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Spatial vision of the achromat: spatial frequency and orientation-specific adaptation.

1. The psychophysical technique of selective adaptation to stationary sine-wave gratings of varying spatial frequency and orientation was used to investigate the central processing of spatial information in the visual system of the complete achromat. 2. For adapting spatial frequencies of 1 and 2 cycles/deg, the spatial frequency and orientation selectivity of contrast threshold elevation is similar for achromatic and trichromatic vision. 3. For adapting frequencies below 1 cycle/deg, the achromat shows threshold elevations of normal magnitude with symmetrical spatial frequency and orientation tuning for adapting frequencies as low as 0.09 cycles/deg with 'bandwidth' estimates similar to those found at high frequencies in the trichromat. Below 0.66 cycles/deg no after-effect could be obtained in the trichromat, and the frequency tuning at 0.66 cycles/deg was skewed towards higher frequencies. 4. The interocular transfer of low-frequency adaptation in the achromat was 50%, which is the same value obtained at higher frequencies. 5. The time course of the decay of low spatial frequency adaptation in the achromat was similar to that found at higher frequencies. 6. Control experiments show no low-frequency adaptation in peripheral vision or in central vision in the dark-adapted trichromat indicating that low spatial frequency adaptation cannot be elicited through the rod system of the trichromat. 7. It is proposed that the observed range shift of adaptable spatial frequency mechanisms in the achromat's visual cortex is the result of an arrest at an early stage of sensory development. The visual cortex of the achromat is comparable, with respect to spatial processing, to that of the young, visually normal human infant.

Adaptation, Ocular↗

The effect of caged calcium release on the adaptation of the transduction current in chick hair cells.

1. Intracellular Ca2+ concentration ([Ca2+]i) was raised by photolysis of a caged calcium compound, nitr-5, and its effects on the mechano-electrical transduction (MET) current were studied by a whole-cell patch electrode voltage clamp technique in dissociated hair cells of a chick. Nitr-5 was loaded into the hair cell by incubation with the membrane-permeable form of the compound (nitr-5 AM). 2. Photolysis of nitr-5 by ultraviolet (UV) light irradiation induced outward currents at -50 mV when recorded with a KCl-based intracellular medium without Ca2+ chelating compounds. The average amplitude of the photo-activated outward current was 115 +/- 82 pA (mean +/- S.D., n = 5). 3. The MET current generated at -50 mV showed a decay after step displacement of the hair bundle. This adaptation was accelerated after UV exposure of the cell. The adaptation was further accelerated by hyperpolarization of the membrane and was eliminated in 20-100 microM Ca2+ extracellular media. 4. The displacement-response relationship was shifted towards the positive direction after the UV irradiation. 5. The recovery of the transducer current after step displacement of the hair bundle was accelerated after UV irradiation, for both the inward-going MET current recorded at -50 mV and the outward-going MET current at +54 mV. However, the adaptation was not observed at positive membrane potentials even after the photolysis of nitr-5. 6. The extent of MET current decay was reduced or disappeared in 20-100 microM Ca2+ extracellular media and the offset time course was prolonged at the membrane potential of -50 mV. The current decay was not observed even after the photo-release of intracellular Ca2+ in 50-100 microM Ca2+ extracellular media. 7. These results (paragraphs 3-6) suggest that the MET current adaptation is accelerated by the increase of [Ca2+]i, and that Ca2+ ions entering through MET channels are essential in the development of adaptation. 8. The adaptation of the MET current was reversibly reduced in a dihydrostreptomycin (DHSM, 20-50 microM) medium. The time course of the adaptation changes lagged the changes in the MET current amplitude. 9. The adaptation developed or disappeared with a delay of 10-20 s after the introduction of either the normal-Ca2+ (2.5 mM) or the low-Ca2+ (50-100 microM) extracellular medium, respectively. These delays in the development and the subsidence of adaptation suggest a presence of a Ca2+ buffer site intracellularly between the adaptative site and the MET channel.

Adaptation, Physiological↗

Adaptation to calcium deprivation in the rat: effects of parathyroidectomy.

