively. On day 11, saccade amplitude no longer differed from the pre-adaptation value. Adaptation was more effective and more resistant to recovery for leftward saccades than for rightward ones. Lastly, modifications of saccade gain related to adaptation were accompanied by a decrease of both saccade duration and peak velocity. A control experiment indicated that all these findings were specifically related to the adaptation protocol, and further revealed that no change in the main sequence relationships could be specifically related to adaptation. We conclude that in humans, the modifications of saccade amplitude that quickly develop during a double-step target adaptation protocol can remain in memory for a much longer period of time, reflecting enduring plastic changes in the brain.

Adaptation, Physiological↗

Adaptation of rat olfactory bulb neurones.

1. Single-unit activity was recorded from olfactory bulb neurones driven by odorous stimuli. Neural responses were quantified as averaged peristimulus time histograms. 2. Successive presentations of the same stimulus evoked similar patterns of activity during each presentation. Some neurones exhibited increased and others decreased excitability in the adapted state. The occurrence of such facilitative or suppressive self-adaptation was not determined by odorant concentration or by the number of action potentials evoked by a given stimulus. Neurones driven by more than one odorant exhibited the same type of adaptation (facilitative or suppressive) for all effective stimuli. 3. When the first odorant differed from the second, the number but not the pattern of action potentials evoked by the second odorant differed from the non-adapted state. Some neurones exhibited increased and others decreased excitability in the cross-adaptation state. Neurones exhibiting suppressive self-adaptation did not exhibit facilitative cross-adaptation and those exhibiting facilitative self-adaptation did not exhibit suppressive cross-adaptation. Instances of asymmetrical cross-adaptation were noted in which two odorants differed in the extent to which they affected subsequent sensitivity to each other. The degree of symmetry for a given pair of odorants differed for different neurones. It is concluded that neurones in the olfactory bulb differ in both the type (suppressive or facilitative) and extent of adaptation evoked by a given odorant.

1-Butanol↗

Recovering from long-term and short-term adaptation of the whole nerve action potential.

Properties of adaptation and recovery from adaptation are measured in response to adapter tones of short duration (100 ms), intermediate duration (1 m), and long duration (2-15 m). The decrease in N1 potential in response to a probe tone burst was used to assess the magnitude of adaptation. By measuring the response at different times after adapter offset the time course of recovery was assessed. By measuring the response to different probe frequencies, the spread of adaptation across place in the cochlea was assessed. Adapters of different duration showed quite different spread of adaptation across probe frequency. Short-duration adapters resulted in decrements of probe response greatest at and above probe frequency. Intermediate- and long-duration adapters showed progressively greater shifts in peak decrement to higher probe frequencies as adapter level was increased.

Action Potentials↗

Short-term adaptation of auditory receptive fields to dynamic stimuli.

Short-term adaptation and recovery from adaptation have a strong impact on the processing of dynamic stimuli. Adaptive effects on neuronal activity have been studied most commonly for changes in first-order statistics of stimuli such as stepwise increments or decrements in stimulus amplitude. However, changes in higher moment statistics, such as the variance of the amplitude distribution in visual stimuli, also can invoke pronounced adaptation behavior. We demonstrate here that neurons in the inferior colliculus (ICC) of the cat show adaptation to dynamic auditory stimuli that differ in the variance of their modulation depth distribution. In addition, it is shown that neurons show adaptation to other higher moment statistics (e.g., kurtosis) of the modulation envelope. The time course of adaptation is specific for the altered stimulus property and the direction of parameter change. The use of dynamic stimuli allows an estimate of the effects of the adaptation on the temporal response properties of the neurons. We demonstrate that temporal receptive fields of neurons undergo change during the course of adaptation. We show that adaptation to variance in the ICC has many similarities to that in the retina and suggest that adaptation to variance is a general property of sensory systems that allows them to effectively deal with a nonstationary environment.

Acoustic Stimulation↗

Orientation-selective adaptation to first- and second-order patterns in human visual cortex.

