Daniel A. Pollen

Visual cortical neurons as localized spatial frequency filters

This paper relates to the receptive field properties of neurons in the primary visual cortex, i.e. the striate cortex, to current issues in spatial visual information processing. Particular attention is given to the fact that receptive field profiles of simple cells in the visual cortex often resemble even-symmetric or odd-symmetric Gabor filters; i.e. their receptive field profiles can be described by the product of a Gaussian and either a cosine or sine function. Their spatial frequency tuning is of medium bandwidth (~one octave) which is narrow enough for a cell to distinguish the third harmonic from the fundamental frequency for square-wave gratings of low spatial frequency. The responses of adjacent simple cells, tuned to the same spatial frequency, orientation, and direction, differ in their phase response to drifting sine-wave gratings by approximately either 90° or 180°. This latter result makes it possible to consider two adjacent simple cell pairs as operating like paired Gaussian-attenuated sine and cosine filters of Gabor filters for restricted regions of visual space. The entire set of simple cells provides a complete representation of the visual scene, yet each simple cell is unique in its response properties. At the complex cell stage, the cells mean firing rate appears to represent the amplitude of a local Fourier coefficient, but phase information is seldom conveyed with much precision in the action potential code.

Amyloid Deposition Begins in the Striatum of Presenilin-1 Mutation Carriers from Two Unrelated Pedigrees

The amyloid cascade hypothesis suggests that the aggregation and deposition of amyloid-β protein is an initiating event in Alzheimers disease (AD). Using amyloid imaging technology, such as the positron emission tomography (PET) agent Pittsburgh compound-B (PiB), it is possible to explore the natural history of preclinical amyloid deposition in people at high risk for AD. With this goal in mind, asymptomatic (n = 5) and symptomatic (n = 5) carriers of presenilin-1 (PS1) mutations (C410Y or A426P) that lead to early-onset AD and noncarrier controls from both kindreds (n = 2) were studied with PiB–PET imaging and compared with sporadic AD subjects (n = 12) and controls from the general population (n = 18). We found intense and focal PiB retention in the striatum of all 10 PS1 mutation carriers studied (ages 35–49 years). In most PS1 mutation carriers, there also were increases in PiB retention compared with controls in cortical brain areas, but these increases were not as great as those observed in sporadic AD subjects. The two PS1 mutation carriers with a clinical diagnosis of early-onset AD did not show the typical regional pattern of PiB retention observed in sporadic AD. Postmortem evaluation of tissue from two parents of PS1C410Y subjects in this study confirmed extensive striatal amyloid deposition, along with typical cortical deposition. The early, focal striatal amyloid deposition observed in these PS1 mutation carriers is often is not associated with clinical symptoms.

Neuroglia: Biophysical Properties and Physiologic Function

The membrane time constant of neocortical glial cells is abolut 385 microseconds, less than one-twentieth the known value for the Betz cell. Glial membrane specific resistance is low (approximately 200 to 500 ohm centimeters squared. Neuroglial cells are ideally suited to buffer the immediate extraneuronal space at areas of synaptic contact against the increases in external potassium ion concentration that accompany postsynaptic and spike activity and to minimize the spread of potassium ions to other pre- and postsynaptic regions.

Neuroglia: Gliosis and Focal Epilepsy

Normal neuroglial cells buffer the extracellular space around neurons and presynaptic terminals against increases in potassium ions. Epileptic foci resulting from brain injury are characterized by areas of intense fibrillary gliosis bordering neuronal tissue. The known pathological changes that occur in gliosis may impair glial control of extracellular potassium ions and lead to excessively excitable neuronal border regions.

Altered expression of transforming growth factor-beta in Alzheimer's disease

We compared immunohistochemical expression of the transforming growth factor-beta s (TGF-beta 1, TGF-beta 2, and TGF-beta 3) using brain tissue from patients with nondominantly inherited Alzheimers disease (NDAD) (n equals 9), autosomal dominantly inherited Alzheimers disease with linkage to 14q24.3 (FAD-14) (n equals 4), and cognitively normal controls (n equals 10) to determine whether their pathologic changes are associated with an altered distribution of the TGF-beta s. We found increased expression of TGF-beta 2 in large, tangle-bearing neurons with widespread staining of glia in NDAD and FAD-14 patients compared with control cases. This result was confirmed with sandwich ELISA assays of brain tissue, which showed TGF-beta 2 levels in AD and NDAD to average 3.2 times the average level of control cases. Despite proximity of TGF-beta 1 and TGF-beta 3 to the sites of susceptibility loci on chromosomes 19 and 14, we did not find that TGF-beta 1 and TGF-beta 3 were selectively altered in any AD subtypes. However, selective induction of TGF-beta 2 may occur in NDAD and FAD-14.

Spatial computation performed by simple and complex cells in the visual cortex of the cat

Simple and complex cells have been tested with drifting sine-wave and square-wave gratings. Despite the known differences in the response pattern of each cell type to drifting sine-wave gratings, the tuning curves for square-wave gratings for both cell types show a similar secondary response band peaking at one-third the preferred spatial frequency as determined from sine-wave studies. These results establish that both cell types respond predominantly to the third harmonic of square-wave gratings in this frequency range. At the simple cell stage, all the information required to specify the amplitude and phase for channel at a given orientation, direction and spatial frequency can be conveyed by four cells for a given subsection of visual space. At the complex cell stage, the cells mean firing rate appears to represent the amplitude of a local Fourier coefficient, but phase information is not conveyed in the action potential code.

How Does the Striate Cortex Begin the Reconstruction of the Visual World

The striate cortex transforms the topographic representation of visual space in the lateral geniculate body into a Fourier transform or frequency representation at the complex cell level via the intermediary simple cell stage of strip integration. Each of these three stages contains essentially the same amount of information, which expresses a conservation of information principle; however, the form of the information is changed. In the transform domain, invariant descriptions of visual objects can be derived to serve as the basic sets required for pattern recognition and memory. We believe that our experimental and theoretical findings are fundamental for understanding the functional organization of the striate cortex.

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.

Familial and sporadic Alzheimer's disease Neuropathology cannot exclude a final common pathway

Whether all etiologic forms of Alzheimers disease (AD) share a final common pathway is a major issue.We determined the severity and regional distribution of neuronal loss, amyloid plaques, neuritic plaques (NPs), and neurofibrillary tangles (NFTs), and calculated the ratio of neuronal loss to NPs and NFTs in brains of 19 familial AD (FAD) patients with linkage to chromosome 14, six AD patients with mutations of chromosome 21 (codon 717 of the beta-amyloid precursor protein gene), and 11 sporadic AD (SAD) patients. There was no difference in the pattern of distribution of the various pathologic features or in the ratio of neuronal loss to NPs or NFTs in any AD group. However, FAD groups could be distinguished from SAD by the greater severity and the lack of influence of apolipoprotein E genotype on pathology. These differences may reflect differences in age at onset rather than different etiopathologic mechanisms. The similarity of pathologic findings in the different AD groups provides evidence for a final common pathophysiologic pathway in AD. NEUROLOGY 1996;46: 406-212

Postmenopausal Hormone Therapy and Cognitive Function in Healthy Older Women

OBJECTIVE: Accumulating biologic evidence suggests that estrogen is related to cognitive function. Several epidemiologic investigations have reported that hormone therapy may reduce the risk of Alzheimers disease. However, fewer studies have examined the relation of postmenopausal hormone use to general cognitive function in nondemented older women. Thus, we examined the association of hormone therapy to performance on four cognitive tests among healthy participants of the Nurses Health Study.