The role of parathyroid hormone (PTH) in the adaptive response in gut calcium transport to calcium deprivation has been studied in the rat using both the in vitro everted duodenal sac and the in situ ligated duodenal segment technique. Intact or parathyroidectomized (PTX) young rats were placed on a low calcium (0.01%) diet for 7-, 14-, or 21-day adaptation periods and compared with control rats maintained on a high calcium (1.5%) diet. Prior PTX (3 days before the start of the adaptation period) abolished the adaptive response (enhanced calcium transport) induced by calcium deprivation for a 7-day adaptation period, but did not abolish a response after a 21-day period. A 14-day adaptation period gave equivocal results. It is concluded that PTH appears to be necessary for short-term (7-day) adaptation, but not for long-term (21-day) adaptation to calcium deprivation. However, if accessory parathyroid tissue is present, the data could be interpreted differently: the essentiality of PTH for the adaptive response might be independent of the length of the adaptation period. The data also contribute to a possible resolution of the controversy concerning the involvement of PTH in the regulation of intestinal calcium transport in the rat.

Adaptation, Physiological↗

Microcirculatory changes during chronic adaptation to hypoxia.

Microcirculatory changes in the window chamber preparation in Syrian golden hamsters, secondary to chronic hypoxia adaptation, are presented herein. Adaptation was attained by keeping animals in a 10% oxygen environment for 1 wk and 5% the following week. The following groups were studied: group 1, adapted to chronic hypoxia and kept in a 5% oxygen environment throughout the experiment; group 2, adapted to chronic hypoxia and kept in a 21% oxygen environment 24 h before and during the experiment; and group 3, control. Adaptation caused venule enlargement and hematocrit increase (68.6 +/- 2.44 in group 1, 70 +/- 2.66 in group 2, and 43.27 +/- 2.30 in group 3; P < 0.05). Whereas heart rate decreased in adapted animals, blood pressure remained constant. Group 1 presented alkalosis, hypocapnia, and hypoxemia. The adapted groups had decreased blood flow velocity in arterioles and veins. We found no difference in microvasculature oxygen tension between groups 2 and 3; however, the number of capillaries with flow was markedly reduced in group 1 but significantly increased in group 2. Our findings suggest that, as an adaptation to hypoxia, erythropoiesis may prove beneficial by increasing blood viscosity and shear stress, leading to vasodilatation, in addition to the increase in oxygen-carrying capacity. Calculations show that oxygen extraction in the tissue of the window chamber model was significantly lowered in adapted animals breathing 5% oxygen, but was unchanged from the control when breathing 21% oxygen, even though blood hemoglobin content was increased from 14.5 +/- 0.07 g/dl at control to 21.04 +/- 1.24 g/dl in the adapted animals (P < 0.05).

Adaptation, Physiological↗

Motion adaptation in area MT.

In many sensory systems, exposure to a prolonged stimulus causes adaptation, which tends to reduce neural responses to subsequent stimuli. Such effects are usually stimulus-specific, making adaptation a powerful probe into information processing. We used dynamic random dot kinematograms to test the magnitude and selectivity of adaptation effects in the middle temporal area (MT) and to compare them to effects on human motion discrimination. After 3 s of adaptation to a random dot pattern moving in the preferred direction, MT neuronal responses to subsequent test patterns were reduced by 26% on average compared with adaptation to a static pattern. This reduction in response magnitude was largely independent of what test stimulus was presented. However, adaptation in the opposite direction changed responses less often and very inconsistently. Therefore motion adaptation systematically and profoundly affects the neurons in MT representing the adapted direction, but much less those representing the opposite direction. In human psychophysical experiments, such adapting stimuli affected direction discrimination, biasing choices away from the adaptation direction. The magnitude of this perceptual shift was consistent with the magnitude of the changes seen in area MT, if one assumes that a motion comparison step occurs after MT.

Adaptation, Physiological↗

Hair-cell versus afferent adaptation in the semicircular canals.

