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D A Pollen

Publications and source records attributed to D A Pollen.

45 records · Page 3Linked to original sources
PubMedDate not supplied

Structural testing of multi-input linear-nonlinear cascade models for cells in macaque striate cortex.

Structural testing methods based on experimental white noise stimulus-response data were used to evaluate multi-input linear-nonlinear (LN) cascade models for simple and complex cells in macaque striate cortex. An LN structural test index, based on white noise stimulation, was developed and found to be suitable for classifying cells as simple vs complex. In particular, classification results based on the LN structural test index were similar to classification results based on a traditional modulation index derived from cell responses to drifting sinewave gratings. Judging from their structural test indices, complex cells deviated more strongly from LN behavior than did simple cells. Yet, even with simple cells, on average, only about 60% of the first- and second-order white noise stimulus-response relation was consistent with LN behavior. Just two of thirteen simple cells studied had an LN consistency level that exceeded 80%. Similar results were found in tests for consistency with an LNL model which includes an additional linear post-filter. We conclude that a conventional multi-input LN network model may be a useful approximation to the response behavior of some simple cells. However, even during steady state stimulus conditions, subcortical and/or cortical nonlinearities other than a static output nonlinearity play a very significant role in shaping the responses of most simple cells in the macaque striate cortex.

Animals↗
PubMedDate not supplied

Distinguishable effects of presenilin-1 and APP717 mutations on amyloid plaque deposition.

Both APP and PS-1 are causal genes for early-onset familial Alzheimer's disease (AD) and their mutation effects on cerebral Abeta deposition in the senile plaques were examined in human brains of 29 familial AD (23 PS-1, 6 APP) cases and 14 sporadic AD cases in terms of Abeta40 and Abeta42. Abeta isoform data were evaluated using repeated measures analysis of variance which adjusted for within-subject measurement variation and confounding effects of individual APP and PS-1 mutations, age at onset, duration of illness and APOE genotype. We observed that mutations in both APP and PS-1 were associated with a significant increase of Abeta42 in plaques as been documented previously. In comparison to sporadic AD cases, both APP717 and PS-1 mutation cases had an increased density (measured as the number of plaques/mm(2)) and area (%) of Abeta42 plaques. However, we found an unexpected differential effect of PS-1 but not APP717 mutation cases. At least some of PS-1 but not APP717 mutation cases had the significant increase of density and area of Abeta40-plaques as compared to sporadic AD independently of APOE genotype. Our results suggest that PS-1 mutations affect cerebral accumulation of Abeta burden in a different fashion from APP717 mutations in their familial AD brains.

Adult↗
PubMedDate not supplied

Space-time spectra of complex cell filters in the macaque monkey: a comparison of results obtained with pseudowhite noise and grating stimuli.

White noise stimuli were used to estimate second-order kernels for complex cells in cortical area V1 of the macaque monkey, and drifting grating stimuli were presented to the sample of neurons to obtain orientation and spatial-frequency tuning curves. Using these data, we quantified how well second-order kernels predict the normalized tuning of the average response of complex cells to drifting gratings. The estimated second-order kernel of each complex cell was transformed into an interaction function defined over all spatial and temporal lags without regard to absolute position or delay. The Fourier transform of each interaction function was then computed to obtain an interaction spectrum. For a cell that is well modeled by a second-order system, the cell's interaction spectrum is proportional to the tuning of its average spike rate to drifting gratings. This result was used to obtain spatial-frequency and orientation tuning predictions for each cell based on its second-order kernel. From the spatial-frequency and orientation tuning curves, we computed peaks and bandwidths, and an index for directional selectivity. We found that the predictions derived from second-order kernels provide an accurate description of the change in the average spike rate of complex cells to single drifting sine-wave gratings. These findings are consistent with a model for complex cells that has a quadratic spectral energy operator at its core but are inconsistent with a spectral amplitude model.

Animals↗
PubMedDate not supplied

Striate cortex increases contrast gain of macaque LGN neurons.