Second-order textures-patterns that cannot be detected by mechanisms sensitive only to luminance changes-are ubiquitous in visual scenes, but the neuronal mechanisms mediating perception of such stimuli are not well understood. We used an adaptation protocol to measure neural activity in the human brain selective for the orientation of second-order textures. Functional MRI (fMRI) responses were measured in three subjects to presentations of first- and second-order probe gratings after adapting to a high-contrast first- or second-order grating that was either parallel or orthogonal to the probe gratings. First-order (LM) stimuli were generated by modulating the stimulus luminance. Second-order stimuli were generated by modulating the contrast (CM) or orientation (OM) of a first-order carrier. We used four combinations of adapter and probe stimuli: LM:LM, CM:CM, OM:OM, and LM:OM. The fourth condition tested for cross-modal adaptation with first-order adapter and second-order probe stimuli. Attention was diverted from the stimulus by a demanding task at fixation. Both first- and second-order stimuli elicited orientation-selective adaptation in multiple cortical visual areas, including V1, V2, V3, V3A/B, a newly identified visual area anterior to dorsal V3 that we have termed LO1, hV4, and VO1. For first-order stimuli (condition LM:LM), the adaptation was no larger in extrastriate areas than in V1, implying that the orientation-selective first-order (luminance) adaptation originated in V1. For second-order stimuli (conditions CM:CM and OM:OM), the magnitude of adaptation, relative to the absolute response magnitude, was significantly larger in VO1 (and for condition CM:CM, also in V3A/B and LO1) than in V1, suggesting that second-order stimulus orientation was extracted by additional processing after V1. There was little difference in the amplitude of adaptation between the second-order conditions. No consistent effect of adaptation was found in the cross-modal condition LM:OM, in agreement with psychophysical evidence for weak interactions between first- and second-order stimuli and computational models of separate mechanisms for first- and second-order visual processing.

Adaptation, Physiological↗

Effect of short-term saccadic adaptation on saccades evoked by electrical stimulation in the primate superior colliculus.

The brain maintains the accuracy of visually guided movements by using visual feedback to correct for changes in the nervous system and musculature that would otherwise result in dysmetria. In monkeys, evidence suggests that an adaptive mechanism can compensate for weakness in an extraocular muscle by changing the gain of the neural signal to the weakened muscle. The visual effects of such neuromuscular changes have been simulated using a short-term saccade adaptation paradigm, in which the target spot jumps to a new location during the initial saccade. Under these circumstances, over several hundred trials, monkeys gradually change the amplitude of their saccades so that the eye lands closer to the final location of the target spot. There is considerable evidence from lesion and single-unit recording studies that the locus of such saccade adaptation is downstream of the superior colliculus in the cerebellum. Paradoxically, previous research has indicated that saccades evoked by electrical stimulation in the superior colliculus are not modified by short-term saccade adaptation, suggesting that adaptation occurs in the oculomotor system upstream of the superior colliculus or else in a pathway that bypasses the superior colliculus. We tested whether this result was due to using suprathreshold stimulation currents. Stimulating at 44 low-threshold sites in the superior colliculi of three monkeys revealed that using low current levels evoked saccades that were modified by adaptation. Adaptation for visually guided and electrically evoked saccades had similar time courses and tended to be accomplished by a reduction in saccade velocity rather than a decrease in duration. Moreover, the more similar the velocity of electrically evoked and visually guided saccades prior to the start of saccadic adaptation the greater the effect of adaptation on electrically evoked saccades. These results suggest that the superior colliculus is indeed upstream of the locus of adaptation, corroborating previous lesion and single-cell recording studies, but that the mechanism mediating saccade adaptation is sensitive to the parameters of electrical stimulation.

Adaptation, Physiological↗

Adaptation in the auditory space map of the barn owl.

