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PubMed2006

Adaptation of clinical guidelines: literature review and proposition for a framework and procedure.

PURPOSE: The development and updating of high-quality clinical practice guidelines require substantial resources. Many guideline programmes throughout the world are using similar strategies to achieve similar goals, resulting in many guidelines on the same topic. One method of using resources more efficiently and avoiding unnecessary duplication of effort would be to adapt existing guidelines. The aim was to review the literature on adaptation of guidelines and to propose a systematic approach for adaptation of guidelines. DATA SOURCES: We selected and reviewed reports describing the methods and results of adaptation of guidelines from those found by searching Medline, Internet, and reference lists of relevant papers. On the basis of this review and our experience in guideline development, we proposed a conceptual framework and procedure for adaptation of guidelines. RESULTS: Adaptation of guidelines is performed either as an alternative to de novo guideline development or to improve guideline implementation through local tailoring of an international or national guideline. However, no validated process for the adaptation of guidelines produced in one cultural and organizational setting for use in another (i.e. trans-contextual adaptation) was found in the literature. The proposed procedure is a stepwise approach to trans-contextual adaptation, including searching for existing guidelines, quality appraisal, detailed analysis of the coherence between the evidence and the recommendations, and adaptation of the recommendations to the target context of use, taking into account the organization of the health care system and cultural context. CONCLUSIONS: Trans-contextual adaptation of guidelines is increasingly being considered as an alternative to de novo guideline development. The proposed approach should be validated and evaluated to determine if it can reduce duplication of effort and inefficient use of resources, although guaranteeing a high-quality product, compared with de novo development.

Diffusion of Innovation↗
PubMed1983

Solutes contributing to osmotic adjustment in cultured plant cells adapted to water stress.

Osmotic adjustment was studied in cultured cells of tomato (Lycopersicon esculentum Mill cv VFNT-Cherry) adapted to different levels of external water potential ranging from -4 bar to -28 bar. The intracellular concentrations of reducing sugars, total free amino acids, proline, malate, citrate, quaternary ammonium compounds, K(+), NO(3) (-), Na(+), and Cl(-) increased with decreasing external water potential. At any given level of adaptation, the maximum contribution to osmotic potential was from reducing sugars followed by potassium ions. The sucrose levels in the cells were 3- to 8-fold lower than reducing sugar levels and did not increase beyond those observed in cells adapted to -16 bar water potential. Concentrations of total free amino acids were 4- to 5-fold higher in adapted cells. Soluble protein levels declined in the adapted cell lines, but the total reduced nitrogen was not significantly different after adaptation. Uptake of nitrogen (as NH(4) (+) or NO(3) (-)) from the media was similar for adapted and unadapted cells. Although the level of quaternary ammonium compounds was higher in the nonadapted cells than that of free proline, free proline increased as much as 500-fold compared to only a 2- to 3-fold increase observed for quaternary ammonium compounds. Although osmotic adjustment after adaptation was substantial (up to -36 bar), fresh weight (volume increase) was restricted by as much as 50% in the adapted cells. Altered metabolite partitioning was evidenced by an increase in the soluble sugars and soluble nitrogen in adapted cells which occurred at the expense of incorporation of sugar into cell walls and nitrogen into protein. Data indicate that the relative importance of a given solute to osmotic adjustment may change depending on the level of adaptation.

Journal Article↗
PubMed1990

Adaptation of the exocrine pancreas to diet.

Pancreatic adaptation represents dietary regulation of gene expression; dietary substrates alter the synthesis and mRNA levels of their respective digestive enzymes. The mechanisms whereby mRNA levels change are not understood, but they must be elucidated. Although the changes in synthesis of proteases, amylase, and lipase parallel the changes in their mRNA levels in response to respective substrates, the concomitant changes in the synthesis of the other enzymes can be discordant with mRNA levels. The evidence supports a pretranslational mechanism of the adaptation of proteases, amylase, and lipase to their respective substrates and suggests potential translational mechanisms of other enzymes in these adaptations. Changes in synthesis occur within hours after a dietary change, but whether mRNA levels also change so early is unknown. Rapid, adaptive changes may occur by a different mechanism from later adaptation, possibly by translational control or nuclear transport. The differential effects of acute and chronic caerulein administration support the possibility of multiple mechanisms of regulation by a single effector. The mediators of pancreatic adaptations have not yet been identified, except for adaptation to dietary protein. CCK appears to mediate protease adaptation through the feedback regulation of its release by dietary protein. Available evidence supports a role of insulin and glucose in the adaptation to carbohydrate and a role of secretin and ketones in the adaptation to dietary fat. Elucidation of the mediators of pancreatic adaptation to carbohydrate and fat and their mechanisms is needed.

