Disease relevance of CORTICOSTERONE

• It is therefore hypothesized that similarities and differences between Parkinson's disease and catatonia may be accounted for by distinct kinds of modulation between cortico-cortical and cortico-subcortical relations [1].
• Abundant cytoplasmic inclusions consisting of aggregated hyperphosphorylated protein tau are a characteristic pathological observation in several neurodegenerative disorders such as Alzheimer's disease, Pick's disease, frontotemporal dementia, cortico-basal degeneration and progressive supranuclear palsy [2].
• Functional abnormalities reversed after liver transplantation and were associated with normalization of T2 cortico-spinal hyperintensity and with improvement of minimal hepatic encephalopathy [3].
• T2 hyperintensity along the cortico-spinal tract in cirrhosis relates to functional abnormalities [3].
• These findings suggest that mild cerebral edema along the cortico-spinal pathway may cause neuronal dysfunction [3].

Psychiatry related information on CORTICOSTERONE

• Cortico-basal ganglia circuit mechanism for a decision threshold in reaction time tasks [4].
• Cortico-cortical disconnection of association areas may disrupt widespread networks mediating attention and semantic knowledge in Alzheimer's disease [5].
• Visuomotor apraxia has traditionally been assumed to result from a disconnection of cortico-cortical fibres between visual and motor areas following occipito-parietal lesions [6].
• A cortico-spinal model of reaching and proprioception under multiple task constraints [7].
• The locus ceruleus and cortico-releasing factor are implicated in the biological circuit associated with panic attacks, while psychological research indicates that catastrophic thinking, phobic responses to somatic sensations, and repressed anger, grief, and traumatic events play a part in triggering attacks [8].

High impact information on CORTICOSTERONE

• The visual cortex is thus served by many cortico-cortical connections to form a network of considerable complexity [9].
• In 2-6-week-old rats we made complete transections of the cortico-spinal tract, a major fibre tract of the spinal cord, the axons of which originate in the motor and sensory neocortex [10].
• Corticosterone sulphate (once called compound B, and abbreviated to BS) is produced by fetal adrenal glands and is present in greater concentrations in human fetal plasma than in maternal plasma [11].
• The basal ganglia are thought to modulate the release or inhibition of movements by way of direct and indirect pathways that act as a push-pull system of cortico-basal ganglia circuits [12].
• Prediction of immediate and future rewards differentially recruits cortico-basal ganglia loops [13].

Chemical compound and disease context of CORTICOSTERONE

• Corticosterone (CS) has been shown to regulate behavior in the learned helplessness (LH) paradigm [14].
• Further studies on the treatment of congenital adrenal hyperplasia with cortisone: IV. Effect of cortisone and compound B in infants with disturbed electrolyte metabolism, by John F. Crigler Jr, MD, Samuel H. Silverman, MD, and Lawson Wilkins, MD, Pediatrics, 1952;10:397-413 [15].
• Ethanol enhanced the hyperthermic response and desensitized the adrenal response to microwave hyperthermia by increased baseline CS [16].
• The effect of early in life instituted undernutrition on the calibre growth of cortico-spinal motor fibres was studied electron microscopically at three different developmental stages in the rat [17].
• METHODS: Paired transcranial magnetic stimulation (TMS) was used to assess cortico-cortical inhibition (CCI) and facilitation (CCF) in the opponens pollicis muscle of patients with atypical, non-L-dopa- (LD) responsive parkinsonism [18].

Biological context of CORTICOSTERONE

• Human fetal movements in utero have been analysed by conventional compound B-scan ultrasound techniques [19].
• Upregulation elicited by exposure to compound A persisted in the presence of 1 mumol/L carbenoxolone, which completely prevented the conversion of compound A to compound B [20].
• Cirrhotic patients exhibited increased T2 signal and several functional abnormalities along the cortico-spinal tract (increased central motor conduction time, increased motor cortical threshold, and decreased motor-evoked potential amplitude) [3].
• In two subjects, involvement of the cortico-spinal tract was demonstrated by magnetic evoked potentials [21].
• The excitatory postsynaptic potentials elicited by presynaptic, phasically firing cortico-cortical pyramids in all classes of postsynaptic infragranular layer pyramidal cells exhibited strong, presynaptically mediated paired pulse and brief train depression [22].