Auditory neurons in the owl's external nucleus of the inferior colliculus (ICX) integrate information across frequency channels to create a map of auditory space. This study describes a powerful, sound-driven adaptation of unit responsiveness in the ICX and explores the implications of this adaptation for sensory processing. Adaptation in the ICX was analyzed by presenting lightly anesthetized owls with sequential pairs of dichotic noise bursts. Adaptation occurred in response even to weak, threshold-level sounds and remained strong for more than 100 ms after stimulus offset. Stimulation by one range of sound frequencies caused adaptation that generalized across the entire broad range of frequencies to which these units responded. Identical stimuli were used to test adaptation in the lateral shell of the central nucleus of the inferior colliculus (ICCls), which provides input directly to the ICX. Compared with ICX adaptation, adaptation in the ICCls was substantially weaker, shorter lasting, and far more frequency specific, suggesting that part of the adaptation observed in the ICX was attributable to processes resident to the ICX. The sharp tuning of ICX neurons to space, along with their broad tuning to frequency, allows ICX adaptation to preserve a representation of stimulus location, regardless of the frequency content of the sound. The ICX is known to be a site of visually guided auditory map plasticity. ICX adaptation could play a role in this cross-modal plasticity by providing a short-term memory of the representation of auditory localization cues that could be compared with later-arriving, visual-spatial information from bimodal stimuli.

Acoustic Stimulation↗

Interocular transfer of adaptation after effect in neurons of area 17 and 18 of split chiasm cats.

Responses to sinusoidal gratings for neurons in area 17 and 18 of split chiasm cats were recorded extracellularly, and the interocular transfer of the effect of adaptation to high-contrast gratings was studied. In area 17 all but one of the simple cells showed the phenomenon of adaptation and its interocular transfer; 60% of the complex cells showed the effect of adaptation, and of these cells 35% showed an interocular transfer of adaptation. The adaptation aftereffect was comparable both in strength and duration for the direct and the callosal pathway. The strength of the adaptation aftereffect through the callosal pathway was not related to the strength of the input from the contralateral eye. An interocular transfer of the adaptation aftereffect was found in several neurons with a very weak input from the contralateral eye and in five simple cells apparently responding only to the ipsilateral eye. Fifty-eight percent of the neurons in area 18 showed the effect of adaptation, and 55% of them showed interocular transfer. No interocular transfer of the adaptation aftereffect was found in those neurons where an input from the contralateral eye was undetectable. Interocular transfer of the adaptation was found in all the neurons recorded in area 17 of animals with section of the corpus callosum but intact chiasm. No interocular transfer was found in neurons recorded in area 17 of cats with both the optic chiasm and the corpus callosum sectioned. We conclude that callosal connections are sufficient for the transfer of the adaptation aftereffect, although they are not necessary.

Adaptation, Ocular↗

Responses of gustatory cells in the nucleus of the solitary tract of the hamster after NaCl or amiloride adaptation.