Animals↗
PubMed1992

Role of monkey midbrain near-response neurons in phoria adaptation.

1. One striking characteristic of the way in which accommodation and convergence of the eyes are organized is that although the two responses are usually tightly coupled, a brief period of binocular viewing through prisms that require extra convergence brings about a persistent, adaptive alteration in the relationship between the two responses: the vergence during monocular viewing of a target at a given distance is biased in a convergent direction. We sought to discover the role of the near-response neurons we have previously described in the monkey midbrain in such phoria adaptation. 2. Phoria adaptation was produced in two monkeys by having them view binocularly stereoscopic targets under conditions that mimicked prism viewing, i.e., the mirrors of the stereoscope were set so as to require more convergence than that associated with a real target at the same distance as the images seen in the stereoscope. The activity of 57 near-response neurons located dorsally and dorsolaterally to the oculomotor nucleus was recorded before and after adaptation while the monkeys monocularly viewed targets at a range of distances. 3. Comparison of a neuron's response in normal binocular viewing with the response when the accommodation and vergence stimuli were in conflict allowed us to distinguish 24 neurons that behaved as though they were related exclusively to the vergence response. 5 neurons that behaved as though they were exclusively related to the accommodation response, and 12 neurons whose firing was not so simply related to either response. We were unable to classify the remaining 16 near-response cells by this method. 4. In accommodation-related neurons, the relationship between firing rate and accommodation did not alter, or only altered slightly, when the animal's phoria was adapted. 5. The relationship between firing rate and vergence was unaltered by phoria adaptation in only a small proportion of vergence-related neurons, showing that most neurons do not carry the entire signal responsible for phoria adaptation. On the other hand, in the majority of vergence-related neurons the relationship between firing rate and accommodation was altered by phoria adaptation, showing that most neurons do carry part of the phoria adaptation signal. 6. The implication is that the increase in vergence observed after adaptation is mediated at more than one site. A proportion of the phoria adaptation signal is present at the level of the midbrain vergence-related neurons, with the remainder of the signal being added later, presumably at the motoneurons.

Accommodation, Ocular↗
PubMed1997

Contribution of outward currents to spike-frequency adaptation in hypoglossal motoneurons of the rat.

Contribution of outward currents to spike-frequency adaptation in hypoglossal motoneurons of the rat. J. Neurophysiol. 78: 2246-2253, 1997. Spike-frequency adaptation has been attributed to the actions of several different membrane currents. In this study, we assess the contributions of two of these currents: the net outward current generated by the electrogenic Na+-K+ pump and the outward current that flows through Ca2+-activated K+ channels. In recordings made from hypoglossal motoneurons in slices of rat brain stem, we found that bath application of a 4-20 microM ouabain solution produced a partial block of Na+-K+ pump activity as evidenced by a marked reduction in the postdischarge hyperpolarization that follows a period of sustained discharge. However, we observed no significant change in either the initial, early, or late phases of spike-frequency adaptation in the presence of ouabain. Adaptation also has been related to increases in the duration and magnitude of the medium-duration afterhyperpolarization (mAHP) mediated by Ca2+-activated K+ channels. When we replaced the 2 mM Ca2+ in the bathing solution with Mn2+, there was a significant decrease in the amplitude of the mAHP after a spike. The decrease in mAHP amplitude resulted in a decrease in the magnitude of the initial phase of spike-frequency adaptation as has been reported previously by others. However, quite unexpectedly we also found that reducing the mAHP resulted in a dramatic increase in the magnitude of both the early and late phases of adaptation. These changes could be reversed by restoring the normal Ca2+ concentration in the bath. Our results with ouabain indicate that the Na+-K+ pump plays little, if any, role in the three phases of adaptation in rat hypoglossal motoneurons. Our results with Ca2+ channel blockade support the hypothesis that initial adaptation is, in part, controlled by conductances underlying the mAHP. However, our failure to eliminate initial adaptation completely by blocking Ca2+ channels suggests that other membrane mechanisms also contribute. Finally, the increase in both the early and late phases of adaptation in the presence of Mn2+ block of Ca2+ channels lends further support to the hypothesis that the initial and later (i.e., early and late) phases of spike-frequency adaptation are mediated by different cellular mechanisms.