The time course and extent of adaptation in semicircular canal hair cells was compared to adaptation in primary afferent neurons for physiological stimuli in vivo to study the origins of the neural code transmitted to the brain. The oyster toadfish, Opsanus tau, was used as the experimental model. Afferent firing-rate adaptation followed a double-exponential time course in response to step cupula displacements. The dominant adaptation time constant varied considerably among afferent fibers and spanned six orders of magnitude for the population ( approximately 1 ms to >1,000 s). For sinusoidal stimuli (0.1-20 Hz), the rapidly adapting afferents exhibited a 90 degrees phase lead and frequency-dependent gain, whereas slowly adapting afferents exhibited a flat gain and no phase lead. Hair-cell voltage and current modulations were similar to the slowly adapting afferents and exhibited a relatively flat gain with very little phase lead over the physiological bandwidth and dynamic range tested. Semicircular canal microphonics also showed responses consistent with the slowly adapting subset of afferents and with hair cells. The relatively broad diversity of afferent adaptation time constants and frequency-dependent discharge modulations relative to hair-cell voltage implicate a subsequent site of adaptation that plays a major role in further shaping the temporal characteristics of semicircular canal afferent neural signals.

Adaptation, Physiological↗

Spike-frequency adaptation in the inferior colliculus.

We investigated spike-frequency adaptation of neurons sensitive to interaural phase disparities (IPDs) in the inferior colliculus (IC) of urethane-anesthetized guinea pigs using a stimulus paradigm designed to exclude the influence of adaptation below the level of binaural integration. The IPD-step stimulus consists of a binaural 3,000-ms tone, in which the first 1,000 ms is held at a neuron's least favorable ("worst") IPD, adapting out monaural components, before being stepped rapidly to a neuron's most favorable ("best") IPD for 300 ms. After some variable interval (1-1,000 ms), IPD is again stepped to the best IPD for 300 ms, before being returned to a neuron's worst IPD for the remainder of the stimulus. Exponential decay functions fitted to the response to best-IPD steps revealed an average adaptation time constant of 52.9 +/- 26.4 ms. Recovery from adaptation to best IPD steps showed an average time constant of 225.5 +/- 210.2 ms. Recovery time constants were not correlated with adaptation time constants. During the recovery period, adaptation to a 2nd best-IPD step followed similar kinetics to adaptation during the 1st best-IPD step. The mean adaptation time constant at stimulus onset (at worst IPD) was 34.8 +/- 19.7 ms, similar to the 38.4 +/- 22.1 ms recorded to contralateral stimulation alone. Individual time constants after stimulus onset were correlated with each other but not with time constants during the best-IPD step. We conclude that such binaurally derived measures of adaptation reflect processes that occur above the level of exclusively monaural pathways, and subsequent to the site of primary binaural interaction.

Acoustic Stimulation↗

Adaptation at synaptic connections to layer 2/3 pyramidal cells in rat visual cortex.

Neocortical synapses express differential dynamic properties. When activated at high frequencies, the amplitudes of the subsequent postsynaptic responses may increase or decrease, depending on the stimulation frequency and on the properties of that particular synapse. Changes in the synaptic dynamics can dramatically affect the communication between nerve cells. Motivated by this question, we studied dynamic properties at synapses to layer 2/3 pyramidal cells with intracellular recordings in slices of rat visual cortex. Synaptic responses were evoked by trains of test stimuli, which consisted of 10 pulses at different frequencies (5-40 Hz). Test stimulation was applied either without any adaptation (control) or 2 s after an adaptation stimulus, which consisted of 4 s stimulation of these same synapses at 10, 25, or 40 Hz. The synaptic parameters were then assessed from fitting the data with a model of synaptic dynamics. Our estimates of the synaptic parameters in control, without adaptation are broadly consistent with previous studies. Adaptation led to pronounced changes of synaptic transmission. After adaptation, the amplitude of the response to the first pulse in the test train decreased for several seconds and then recovered back to the control level with a time constant of 2-18 s. Analysis of the data with extended models, which include interaction between different pools of synaptic vesicles, suggests that the decrease of the response amplitude was due to a synergistic action of two factors, decrease of the release probability and depletion of the available transmitter. After a weak (10 Hz) adaptation, the decrease of the response amplitude was accompanied by and correlated with the decrease of the release probability. After a strong adaptation (25 or 40 Hz), the depletion of synaptic resources was the main cause for the reduced response amplitude. Adaptation also led to pronounced changes of the time constants of facilitation and recovery, however, these changes were not uniform in all synapses, and on the population level, the only consistent and significant effect was an acceleration of the recovery after a strong adaptation. Taken together, our results suggest, that apart from decreasing the amplitude of postsynaptic responses, adaptation may produce synapse-specific effects, which could result in a kind of re-distribution of activity within neural networks.