Recurrent projections comprise a universal feature of cerebral organization. Here, we show that the corticofugal projections from the striate cortex (VI) to the lateral geniculate nucleus (LGN) robustly and multiplicatively enhance the responses of parvocellular neurons, stimulated by gratings restricted to the classical receptive field and modulated in luminance, by over two-fold in a contrast-independent manner at all but the lowest contrasts. In the equiluminant plane, wherein stimuli are modulated in chromaticity with luminance held constant, such enhancement is strongly contrast dependent. These projections also robustly enhance the responses of magnocellular neurons but contrast independently only at high contrasts. Thus, these results have broad functional significance at both network and neuronal levels by providing the experimental basis and quantitative constraints for a wide range of models on recurrent projections and the control of contrast gain.

Animals↗
PubMedDate not supplied

On the neural correlates of visual perception.

Neurological findings suggest that the human striate cortex (V1) is an indispensable component of a neural substratum subserving static achromatic form perception in its own right and not simply as a central distributor of retinally derived information to extrastriate visual areas. This view is further supported by physiological evidence in primates that the finest-grained conjoined representation of spatial detail and retinotopic localization that underlies phenomenal visual experience for local brightness discriminations is selectively represented at cortical levels by the activity of certain neurons in V1. However, at first glance, support for these ideas would appear to be undermined by incontrovertible neurological evidence (visual hemineglect and the simultanagnosias) and recent psychophysical results on 'crowding' that confirm that activation of neurons in V1 may, at times, be insufficient to generate a percept. Moreover, a recent proposal suggests that neural correlates of visual awareness must project directly to those in executive space, thus automatically excluding V1 from a related perceptual space because V1 lacks such direct projections. Both sets of concerns are, however, resolved within the context of adaptive resonance theories. Recursive loops, linking the dorsal lateral geniculate nucleus (LGN) through successive cortical visual areas to the temporal lobe by means of a series of ascending and descending pathways, provide a neuronal substratum at each level within a modular framework for mutually consistent descriptions of sensory data. At steady state, such networks obviate the necessity that neural correlates of visual experience project directly to those in executive space because a neural phenomenal perceptual space subserving form vision is continuously updated by information from an object recognition space equivalent to that destined to reach executive space. Within this framework, activity in V1 may engender percepts that accompany figure-ground segregations only when dynamic incongruities are resolved both within and between ascending and descending streams. Synchronous neuronal activity on a short timescale within and across cortical areas, proposed and sometimes observed as perceptual correlates, may also serve as a marker that a steady state has been achieved, which, in turn, may be a requirement for the longer time constants that accompany the emergence and stability of perceptual states compared to the faster dynamics of adapting networks and the still faster dynamics of individual action potentials. Finally, the same consensus of neuronal activity across ascending and descending pathways linking multiple cortical areas that in anatomic sequence subserve phenomenal visual experiences and object recognition may underlie the normal unity of conscious experience.

Adaptation, Physiological↗
PubMedDate not supplied

Familial Alzheimer's disease and cortical Lewy bodies: is there a genetic susceptibility factor?

The reason for the occurrence of Lewy body disease (LBD) in Alzheimer's disease (AD) patients is unknown. If brains from etiologically different AD groups differ in their tendency to develop cortical Lewy bodies, the concurrence of LBD in AD patients may be a manifestation of the AD process in specific AD subsets. To address this issue, we counted cortical Lewy bodies in AD patients with genetic abnormalities on chromosome 14 (n = 19), and chromosome 21 (n = 3), sporadic AD (n = 27), Down's syndrome (n = 1) and control (n = 26) patients. Cortical Lewy bodies were occasionally present in AD patients with long-duration disease in most of the above AD subgroups, but were not present in any of our age-matched control cases. We suggest that cortical Lewy body formation may be an intrinsic part of the late pathologic changes of AD regardless of etiology and that it is not specific to any of the AD subtypes studied.

Aged↗