Animals↗
PubMed1985

Some characteristics of hyperoxia-adapted HeLa cells. A tissue culture model for cellular oxygen tolerance.

By culturing HeLa cells at stepwise increased oxygen tensions over a prolonged period of time (approximately 21 months) we selected a substrain capable of growing under 80% O2/19% N2/1% CO2, an oxygen level that is lethal to normal HeLa cells, adapted to 20% O2/79% N2/1% CO2. The 80% O2-adapted cells exhibited the following characteristics. At the ultrastructural level an abnormal mitochondrial morphology was observed: compared to normal cells, mitochondria of the hyperoxia-adapted cells exhibited a 3-fold larger mean profile area in sections and were slightly decreased in number; the relative mitochondrial volume was increased 2-fold, whereas the size of both cell types was the same. Mitochondrial matrix appeared less dense in the hyperoxia-adapted cells; no structural damage was detected. Compared to the 20% O2-adapted cells O2 consumption per cell was approximately 40% decreased in the 80% O2-adapted cells. Under hyperoxic conditions 20% O2-adapted and 80% O2-adapted cells exhibited very similar cyanide-resistant respiration rates (0.16 +/- 0.04 and 0.15 +/- 0.02 fmoles/cell/minute, respectively), suggesting that the increased O2 tolerance of the 80% O2-adapted cells was not due to a decreased cellular production of activated oxygen species at hyperoxia. Cellular levels of the enzymes directly involved in protection against activated oxygen species, i.e., superoxide dismutases, catalase, and glutathione peroxidase, were normal or slightly below normal in the 80% O2-adapted cells, implying that these enzymes were of no significance for the increased O2 tolerance. In addition, the specific activity of glucose-6-phosphate dehydrogenase, a key enzyme for cellular production of NADPH, was not related to the degree of O2 tolerance. Our results suggest that the increased O2 tolerance of the 80% O2-adapted cells is neither based on cellular properties controlling the formation or removal of intracellular activated oxygen species nor on the cellular capacity to repair or replace damaged cellular components. We speculate that the increased O2 tolerance is largely due to a genetically determined increased resistance of oxygen-sensitive cellular targets.

DNA↗
PubMed1995

[Cross-adaptation as affected by methylating and ethylating compounds and mitomycin c].

The present study examines cross-adaptation between alkylating agents and antibiotic mitomycin C (MC). Ethylating and methylating agents induce monoadducts in DNA in the form of ethyl and methyl radicals. MC induces DNA cross-links. In our experiments on cross-adaptation, low concentration of ethylenimine (EI) did not induce an adaptive response following posttreatment with methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (NG) at mutagenic concentration. Pretreatment with low EI concentration and posttreatment with MC did not induce adaptive response to late fixation. Pretreatment with NG at low concentration and subsequent posttreatment with EI at high concentration reduced the yield of chromosomal aberrations (adaptive response), compared to the effect of EI alone. Adaptive response is absent when pre- and posttreatment are performed within phase G1, and the effect of sensibilization is noted in this case. After posttreatment with MC at mutagenic concentration, the adaptive response is expressed in the case of increased cell-cycle duration. Posttreatment with MC at low mutagenic concentration did not lead to any adaptive response following NG pretreatment. In experiments with low MC concentration and posttreatment with high EI concentrations, the adaptive response was observed, whereas in experiments with NG posttreatment, an increased yield of aberrations (the effect of sensibilization) was observed. Thus, in cross-adaptation, inducible repair, i.e., adaptive response, is demonstrated by MC, methylating agent NG, and ethylating agent EI despite differing damage to DNA. This effect is dependent on the character of DNA damage following pretreatment, concentration and character of the mutagen used for posttreatment, and the duration and phase of the cell cycle.