Adaptation, Physiological↗

Neural mechanisms in vibrotactile adaptation.

1. Peripheral and central neural contributions to vibrotactile adaptation were investigated in decerebrate or anesthetized cats by recording from sensory nerve fibers associated with Pacinian corpuscle (PC) receptors and from central neurons of the dorsal column nuclei that receive their input from vibration-sensitive receptors of the forelimb footpads. Responsiveness of units was assessed using 1-s duration, test vibration stimuli delivered with 1- to 2-mm-diam probes at different times following adapting trains of vibration (usually 300 Hz) that lasted from less than 1 min up to 50 min. 2. Cuneate neuron responsiveness underwent marked depression following prior vibration. The extent of the depression and the time course of recovery in responsiveness were dependent on the intensity and duration of the adapting vibratory stimulus. The recovery time course (often several minutes) was approximately exponential and resembled the reported time course of subjective vibrotactile adaptation obtained in psychophysical experiments. 3. Response depression in PC fibers was only seen at low amplitudes of the test vibration and displayed a brief time course of recovery in comparison with that seen in cuneate neurons. It is therefore unlikely to account for the adaptation time course either in cuneate neurons or at a subjective level. Furthermore, as the adaptation seen in PC fiber responses had a similar time course in both cutaneous and mesenteric PC fibers it is unlikely that mechanical changes in the skin contribute significantly to the adaptation in PC fiber responses to vibration. 4. The time course of afferent-induced inhibition following long periods of prior vibration was too brief to account for the response adaptation in cuneate neurons. 5. As the long-term response depression in cuneate neurons following their prior activation was seen for inputs from unconditioned sites within the neuron's excitatory receptive field, as well as from the conditioned site, it appears that the response adaptation is attributable to changes in the central neuron or in synaptic processes associated with the central neuron. It is proposed that this adaptation may be due to an increase in extracellular potassium ion concentration that alters the responsiveness of the central neurons.

Adaptation, Physiological↗

Comparison of two methods of producing adaptation of saccade size and implications for the site of plasticity.

Saccade accuracy is known to be maintained by adaptive mechanisms that progressively reduce any visual error that consistently exists at the end of saccades. Experimentally, the visual error is induced using one of two paradigms. In the first, the horizontal and medial recti of trained monkeys are tenectomized and allowed to reattach so that both muscles are paretic. After patching the unoperated eye and forcing the monkey to use the "paretic eye," saccades initially undershoot the intended target, but gradually increase in size until they almost acquire the target in one step. In the second, the target of a saccade is displaced in midsaccade so that the saccade cannot land on target. Again saccade size adapts until the target can be acquired in one step. Because adaptation with the latter paradigm is very rapid but adaptation using the former is slow, it has frequently been questioned whether or not the two forms of adaptation depend on the same neural mechanisms. We show that the rate of adaptation in both paradigms depends on the number of possible visual targets, so that when this variable is equated, adaptation occurs at similar rates in both paradigms. To demonstrate further similarities between the result of the two paradigms, an experiment using intrasaccadic displacements was conducted to show that rapid adaptation possesses the capacity to produce gain changes that vary with orbital position. The relative size of intrasaccadic displacements were graded with orbital position so as to mimic the position-dependent dysmetria initially produced by a single paretic extraocular muscle. Induced changes in saccade size paralleled the size of the displacements, being largest for saccades into one hemifield and being negligible for saccades into the other hemifield or in the opposite direction. Collectively, the data remove the rational for asserting that adaptation produced by the two paradigms depends on separate neural mechanisms. We argue that adaptation produced by both paradigms depends on the cerebellum.

