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Author

Arnold B. Scheibel

Other affiliations: University of Tennessee
Bio: Arnold B. Scheibel is an academic researcher from University of California, Los Angeles. The author has contributed to research in topics: Neuropil & Dendrite. The author has an hindex of 50, co-authored 100 publications receiving 10811 citations. Previous affiliations of Arnold B. Scheibel include University of Tennessee.


Papers
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Journal ArticleDOI
TL;DR: Across subjects, the overall density of callosal fibers had no significant correlation withcallosal area and an increased callosal area indicated an increased total number of fibers crossing through, and this was only true for small diameter fibers, whose large majority is believed to interconnect association cortex.

1,340 citations

Journal Article
TL;DR: An apparently consistent alteration of pyramidal cell orientation in chronic schizophrenic patients compared with eight nonschizophrenic controls is reported, suggesting a histopathological continuum ranging from the clinically nonpsychotic individual, through borderline states to the intractable long-term psychotic.

608 citations

Journal ArticleDOI
TL;DR: Deterioration of psychomotor performance with aging may be conceived in significant degree as a function of the quality of neuropil as well as of the amount of total nerve cell loss.

362 citations

Journal ArticleDOI
TL;DR: The relationship between the basilar dendrites of supragranular pyramidal cells in Wernicke's area is examined and gender and hemisphere and selected intrinsic and extrinsic variables are selected.
Abstract: This quantitative Golgi study extends our investigation of relationships between cortical dendrite systems in humans and higher cognitive functions. Here we examine the relationship between the basilar dendrites of supragranular pyramidal cells in Wernicke's area and selected intrinsic (i.e., gender and hemisphere) and extrinsic (i.e., education and personal history) variables. Tissue was obtained from 20 neurologically normal right-handers: 10 males (Mage = 52.2) and 10 females (Mage = 47.8). Several independent variables were investigated: GENDER (male, female), HEMISPHERE (left, right), and EDUCATION (less than high school, high school, and university). These were evaluated according to Total Dendritic Length, Mean Dendritic Length, and Dendritic Segment Count. A distinction was made between proximal (1st, 2nd, and 3rd order) and ontogenetically later developing distal (4th order and above) branches. There was significant interindividual variation in dendritic measurements, which roughly reflected individuals' personal backgrounds. Females exhibited slightly greater dendritic values and variability than males across the age range examined. On the whole, the left hemisphere maintained a slight advantage over the right hemisphere for all dendritic measures when all subjects were pooled, but these differences were not in a consistent direction across individuals. Education had a consistent and substantial effect such that dendritic measures increased as educational levels increased. Dendritic differences between independent variable levels were most clearly illustrated in the total dendritic length of 3rd and 4th order branches. Distal dendritic branches appeared to exhibit greater epigenetic flexibility than proximal dendrites. The present findings concur with environmental enrichment research results in animals and suggest that dendritic systems in humans function as a sensitive indicator of an individual's (a)vocational activities.

321 citations


Cited by
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Journal ArticleDOI
TL;DR: Developmental changes in prefrontal cortex and limbic brain regions of adolescents across a variety of species, alterations that include an apparent shift in the balance between mesocortical and mesolimbic dopamine systems likely contribute to the unique characteristics of adolescence.

4,985 citations

Journal ArticleDOI
TL;DR: By better understanding AD inflammatory and immunoregulatory processes, it should be possible to develop anti-inflammatory approaches that may not cure AD but will likely help slow the progression or delay the onset of this devastating disorder.

4,319 citations

Journal ArticleDOI
TL;DR: Astrocyte functions in healthy CNS, mechanisms and functions of reactive astrogliosis and glial scar formation, and ways in which reactive astrocytes may cause or contribute to specific CNS disorders and lesions are reviewed.
Abstract: Astrocytes are specialized glial cells that outnumber neurons by over fivefold. They contiguously tile the entire central nervous system (CNS) and exert many essential complex functions in the healthy CNS. Astrocytes respond to all forms of CNS insults through a process referred to as reactive astrogliosis, which has become a pathological hallmark of CNS structural lesions. Substantial progress has been made recently in determining functions and mechanisms of reactive astrogliosis and in identifying roles of astrocytes in CNS disorders and pathologies. A vast molecular arsenal at the disposal of reactive astrocytes is being defined. Transgenic mouse models are dissecting specific aspects of reactive astrocytosis and glial scar formation in vivo. Astrocyte involvement in specific clinicopathological entities is being defined. It is now clear that reactive astrogliosis is not a simple all-or-none phenomenon but is a finely gradated continuum of changes that occur in context-dependent manners regulated by specific signaling events. These changes range from reversible alterations in gene expression and cell hypertrophy with preservation of cellular domains and tissue structure, to long-lasting scar formation with rearrangement of tissue structure. Increasing evidence points towards the potential of reactive astrogliosis to play either primary or contributing roles in CNS disorders via loss of normal astrocyte functions or gain of abnormal effects. This article reviews (1) astrocyte functions in healthy CNS, (2) mechanisms and functions of reactive astrogliosis and glial scar formation, and (3) ways in which reactive astrocytes may cause or contribute to specific CNS disorders and lesions.

4,075 citations

Journal ArticleDOI
TL;DR: The findings suggest that nonspecific histopathology exists in the limbic system, diencephalon, and prefrontal cortex, that the pathology occurs early in development, and that the causative process is inactive long before the diagnosis is made.
Abstract: • Recent research on schizophrenia has demonstrated that in this disorder the brain is not, strictly speaking, normal. The findings suggest that nonspecific histopathology exists in the limbic system, diencephalon, and prefrontal cortex, that the pathology occurs early in development, and that the causative process is inactive long before the diagnosis is made. If these findings are valid and not epiphenomena, then the pathogenesis of schizophrenia does not appear to fit either traditional metabolic, posttraumatic, or neurodegenerative models of adult mental illness. The data are more consistent with a neurodevelopmental model in which a fixed "lesion" from early in life interacts with normal brain maturational events that occur much later. Based on neuro-ontological principles and insights from animal research about normal brain development, it is proposed that the appearance of diagnostic symptoms is linked to the normal maturation of brain areas affected by the early developmental pathology, particularly the dorsolateral prefrontal cortex. The course of the illness and the importance of stress may be related to normal maturational aspects of dopaminergic neural systems, particularly those innervating prefrontal cortex. Some implications for future research and treatment are considered.

3,562 citations

Book
05 Jun 1975
TL;DR: Introduction to synaptic circuits, Gordon M.Shepherd and Christof Koch membrane properties and neurotransmitter actions, David A.Brown and Anthony M.Brown.
Abstract: Introduction to synaptic circuits, Gordon M.Shepherd and Christof Koch membrane properties and neurotransmitter actions, David A.McCormick peripheral ganglia, Paul R.Adams and Christof Koch spinal cord - ventral horn, Robert E.Burke olfactory bulb, Gordon M.Shepherd, and Charles A.Greer retina, Peter Sterling cerebellum, Rodolfo R.Llinas and Kerry D.Walton thalamus, S.Murray Sherman and Christof Koch basal ganglia, Charles J.Wilson olfactory cortex, Lewis B.Haberly hippocampus, Thomas H.Brown and Anthony M.Zador neocortex, Rodney J.Douglas and Kevan A.C.Martin Gordon M.Shepherd. Appendix: Dendretic electrotonus and synaptic integration.

3,241 citations