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A Grunewald

Publications and source records attributed to A Grunewald.

17 recordsLinked to original sources
PubMed1999

Responses to auditory stimuli in macaque lateral intraparietal area. I. Effects of training.

The lateral intraparietal area (LIP) of macaques has been considered unresponsive to auditory stimulation. Recent reports, however, indicate that neurons in this area respond to auditory stimuli in the context of an auditory-saccade task. Is this difference in auditory responsiveness of LIP due to auditory-saccade training? To address this issue, LIP responses in two monkeys were recorded at two different times: before and after auditory-saccade training. Before auditory-saccade training, the animals had never been trained on any auditory task, but had been trained on visual tasks. In both sets of experiments, activity of LIP neurons was recorded while auditory and visual stimuli were presented and the animals were fixating. Before training, 172 LIP neurons were recorded. Among these, the number of cells responding to auditory stimuli did not reach significance, whereas about one-half of the cells responded to visual stimuli. An information theory analysis confirmed that no information about auditory stimulus location was available in LIP neurons in the experiments before training. After training, activity from 160 cells was recorded. These experiments showed that 12% of cells in area LIP responded to auditory stimuli, whereas the proportion of cells responding to visual stimuli remained about the same as before training. The information theory analysis confirmed that, after training, information about auditory stimulus location was available in LIP neurons. Auditory-saccade training therefore generated responsiveness to auditory stimuli de novo in LIP neurons. Thus some LIP cells become active for auditory stimuli in a passive fixation task, once the animals have learned that these stimuli are important for oculomotor behavior.

Acoustic Stimulation↗
PubMed1999

Responses to auditory stimuli in macaque lateral intraparietal area. II. Behavioral modulation.

The lateral intraparietal area (LIP), a region of posterior parietal cortex, was once thought to be unresponsive to auditory stimulation. However, recent reports have indicated that neurons in area LIP respond to auditory stimuli during an auditory-saccade task. To what extent are auditory responses in area LIP dependent on the performance of an auditory-saccade task? To address this question, recordings were made from 160 LIP neurons in two monkeys while the animals performed auditory and visual memory-saccade and fixation tasks. Responses to auditory stimuli were significantly stronger during the memory-saccade task than during the fixation task, whereas responses to visual stimuli were not. Moreover, neurons responsive to auditory stimuli tended also to be visually responsive and to exhibit delay or saccade activity in the memory-saccade task. These results indicate that, in general, auditory responses in area LIP are modulated by behavioral context, are associated with visual responses, and are predictive of delay or saccade activity. Responses to auditory stimuli in area LIP may therefore be best interpreted as supramodal responses, and similar in nature to the delay activity, rather than as modality-specific sensory responses. The apparent link between auditory activity and oculomotor behavior suggests that the behavioral modulation of responses to auditory stimuli in area LIP reflects the selection of auditory stimuli as targets for eye movements.

Acoustic Stimulation↗
PubMed1998

Motion after-effect due to binocular sum of adaptation to linear motion.

The motion after-effect (MAE) can be elicited by adapting observers to global motion of randomly distributed dots before they view a display containing dots moving in random directions, but no global motion. Experiments by others have shown that if the adaptation stimulus contains two directions of motion, the MAE points opposite to the vector sum of the adapting directions. The present study investigated whether such vector addition in the MAE could also occur if the two directions of motion were presented to separate eyes. Observers were adapted to different, but not opposite, directions of motion in the two eyes. Either the left eye, the right eye, or both eyes were tested. Observers reported the direction of perceived motion during the test. When they saw the test stimulus with both eyes, observers reported seeing motion in the direction opposite that of the vector sum of the adaptation directions. In the monocular test conditions observers reported MAE directions opposite to the corresponding monocular adaptation directions. In a second experiment we verified that subjects had interocular transfer of the MAE. Together these results are consistent with a model in which (1) addition of adaptation directions occurs at a binocular site; (2) directional adaptation occurs at a monocular site; and (3) monocular adaptation is able to change the threshold for obtaining an MAE at the binocular site, thus acting like binocular adaptation in interocular transfer of the MAE.

Adaptation, Ocular↗
PubMed1998

Self-organization of binocular disparity tuning by reciprocal corticogeniculate interactions.