Adaptation, Physiological↗

Dark adaptation in diabetics.

Dark adaptation in diabetics was recorded with Goldmann-Weeker's adaptometer and analysed according to the stages of retinopathy by Scott. Dark adaptation curves in diabetics were divided into three groups; normal dark adaptation; subnormal one which showed normal first curve of dark adaptation and impaired second curve; abnormal dark adaptation which showed impaired dark adaptation in the whole course. The cases with normal dark adaptation were found to be few in the stages Ia, II and IIIa of retinopathy. Subnormal dark adaptation was rarely found in the stages Ia, II, IIIa and IIb of retinopathy. Abnormal dark adaptation was recorded in most patients with diabetic retinopathy and found in all th stages of retinopathy. A 5% level of significance was statistically recognized in the thresh old at 35 min after light adaptation between the stages IIIa and IIIb of retinopathy. From this viewpoint, significance in severity of diabetic retinopathy was discussed.

Dark Adaptation↗

Stereo-slant adaptation is high level and does not involve disparity coding.

We have investigated the potential stages of visual processing at which adaptation may occur to a slanted surface produced by horizontal magnification. Predictions of three hypotheses were tested utilizing a property of depth from binocular disparity, namely that slant scales with distance. If adaptation occurs at the disparity level, then the after-effect expressed in units of horizontal magnification will be independent of the test distance. If adaptation occurs at either a perceived slant or mapping level, then the after-effect, expressed in units of slant, will be independent of the test distance. If adaptation is contingent on distance, then the after-effect will not transfer over distance. Subjects adapted to a stereo-defined slanted surface at a distance of 57 cm. The after-effect was measured with a test stimulus at a distance of 28, 57, 85, or 114 cm by means of a nulling method. When the after-effect was expressed in units of slant, we found that it was larger at the adapting distance than other test distances, and that the after-effect was constant at test distances different from the adaptation distance. These results suggest that two types of adaptation occurred, namely adaptation on a mapping/perception level and adaptation contingent on distance.

Adaptation, Ocular↗

More evidence for sensorimotor adaptation in color perception.

Sensorimotor adaptation can be defined as a perceptual adaptation whose effects depend on the occurrence and nature of the performed motor actions. Examples of sensorimotor adaptation can be found in the literature on prisms concerning several space-related attributes like orientation, curvature, and size. In this article, we show that sensorimotor adaptation can be obtained for color, as a consequence of the introduction of a new sensorimotor contingency between eye movements and color changes. In an adaptation phase, trials involved the successive presentation of two patches, first on the left, and then on the right or the opposite. The left patch being always red and the right patch green, a correlation is introduced between left-right (respectively right-left) eye saccades and red-green (respectively green-red) color change. After 40 min of adaptation, when two yellow patches are successively presented on each side of the screen, the chromaticity of the left and right patches need respectively to be shifted toward the chromaticity of the red and green adaptation patches for subjective equality to be obtained. When the eyes are kept fixed during the adaptation stage, creating a strong nonhomogeneity in retinal adaptation, no effect is found. This ensures that, if present, adaptation at a given retinal location cannot explain the present effect. A third experiment shows a dependency of the effect on the eyes' saccadic movements and not on the position on the screen, that is, on the position of the eyes in the orbits. These results argue for the involvement of sensorimotor mechanisms in color perception. The relation of these experimental findings toward a sensorimotor theory of color perception is discussed.

Adaptation, Physiological↗

Vitamin A status modulates intestinal adaptation after partial small bowel resection.