Alkylation↗
PubMed1992

Rapid and slow changes in the human cone electroretinogram during light and dark adaptation.

Changes in the response characteristics of the human cone electroretinogram (ERG) during light and dark adaptation were studied in two visually normal subjects. Cone ERG responses were isolated under all adaptation conditions through the use of 31 Hz flicker. To determine the time-course of changes in the cone ERG during adaptation, responses to stimuli of constant luminance were measured repeatedly during 15 min of exposure to an adapting field of 2.0 log cd/m2 and during 30 min of dark adaptation following adapting field termination. In addition, luminance-response functions were obtained before and immediately after adapting field onset, as well as before and immediately after adapting field termination. The results indicate that the human cone ERG is influenced by two major processes. One process has a relatively rapid time-course and serves to reposition the luminance-response function along the luminance axis following changes in ambient light levels. The second process, which has a slow time-course, scales response amplitudes during light and dark adaptation by the same proportion at all stimulus luminances. The results provide a framework for predicting the manner in which the cone ERG will change with alterations in the state of retinal adaptation.

Adaptation, Ocular↗
PubMed2006

Cone phototransduction and growth of the ERG b-wave during light adaptation.

The purpose of this study was to determine whether cone redepolarization accounts for the amplitude increase of the b-wave of the human electroretinogram (ERG) during light adaptation. The time course of the b-wave amplitude increase was compared to the time course of the change in the activation phase of cone phototransduction, as derived from a delayed Gaussian model applied to the leading edge of the ERG a-wave. ERG recordings were obtained from five visually normal subjects, alternately in the presence of the adapting field (adapt-on condition) and 300ms after its temporary extinction (adapt-off condition). The proportional increase in amplitude was less for R(mp3) (maximum amplitude of P3, the massed cone photoreceptor response) than for the b-wave for both adaptation conditions, and the time course of the amplitude increase for R(mp3) was faster than that for the b-wave in the adapt-off condition. The results demonstrate that time-dependent changes in the activation phase of cone phototransduction have only a minimal role in governing the increase in the amplitude of the human cone-derived ERG b-wave during light adaptation. In addition, the systematic increase in b-wave amplitude and the decrease in b-wave implicit time in the adapt-off condition indicates that the ERG response measured shortly after adapting field offset does not necessarily represent the waveform of the dark-adapted cone ERG.

Adaptation, Ocular↗
PubMed1992

Light adaptation, rods, and the human cone flicker ERG.

During the course of light adaptation, the amplitude and implicit time of the human cone ERG change systematically. In the present study, the effect of adapting field luminance on these ERG changes was assessed, and the hypothesis that light adaptation of the rod system is the primary determining factor was evaluated. Cone ERG responses, isolated through the use of 31.1-Hz flicker, were obtained from two visually normal subjects, initially under dark-adapted conditions and then repeatedly for 30 min following the onset of each of a series of ganzfeld adapting fields with luminances that ranged from -1.2 to 2.1 log cd/m2. The increase in flicker ERG amplitude and decrease in implicit time during light adaptation were greatest at the highest adapting field luminances. Photopically equivalent achromatic and long-wavelength adapting fields induced comparable increases in flicker ERG amplitude, while scotopically equivalent adapting fields had considerably different effects. This latter finding demonstrates that the rod system is not a major determinant of the adaptation-induced increase in cone ERG amplitude.

Adaptation, Ocular↗
PubMed1990

[Adaptational changes in cone electroretinograms in man].

Changes of amplitude and implicit time of human cone electroretinogram (ERG) were studied during dark adaptation and succeeding light adaptation. Dark-adapted cone ERG was isolated by subtracting scotopic blue response from matched scotopic red response. The former represented the rod-mediated b-wave, while the latter consisted of both rod-mediated b-wave and cone-mediated b-wave or x-wave. The b-wave amplitude of dark-adapted cone ERG remained unchanged during dark adaptation, while the implicit time increased systematically, reaching a plateau. Light-adapted cone ERG was obtained by red stimulus lights under a bright background light. The amplitude of light-adapted cone ERG was markedly suppressed through dark adaptation but it recovered gradually during light adaptation, reaching the base line level. The implicit time was unchanged during light adaptation.