Anatomical context of CORTICOSTERONE

• Mena-deficient mice are viable; however, axons projecting from interhemispheric cortico-cortical neurons are misrouted in early neonates, and failed decussation of the corpus callosum as well as defects in the hippocampal commissure and the pontocerebellar pathway are evident in the adult [23].
• This finding demonstrates a cortico-cortical mechanism subserving the transformation from the geometrical properties of an object to the outputs from motor cortex before grasp that is specific for object-driven movements [24].
• Cortico-basal ganglia circuits are key parts of the brain's habit system, but little is yet known about how these forebrain pathways function as ingrained habits are performed [25].
• The patterns of cortico-cortical and cortico-thalamic connections of auditory cortical areas in the rhesus monkey have led to the hypothesis that acoustic information is processed in series and in parallel in the primate auditory cortex [26].
• In all three species visual, auditory, and somatosensory information is transmitted to the amygdala by a series of modality-specific cortico-cortical pathways ("cascades") that originate in the primary sensory cortices and flow toward higher order association areas [27].

Associations of CORTICOSTERONE with other chemical compounds

• In cultured vascular smooth muscle cells, 10% of compound B was converted to compound A, whereas > 60% of compound A was converted to compound B [20].
• These data suggest that both types I and II 11beta HSD in Leydig cells play a protective role, opposing the adverse effects of excessive CORT on testosterone production [28].
• Lipid A monoclonal antibodies, which require for binding the presence of the bisphosphorylated D-glucosamine disaccharide lipid A backbone, were tested against synthetic lipid A precursor Ia and compound B 1047 by enzyme immunoassay [29].
• A proposed combination of CGP-60474 and compound B led to the discovery of [1,3,5]triazine-pyridine as a new series of potent CDK inhibitors [30].
• Moreover, an important role for GR was further shown by means of the specific GR antagonist, RU 38486, which blocked the reduction of LH in ADX rats that were given 100 microg/ml CS [14].
• The maintenance of glycemia and increasing insulin in parallel to the dose of corticosterone indicate a decrease in insulin sensitivity, which is enhanced by OE [31].
• These results demonstrated the hypotheses that IL-1 effects may be via PLA2-PGE2-corticosterone pathway and EPA attenuated IL-1 effects may be through the suppression of PLA2 expression, which then reduced PGE2 synthesis and corticosterone secretion [32].
• Flutamide treatment increased the baseline levels of corticosterone, whereas letrozole treatment attenuated the stress response of corticosterone [33].

Gene context of CORTICOSTERONE

• A graded decrease of body temperature induced a progressive increase in the plasma level of CS, whereas that of PRL showed a drastic decrease [34].
• We observed that prolonged estrogen treatment (6 weeks) of old rats normalized the termination of the stress response, restored dexamethasone inhibition of plasma CORT, and increased GR immunoreactivity in CA1 and CA2 hippocampal subfields and subiculum [35].
• Binding of the positron emission tomography tracer Pittsburgh compound-B reflects the amount of amyloid-beta in Alzheimer's disease brain but not in transgenic mouse brain [36].
• An opioid receptor like 1 antagonist, compound B (10 microM), induced a phase delay, and this effect was blocked by nociceptin (10 microM) [37].
• Architectural changes of the cortico-spinal system in the dystrophin defective mdx mouse [38].

Analytical, diagnostic and therapeutic context of CORTICOSTERONE

• Pairs of transcranial magnetic stimulation pulses were delivered at precise intervals to detect changes in the excitability of cortico-cortical inputs to motor cortex when subjects prepared to grasp different objects [24].
• This report describes the first human study of a novel amyloid-imaging positron emission tomography (PET) tracer, termed Pittsburgh Compound-B (PIB), in 16 patients with diagnosed mild AD and 9 controls [39].
• Cortico-muscular synchronization during isometric muscle contraction in humans as revealed by magnetoencephalography [40].
• In addition to establishing the validity of EEG coherence analysis for assaying cortico-cortical connectivity, this study extends to the human brain the finding that visual stimuli cause interhemispheric synchronization, particularly in frequencies of the gamma band [41].
• Fos expression in the suprachiasmatic nucleus of rats induced by photic stimulation (50 lux, 30 min) during the early subjective night was inhibited by treatment with nociceptin (0.5-10 nM, i.c.v.). The effect of nociceptin (10nM, i.c.v.) was blocked by pretreatment with compound B (30 mg/kg, i.p) [37].

References