BACKGROUND: Intestinal adaptation after loss of functional small bowel surface area is characterized by cellular hyperplasia and increased absorptive function. Interventions to enhance the adaptive response are needed to decrease the morbidity and mortality associated with short bowel syndrome. Retinoic acid was shown to stimulate crypt cell proliferation in the adapting remnant rat ileum by 6 hours after resection. Thus, vitamin A, which is required for normal epithelial cell proliferation and differentiation and which can modulate programmed cell death, may play an important role in the adapting intestine. On the basis of these observations, the effects of vitamin A deficiency on intestinal morphology, epithelial cell proliferation, and apoptosis in the adapting intestine after resection were investigated. METHODS: Weanling male Sprague-Dawley rats fed either a vitamin A-deficient or -sufficient diet for 58 days underwent 70% proximal small bowel resection. The deficient rats were divided into cohorts that were either maintained on the experimental diet after surgery or replenished with vitamin A 20 hours before surgery and switched to the control diet after surgery. RESULTS: Ten days after resection, vitamin A-deficient rats exhibited a markedly blunted adaptive response. The adaptive increase in villus height and crypt depth was absent in the deficient rats. However, adaptive increases in crypt cell proliferation were not attenuated by vitamin A deficiency, and there were no differences in apoptotic indices. CONCLUSIONS: Vitamin A deficiency inhibits the adaptive response to partial small bowel resection, supporting a role for vitamin A in the adaptive process. Changes in cellular proliferation or programmed cell death are not sufficient to account for this inhibition. This model system will be useful for examining the role of other mechanisms, such as changes in cell-cell and cell-extracellular matrix interactions, and rates of epithelial cell migration and cell extrusion.

Adaptation, Physiological↗

Adaptation to chemotactic cyclic AMP signals in Dictyostelium involves the G-protein.

Amoebae of Dictyostelium discoideum show adaptation towards a chemotactic cyclic AMP signal. Within a few seconds of receipt of the signal they are inhibited for a period of 1-2 min from further chemotactic responses to subsequent cyclic AMP signals of similar or smaller magnitude. The site of this adaptation mechanism in the chemotactic transduction pathway was investigated by addition of components of the transduction chain (GTP analogues, myo-inositol-1,4,5-trisphosphate (InsP3) and Ca2+) to permeabilized cells followed by determination of the amount of cyclic GMP formed as a measure of the chemotactic response. This approach was made possible by finding that permeabilization of amoebae with saponin did not uncouple the cell surface cyclic AMP receptors from stimulation of cyclic GMP formation. It was found that InsP3 and Ca2+ were 'downstream' from the adaptation mechanism: they could trigger a cyclic GMP response in cyclic AMP-adapted amoebae but could not themselves induce adaptation. In contrast, GTP gamma S was unable to trigger a cyclic GMP response in cyclic AMP-adapted cells, although it could trigger multiple cyclic GMP responses in non-adapted cells. We deduce that the site of adaptation to cyclic AMP stimulation is at the G-protein involved in this signalling pathway. Moreover, as GTP gamma S was found to be unable to induce adaptation, we conclude that the mechanism of adaptation involves an action of the cyclic AMP receptor on the G-protein that is distinct from its commonly reported action of stimulating G-protein binding of GTP.

Adaptation, Physiological↗

Assessment of the dark-adaptation time required for recovery of electroretinographic responses in dogs after fundus photography and indirect ophthalmoscopy.

OBJECTIVE: To investigate the duration of dark-adaptation time required for recovery of electroretinographic responses after fundus photography or indirect ophthalmoscopy in dogs. ANIMALS: 6 dogs. PROCEDURE: Initially, scotopic-intensity series of electroretinograms (ERGs) were recorded after 20 minutes of dark adaptation. The fundus of the left eye of each dog was photographed (n = 10) or examined via indirect ophthalmoscopy for 5 minutes with moderate- (117 candela [cd]/m2) or bright-intensity (1,693 cd/m2) light; ERGs were repeated after a further 20 or 60 minutes of dark adaptation (6 procedures/dog). RESULTS: Following 20 minutes of dark adaptation after fundus photography, the b- and a-wave amplitudes were reduced in response to brighter stimuli, compared with pretest ERGs; after 60 minutes of dark adaptation, ERG amplitudes had recovered. Following 20 minutes of dark adaptation after indirect ophthalmoscopy (moderate-intensity light), significantly lower b-wave amplitudes were recorded in response to 2 of the brighter flash stimuli, compared with pretest ERGs; after 60 minutes of dark adaptation, ERG amplitudes had recovered. Following 20 minutes of dark adaptation after indirect ophthalmoscopy (bright-intensity light), all ERG amplitudes were significantly decreased and implicit times were significantly decreased at several flash intensities, compared with pretest ERGs; after 60 minutes of dark adaptation, ERG amplitudes and implicit times had returned to initial values, except for b-wave amplitudes recorded in response to dimmer stimuli. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that at least 60 minutes of dark adaptation should be allowed before ERGs are performed in dogs after fundus photography or indirect ophthalmoscopy.