Adaptation, Ocular↗
PubMed2001

Functional organization of the suprachiasmatic nucleus of Xenopus laevis in relation to background adaptation.

The process of background adaptation in the toad Xenopus laevis is controlled by neurons in the suprachiasmatic nucleus (SC) that inhibit the release of alpha-melanophore-stimulating hormone from the neuroendocrine melanotrope cells in the pituitary gland. We have identified the structural and functional organization of different neuropeptide Y (NPY)-containing cell groups in the Xenopus SC in relation to background adaptation. A ventrolateral, a dorsomedial, and a caudal group were distinguished, differing in location as well as in number, size, and shape of their cells. They also show different degrees of NPY immunoreactivity in response to different background adaptation conditions. In situ hybridization using a Xenopus mRNA probe for the exocytosis protein DOC2 revealed that melanotrope cells of black-adapted animals have a much higher expression of DOC2-mRNA than white-adapted ones. This establishes that the degree of DOC2-mRNA expression is a good parameter to measure cellular secretory activity in Xenopus. We show that in the ventrolateral SC group, more NPY-positive neurons express DOC2-mRNA in white- than in black-adapted animals. In contrast, NPY-positive neurons in the dorsomedial group have a high secretory activity under the black-adaptation condition. We propose that in black-adapted animals, NPY-positive neurons in the ventrolateral group, known to inhibit the melanotrope cells in white-adapted animals synaptically, are inhibited by NPY-containing interneurons in the dorsmedial group. NPY-positive neurons in the caudal group have similar secretory dynamics as the dorsomedial NPY neurons, indicating that they also play a role in background adaptation, distinct from that exerted by the ventrolateral and dorsomedial group.

Adaptation, Physiological↗
PubMed1995

Ozone adaptation in rats after chronic exposure to a simulated urban profile of ozone.

Studies in both humans and rats have indicated that certain pulmonary responses induced by exposure to an acute provocative concentration of ozone (O3) will eventually attenuate if the exposure is repeated on a daily basis. This phenomenon is commonly referred to as O3 adaptation. Whether or not a "state" of adaptation develops due to long-term low level O3 exposure is unknown. Two human studies have reported adaptation in subjects living in Los Angeles during periods when ambient O3 concentrations have been relatively high. At present, however, we are not aware of comparable information from rats. This study assessed O3 adaptation in rats following chronic (12 or 18 months) exposure and after a 4-month recovery period. A chronic exposure pattern, similar to that found in an urban area during the summer (0.06 ppm O3 for 13 hr/day, 7 days/week; Monday-Friday, peak to 0.25 ppm O3, over 9 hr), was used. To assess whether adaptation had occurred and/or persisted, awake rats were challenged with high provocative concentrations of O3 for up to 2 hr. During a challenge, rats were monitored for typical O3-induced alterations in spontaneous breathing parameters (e.g., increase in breathing frequency and decrease in tidal volume). Adaptation was defined as attenuation of breathing response during the challenge in rats chronically exposed to O3 as compared to that in "control" rats (chronically exposed to air). Adaptation was found in the rats within 8 hr following the chronic O3 exposure but not after the 4-month recovery period. Spontaneous breathing parameters that were significantly attenuated in the chronically exposed rats were breathing frequency, tidal volume, inspiratory and expiratory times, and maximum expiratory flow. We conclude that rats demonstrated adaptation to O3 after long-term exposure to an urban-type O3 profile and that the adaptation was not seen 4 months postexposure. These results suggest that exposure to environmental O3 in Los Angeles air may have been responsible for the adaptation found in residential subjects.

Adaptation, Physiological↗
PubMed1994

The effects of adaptation to visual stimuli on the velocity of subsequent ocular following responses.