1. The responses of single nucleus of the solitary tract (NST) neurons in the hamster were recorded to an array of Na+ and non-Na+ stimuli under each of three adaptation conditions: distilled H2O, 0.032 M NaCl, and 10 microM amiloride. Each adapting solution flowed for 60 s before delivery of one of seven test stimuli: 0.032 M NaCl, NaNO3, and Na-gluconate, 0.1 M KCl and sucrose, 1 mM HCl, and 3 mM quinine hydrochloride (QHCl). Stimuli were dissolved in distilled H2O (H2O and NaCl adaptation conditions) or 10 microM amiloride (amiloride adaptation condition). 2. Both amiloride treatment and NaCl adaptation reduced responses to the Na+ stimuli. The effects of NaCl adaptation were generally greater than those of amiloride, and the responses to the Na+ salts were reduced by NaCl adaptation in every cell that responded to NaCl, regardless of its best-stimulus classification. Amiloride treatment suppressed the responses to Na+ salts with larger anions (NaNO3 and Na-gluconate) more than the response to NaCl. 3. Unlike amiloride treatment, NaCl adaptation also reduced responses to several non-Na+ stimuli (KCl, HCl, and QHCl). This effect occurred primarily in the NaCl-best neurons that were most highly responsive to NaCl and that showed a postexcitatory suppression after NaCl. This suppression has been observed in recordings from the chorda tympani nerve in both rats and hamsters and in taste receptor cell responses recorded in situ in the rat. If it is a receptor phenomenon, these data would imply that some NaCl-sensitive receptor cells are also responsive to these non-Na+ electrolytes. 4. The effects of amiloride on the responses to Na+ stimuli were not limited to NaCl-best neurons, but occurred in sucrose-best cells as well. These results suggest that the sucrose-best cells in the NST receive converging input from sucrose- and NaCl-best chorda tympani fibers, because there is little Na+ sensitivity in the peripheral sucrose-best fibers and the amiloride sensitivity is restricted to NaCl-best chorda tympani fibers. The responses to NaCl in the few HCl- and QHCl-best NST neurons were not affected by amiloride. 5. Rinsing the tongue with amiloride for 60 s resulted in a reduction in the baseline response rate of NST cells. This effect occurred primarily in NaCl- and sucrose-best NST neurons and implies that much of the spontaneous activity in these brain stem cells arises from amiloride-sensitive channel activity in the peripheral receptor cells. 6. The results of human psychophysical studies show very different effects of NaCl adaptation and amiloride treatment. Adaptation to NaCl produces a robust and specific reduction in the saltiness of all salts. The present results show that NaCl adaptation reduces the responses of all cells sensitive to NaCl. Treatment of the human tongue with amiloride produces a proportionately smaller reduction in the response to NaCl than it does in rodents, and it appears to have no effect on saltiness. Rather, amiloride has been shown to specifically reduce the sour side taste of NaCl, Nagluconate, and LiCl. Therefore conclusions about the effects of amiloride on taste quality based on rodent electrophysiology are questionable.

Adaptation, Physiological↗

Saccadic gain modification: visual error drives motor adaptation.

The brain maintains the accuracy of saccadic eye movements by adjusting saccadic amplitude relative to the target distance (i.e., saccade gain) on the basis of the performance of recent saccades. If an experimenter surreptitiously moves the target backward during each saccade, thereby causing the eyes to land beyond their targets, saccades undergo a gradual gain reduction. The error signal driving this conventional saccadic gain adaptation could be either visual (the postsaccadic distance of the target from the fovea) or motoric (the direction and size of the corrective saccade that brings the eye onto the back-stepped target). Similarly, the adaptation itself might be a motor adjustment (change in the size of saccade for a given perceived target distance) or a visual remapping (change in the perceived target distance). We studied these possibilities in experiments both with rhesus macaques and with humans. To test whether the error signal is motoric, we used a paradigm devised by Heiner Deubel. The Deubel paradigm differed from the conventional adaptation paradigm in that the backward step that occurred during the saccade was brief, and the target then returned to its original displaced location. This ploy replaced most of the usual backward corrective saccades with forward ones. Nevertheless, saccadic gain gradually decreased over hundreds of trials. Therefore, we conclude that the direction of saccadic gain adaptation is not determined by the direction of corrective saccades. To test whether gain adaptation is a manifestation of a static visual remapping, we decreased the gain of 10 degrees horizontal saccades by conventional adaptation and then tested the gain to targets appearing at retinal locations unused during adaptation. To make the target appear in such "virgin territory," we had it jump first vertically and then 10 degrees horizontally; both jumps were completed and the target spot extinguished before saccades were made sequentially to the remembered target locations. Conventional adaptation decreased the gain of the second, horizontal saccade even though the target was in a nonadapted retinal location. In contrast, the horizontal component of oblique saccades made directly to the same virgin location showed much less gain decrease, suggesting that the adaptation is specific to saccade direction rather than to target location. Thus visual remapping cannot account for the entire reduction of saccadic gain. We conclude that saccadic gain adaptation involves an error signal that is primarily visual, not motor, but that the adaptation itself is primarily motor, not visual.

Adaptation, Physiological↗

Protective effects of intermittent hypoxic adaptation on myocardium and its mechanisms.

