Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.9.3.1 (cytochrome oxidase)
 8,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study describes the location and anatomical subdivisions of the auditory cortex of the horseshoe bat, Rhinolophus rouxi. The basic cyto- and myeloarchitectural features and cytochrome oxidase reactivity patterns are evaluated in brains where auditory fields have been previously established neurophysiologically (Radtke-Schuller and Schuller 1995). Thus, the neuroanatomical findings from these brains and additional analyzed material are related to neurophysiological characteristics. The neocortex of Rhinolophus shows a typical mammalian six-layered organization. It is poorly laminated, has a low density of granular elements, a wide layer I, and a phylogenetically old pyramidal cell type in a sharply accentuated layer II. These features are generally considered 'primitive' or conservative. Frontal, parietal, temporal and occipital regions can be distinguished. In the temporal cortex, layers III and IV are found to be markedly thicker than layer V, in contrast to the parietal region, where a prominent layer V, containing a high concentration of large pyramidal cells is the most outstanding feature. The entire temporal region, most of the parietal and parts of the occipital region are responsive to auditory stimuli. The primary auditory field corresponds to most of the temporal region. The fields of the parietal region almost completely coincide with the dorsal fields of the auditory cortex. Border zones between the temporal, parietal, and occipital regions correspond to the posterior auditory field. The non-primary fields of the auditory cortex occupy a larger area of the bat's neocortex than the primary field. The accentuated neuroarchitectural features, like cortical thickness and staining intensity, are shown to coincide with the physiological representation of biologically significant parameters.
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PMID:Neuroarchitecture of the auditory cortex in the rufous horseshoe bat (Rhinolophus rouxi). 1150 34

Evidence indicates that the degeneration of basal forebrain cholinergic neurons may represent an important factor underlying the progressive cognitive decline characterizing Alzheimer's disease (AD). However, the nature of the relationship between cholinergic depletion and AD is not fully elucidated. This study aimed at clarifying some aspects of the relation existing between deficits in cerebral energy metabolism and degeneration of cholinergic system in AD, by investigating the neuronal metabolic activity of several cortical areas after depletion of basal forebrain cholinergic neurons. In cholinergically depleted rats, we evaluated the neuronal metabolic activity by assaying cytochrome oxidase (CO) activity in frontal, parietal and posterior parietal cortices at four different time-points after unilateral injection of 192 IgG-saporin in the nucleus basalis magnocellularis. Unilateral depletion of cholinergic cells in the basal forebrain induced a bilateral decrease of metabolic activity in all the analyzed areas. Frontal and parietal cortices showed decreased metabolic activity even 3 days after the lesion, when the cholinergic degeneration was still incomplete. In posterior parietal cortex metabolic activity decreased only 7 days after the lesion. The possible molecular mechanisms underlying these findings were also investigated. Real-time PCR showed an increase of CO mRNA levels at 3, 7 and 15 days after the lesion both in frontal and parietal cortices, followed by normalization at 30 days. Western Blot analysis did not show any change in CO protein levels at any time-point after the lesion. Our findings support a link between metabolic deficit and cholinergic hypofunctionality characterizing AD pathology. The present model of cholinergic hypofunctionality provides a useful means to study the complex mechanisms linking two fundamental and interrelated phenomena characterizing AD from the early stages.
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PMID:Cortical metabolic deficits in a rat model of cholinergic basal forebrain degeneration. 2392 61