We examined the effect of prior adaptation to moving and flickering stimuli on the velocity of subsequent ocular following responses in man. Experiments consisted of two phases: an adaptation phase in which moving or flickering stimuli were presented while the eyes fixated a small spot and a test phase in which ocular following responses were free to occur. The effects resulting from prior adaptation were characterized by determining the mean initial eye velocities in the period 200-500 ms after the onset of the test stimulus. It was found that 8 s of prior exposure to a grating pattern moving at between 1.5 and 4 cycles.s-1 significantly reduced initial eye velocities in all subjects. Prior exposure to a flickering stimulus (temporal frequency 3.2 cycles.s-1) also attenuated the velocities of initial eye movements, but to a far lesser extent. These results suggest that a motion-dependent and a weaker flicker-dependent process have an adaptive influence on the generation of ocular following responses. Initial eye velocities were measured as a function of the contrast of the prior adapting gratings. The velocities were found to decrease with increasing adapting contrast. The reductions in eye velocity were well described by a decaying exponential function. The motion-dependent adaptive effect showed significant inter-ocular transfer and had the same temporal tuning when transferred (i.e. optimum adaptation at between 1.5 and 4 cycles.s-1). The flicker-dependent effect did not show inter-ocular transfer. There is a distinct similarity between the adaptive process that causes attenuation of ocular following velocities and the adaptive mechanism that induces perceptual motion after-effects. This similarity is discussed.

Acceleration↗
PubMed1996

Gastric mucosal adaptation to diclofenac injury.

Adaptation occurs to the gastric injury produced by nonsteroidal antiinflammatory drugs during continued dosing. The aim of this study was to identify characteristics of this phenomenon that might help in the search for underlying mechanisms. The time frame for onset and offset of adaptation of diclofenac (damage assessed planimetrically) was examined in rats. Adaptation to oral diclofenac took three to five days to develop, and persisted for up to five days after the last dose. It was also demonstrable after subcutaneous dosing or when injury was measured by a change in mucosal potential difference. Diclofenac-adapted rats were protected against injury induced by subsequent exposure to ethanol, indomethacin, aspirin, or piroxicam, indicating that adaptation is not specific to injury by the adapting agent. This cross-adaptation was dose-dependent and characterized histologically by a reduction in deep damage. In conclusion, gastric adaptation to diclofenac is mediated by mechanisms that take several days to develop and be lost. The route of administration appears to be unimportant, but the development of both adaptation and cross-adaptation is influenced by dosage size.

Adaptation, Physiological↗
PubMed1999

Adaptive response to cold temperatures in Vibrio vulnificus.

The effectiveness of rapid chilling or freezing of oysters to reduce Vibrio vulnificus levels in shellfish may be compromised by product handling procedures that permit cold adaptation. When a V. vulnificus culture was shifted from 35 degrees C to 6 degrees C conditions, it underwent transition to a non-culturable state. Cells adapted to 15 degrees C prior to change to 6 degrees C condition, however, remain viable and culturable. In addition, cultures adapted to 15 degrees C were able to survive better upon freezing at -78 degrees C compared with cultures frozen directly from 35 degrees C. Inhibition of protein synthesis by addition of chloramphenicol in a V. vulnificus culture immediately prior to the exposure to the adaptive temperature eliminated inducible cold tolerance. These results suggest that cold-adaptive "protective" proteins may enhance survival and tolerance at cold temperatures. In addition, removal of iron from the growth medium by adding 2,2'-Dipyridyl prior to cold adaptation decreased the viability by approximately 2 logarithm levels. This suggests that iron plays an important role in adaptation at cold temperatures. Analysis of total cellular proteins on an SDS polyacrylamide gel electrophoresis, labeled with 35S-methionine during exposure at 15 degrees C, showed elevated expressions of a 6-kDa and a 40-kDa protein and decreased expression of an 80-kDa protein. These results suggest that, for V. vulnificus, survival and tolerance at cold temperatures could be due to the expression of cold-adaptive proteins other than previously documented major cold shock proteins such as CS7.4 and CsdA. In this study, for the first time we have shown that exposure to an intermediate cold temperature (15 degrees C) causes a cold adaptive response, helping this pathogen remain in culturable state when exposed to a much colder temperature (6 degrees C). This adaptive nature to cold temperatures could be important for shellfish industry efforts to reduce the risk of V. vulnificus infection from consuming raw oysters.