Intermittent hypoxic adaptation offers as many beneficial effects in protecting against myocardial injuries as chronic continuous hypoxic adaptation. However, chronic continuous hypoxic adaptation readily causes some adverse effects on the organism, which may be prevented by intermittent hypoxic adaptation. As an approach to potentiate the protective effects, intermittent hypoxic adaptation is also much easier to apply to subjects who are not living at high altitude. The mechanisms underlying the cardioprotective effects of intermittent hypoxic adaptation are less understood, although great similarities exist between chronic continuous and intermittent hypoxic adaptation. The participation of several factors, such as myocardial vascularity, coronary blood flow, and cardiomyoglobin, which comprise the oxygen uptake system is not apparent, while the more efficient energetic metabolism after intermittent hypoxic adaptation may be a mechanism for cardioprotection. The possible roles of several signaling transduction pathways, including adrenoceptors, prostaglandins, and the adenosinergic system, in the beneficial effects of intermittent hypoxia are compared to those of chronic continuous hypoxic adaptation. Antioxidant enzymes and stress proteins may also be part of the mechanisms contributing to the cardioprotection of the intermittent hypoxic adaptation. As the cardioprotective effects of intermittent hypoxic adaptation employ multifold mechanisms, their clear elucidation needs more efforts.

Adaptation, Physiological↗

A universal model for spike-frequency adaptation.

Spike-frequency adaptation is a prominent feature of neural dynamics. Among other mechanisms, various ionic currents modulating spike generation cause this type of neural adaptation. Prominent examples are voltage-gated potassium currents (M-type currents), the interplay of calcium currents and intracellular calcium dynamics with calcium-gated potassium channels (AHP-type currents), and the slow recovery from inactivation of the fast sodium current. While recent modeling studies have focused on the effects of specific adaptation currents, we derive a universal model for the firing-frequency dynamics of an adapting neuron that is independent of the specific adaptation process and spike generator. The model is completely defined by the neuron's onset f-I curve, the steady-state f-I curve, and the time constant of adaptation. For a specific neuron, these parameters can be easily determined from electrophysiological measurements without any pharmacological manipulations. At the same time, the simplicity of the model allows one to analyze mathematically how adaptation influences signal processing on the single-neuron level. In particular, we elucidate the specific nature of high-pass filter properties caused by spike-frequency adaptation. The model is limited to firing frequencies higher than the reciprocal adaptation time constant and to moderate fluctuations of the adaptation and the input current. As an extension of the model, we introduce a framework for combining an arbitrary spike generator with a generalized adaptation current.

Action Potentials↗

Cone selective adaptation influences L- and M-cone driven signals in electroretinography and psychophysics.

To assess the influence of selective adaptation of long (L) and middle (M) wavelength sensitive cones with electroretinography (ERG) and psychophysics, a novel adaptation procedure was developed, which comprises a selective and quantifiable change in the state of adaptation in the different cone types. One adaptation condition was used as a reference. In four additional conditions, the M-cones or the L-cones were selectively adapted, so that they absorbed either more or less photons. At each of these five states of adaptation, the ERG response amplitudes to 30Hz L- and to M-cone selective stimuli were measured. Furthermore, the psychophysical sensitivities to L- and M-cone selective stimuli were measured at different temporal frequencies. In subjects with normal color vision, adaptation can have a strong influence on the L- and M-cone driven response amplitudes in the ERG and on both the L- and the M-cone sensitivities in the psychophysical luminance channel. As a result, the L- to M-cone ERG and psychophysical ratios can change dramatically at the different states of adaptation. The cone sensitivity thresholds and the L- to M-cone sensitivity ratio in the psychophysical chromatic channel are about unity at all states of adaptation, suggesting the presence of a compensatory mechanism. In dichromats, the responses and sensitivities to stimulation of the absent cone type were generally small at all states of adaptation. But, with reddish backgrounds residual ERG responses and residual psychophysical sensitivities were observed, indicating the presence of either a robust rod driven signal or an additional adaptation mechanisms that are not cone driven and that have not been described before.

Adaptation, Ocular↗