Adaptation, Ocular↗

Changes in VOR adaptation after local injection of beta-noradrenergic agents in the flocculus of rabbits.

Noradrenaline (NA) has been implicated as a neuromodulator in plasticity, presumably facilitating adaptive processes. Since the flocculus receives noradrenergic afferents, and ablation of the flocculus interferes with the normal adaptive changes in the VOR gain, experiments were performed to find out whether bilateral injection of monoaminergic substances into the flocculus of rabbits could modify the adaptive changes of the VOR. The visual world surrounding the rabbit was oscillated in opposite direction to the platform on which the rabbit was mounted, which resulted in an adaptive increase in the VOR gain; this adaptation was measured either in light or in darkness. Floccular injection of the beta-agonist isoproterenol did not greatly affect the adaptation of the VOR measured in light. In darkness, however, the increase in gain after injection of isoproterenol was larger than during normal adaptation. The beta-antagonist sotalol reduced the adaptation of the VOR gain significantly in light as well as in darkness. In a control condition without pressure for adaptation (only intermittent testing of the VOR gain over a period of 2.5 h), the gain of the VOR was not significantly affected by similar injections of beta-adrenergic agents. We conclude that the noradrenergic system facilitates the adaptation of the VOR gain to retinal slip in rabbits without affecting the VOR gain directly. At least part of this influence is exerted through beta-receptors located in the cerebellar flocculus.

Adaptation, Physiological↗

Gastric adaptation to stress: role of sensory nerves, salivary glands, and adrenal glands.

BACKGROUND: Single exposure to water immersion and restraint stress (WRS) in rats produces acute gastric mucosal damage, but repetitive WRS insults lead to gastric adaptation to stress ulcerogenesis. This study was designed to assess the mechanism of this adaptation, particularly the role of sensory nerves, salivary glands, adrenal glands, and gastric acid secretion. METHODS: WRS was applied for a standard period of 3.5 h, either once or repeated every other day for up to 8 days in intact rats and in animals with capsaicin-induced deactivation of sensory nerves, vagotomy, salivectomy, adrenalectomy, and inhibition of gastric acid secretion by H2-blocker. RESULTS: WRS applied once produced multiple gastric erosions accompanied by a significant increase in gastric acid secretion and a decrease in gastric blood flow (GBF) and DNA synthesis. Repeated WRS insults resulted in a significant decrease in the number of gastric lesions, reaching a maximum after four consecutive exposures to WRS. This adaptation to stress ulcerogenesis was accompanied by a decrease in gastric acid secretion and an increase in GBF and mucosal generation of DNA synthesis. Salivectomy, which decreased the luminal content of epidermal growth factor (EGF) (by about 80%), markedly attenuated this adaptation, and this was reversed by the addition of exogenous EGF. Capsaicin-induced ablation of sensory nerves eliminated gastric adaptation to WRS, and this was accompanied by a significant decrease in the GBF, but pretreatment with calcitonin gene-related peptide restored gastric adaptation to stress in capsaicin-denervated rats. Selective vagotomy and adrenalectomy failed to affect gastric adaptation to WRS, whereas gastric acid inhibition by ranitidine enhanced this adaptation. CONCLUSIONS: The stomach is able to adapt to repeated stress insults by enhancing GBF and DNA synthesis, and this adaptation is mediated, at least in part, by sensory nerves and EGF.

Adaptation, Physiological↗