Adaptation, Physiological↗
PubMed2002

Investigating the site of human saccadic adaptation with express and targeting saccades.

To focus on various objects of interest within the visual environment, primates employ rapid eye movements called saccades. When the accuracy of these movements becomes impaired, the brain can adjust their amplitude by a process known as saccadic adaptation. To investigate the locus of this plasticity in the human brain, we behaviorally adapted two types of saccade thought to be generated through different neuronal pathways. Targeting saccades, which are made to sequentially illuminated targets and have long latencies, are thought to involve higher cortical processing whereas express saccades, which have very short latencies, apparently do not. If adaptation transfers between these two types of saccade, one may conclude that the plasticity must exist at a locus common to the two pathways generating these saccades. We directly reduced the gain of either targeting or express saccades by intrasaccadically moving the target one-third of its amplitude back toward the initial fixation location and then examined whether the gain was also reduced in the other type of saccade. When targeting saccades were adapted directly, all subjects showed significant reductions in the gain of these saccades. In 75% of the 32 experimental target conditions across all subjects, there were also significant reductions in the gain of express saccades, thus providing evidence of adaptation transfer. In 71% of these conditions (i.e., 53% of all target conditions) there was no significant difference between the reductions in gain of the two types of saccade, suggesting that adaptation transfer was complete (100%). Similar results were obtained when express saccades were adapted directly: significant reductions in gain occurred in 91% of express saccades and in 100% of targeting saccades. In 86% of the target conditions, across subjects, in which both express and targeting saccades showed significant reductions in gain, the two types of saccade did not differ significantly in the amount of gain reduction. This suggests that adaptation transfer was complete for 78% of all target conditions. Therefore, we conclude that saccadic adaptation transfers robustly between targeting and express saccades. These results suggest that adaptation in humans occurs after the pathways generating these two types of saccade converge, probably at or downstream from the superior colliculus.

Adaptation, Physiological↗
PubMed2000

Flexibility of saccade adaptation in the monkey: different gain states for saccades in the same direction.

Saccadic accuracy, measured as the ratio of the size of a saccade to the size of the target step that elicits it, i.e., saccade gain, can be altered by jumping the target surreptitiously during the targeting saccade. The gain change produced by this paradigm does not generalize or transfer to saccades of all sizes. Instead, the amount of transfer decreases the more the tested saccade differs in amplitude and direction from that adapted. Here, we tested the limits of this saccade-size specificity by attempting to impose quite different gain states on saccades in the same direction. We altered the saccadic gain by intrasaccadic target jumps of 30% of the initial target step, either forward to produce a gain increase or backward to produce a gain decrease. Three different conditions were studied: (1) saccades to target steps of 20 degrees or 7 degrees were adapted in individual sessions with backward and forward jumps, respectively; (2) saccades to target steps of 20 degrees caused backward target jumps during the same session in which saccades to 7 degrees target steps caused forward steps; (3) the target jumps accompanying 20 and 7 degrees saccades were the same as in (2), but in addition, there were intermediate-sized saccades to 13.5 degrees target steps with no intrasaccadic target jumps. Saccadic gain adaptation was quite flexible. In condition 2, we could simultaneously increase the gain of saccades to 7 degrees target steps while decreasing the gain of saccades to 20 degrees steps in the same direction. Intermediate horizontal saccades to 13.5 degrees target steps experienced gain reductions (average: 6.9%), which were not the sum of gain changes expected from separate 20 degrees gain decreases and 7 degrees gain increases alone, as predicted from condition 1. If adaptation at 20 degrees and 7 degrees occurred while an animal also tracked a non-adapting 13.5 degrees target step (paradigm 3), the gain reduction of saccades to the 13.5 degrees step was reduced considerably (3.4%). Thus, the mechanism that adapts saccade size can support a robust gain increase for saccades of one size while simultaneously supporting a robust gain decrease for saccades only 13 degrees larger. Furthermore, the presence during adaptation of a non-adapted target step with a size intermediate to the two adapting steps reestablishes a nearly normal gain within only 6.5 degrees of a robust gain increase and decrease. These data indicate that saccadic gain adaptation can set very different gain states for saccades with rather similar vectors.

Adaptation, Ocular↗