This article develops a neural model of how sharp disparity tuning can arise through experience-dependent development of cortical complex cells. This learning process clarifies how complex cells can binocularly match left and right eye image features with the same contrast polarity, yet also pool signals with opposite contrast polarities. Antagonistic rebounds between LGN ON and OFF cells and cortical simple cells sensitive to opposite contrast polarities enable anticorrelated simple cells to learn to activate a shared set of complex cells. Feedback from binocularly tuned cortical cells to monocular LGN cells is proposed to carry out a matching process that dynamically stabilizes the learning process. This feedback represents a type of matching process that is elaborated at higher visual processing areas into a volitionally controllable type of attention. We show stable learning when both of these properties hold. Learning adjusts the initially coarsely tuned disparity preference to match the disparities present in the environment, and the tuning width decreases to yield high disparity selectivity, which enables the model to quickly detect image disparities. Learning is impaired in the absence of either antagonistic rebounds or corticogeniculate feedback. The model also helps to explain psychophysical and neurobiological data about adult 3-D vision.

Algorithms↗
PubMed1996

Orthogonal motion after-effect illusion predicted by a model of cortical motion processing.

The motion after-effect occurs after prolonged viewing of motion; a subsequent stationary scene is perceived as moving in the opposite direction. This illusion is thought to arise because motion is represented by the differential activities of populations of cortical neurons tuned to opposite directions; fatigue in one population leads to an imbalance that favours the opposite direction once the stimulus ceases. Following adaptation to multiple directions of motion, the after-effect is unidirectional, indicating that motion signals are integrated across all directions. Yet humans can perceive several directions of motion simultaneously. The question therefore arises as to how the visual system can perform both sharp segregation and global integration of motion signals. Here we show in computer simulations that this can occur if excitatory interactions between different directions are sharply tuned while inhibitory interactions are broadly tuned. Our model predicts that adaptation to simultaneous motion in opposite directions will lead to an orthogonal motion after-effect. This prediction was confirmed in psychophysical experiments. Thus, broadly tuned inhibitory interactions are likely to be important in the integration and segregation of motion signals. These interactions may occur in the cortical area MT, which contains motion-sensitive neurons with properties similar to those required by our model.

Afterimage↗
PubMed1994

Isolation and function of human and pig islets.

This report confirms reproducible methods to isolate and assess viability and function of pig and human islets. We processed 10 pig and five human pancreata. The pancreata were digested by a modification of Ricordi's automated method for islet isolation. The number of islet equivalents (150 microns diameter islets) was 335,190 +/- 79,345 islets per pig pancreas (5,146 +/- 1,274 islets/g pig pancreas) and 323,630 +/- 147,810 per human pancreas (6,252 +/- 2,572 islets/g human pancreas). The majority of islets were in the range of 50-200 microns diameter, and 20% of the islet population had a size distribution of 200 microns diameter in both porcine and human models. The purity of the final preparations exceeded 90%. The secretory response of perifused islets showed a biphasic insulin release pattern in both species. Perifused fresh pig islets released 2.5 pmol/L islet-1 min-1 at 2.0 mM glucose and 6.2 pmol/L islet-1 min-1 at 16.7 mM glucose. After 7 days culture at 37 degrees C, human islets released 1.32 pmol/L islet-1 min-1 at 2.0 mM and 12.24 pmol/L islet-1 min-1 at 16.7 mM. These results indicate that this procedure is useful to obtain pure, large, and functional islets from pig and human pancreata.

Adult↗
PubMed1993

Pancreatic islet function in nondiabetic and diabetic BB rats.

A decreased acute insulin response to glucose in islet cell antibody positive humans predicts diabetes. Because the dominant mechanism leading to decreased in vivo acute insulin response to glucose remains unclear, perifused islets were examined before and after diabetes onset in BB rats to assess the role of glucose sensitivity on insulin secretion in individual islets. Islets from normal WF rats, diabetes-prone rats without inflamed islets, diabetes-prone rats with inflamed islets, and diabetic rats were studied at 2.0, 8.3, and 16.7 mM glucose. Immunoreactive insulin from WF islets at 16.7 mM glucose was 0.15 +/- 0.02 ng.0-7 min-1 x islet-1 for the first phase and 1.00 +/- 0.05 ng.7-20 min-1 x islet-1 for the second phase of biphasic secretion, compared with basal secretion of 0.10 +/- 0.03 ng.20 min-1 x islet-1 at 2 mM glucose. Diabetes-prone noninflamed islets showed a 0.20 +/- 0.03 ng first-phase secretion, a 1.32 +/- 0.13 ng second-phase secretion after 16.7 mM glucose, and 0.093 +/- 0.02 ng.20 min-1 x islet-1 at 2 mM glucose, indicating no intrinsic BB rat strain secretion abnormality. Diabetes-prone inflamed islets had secretions of 0.35 +/- 0.02 ng during the first phase (P < 0.05 vs. WF) and 1.78 +/- 0.29 ng during the second phase (P < 0.05 vs. WF) after 16.7 mM glucose, with 0.24 +/- 0.08 ng.20 min-1 x islet-1 at 2 mM glucose.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