magnocellular


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magnocellular

[‚mag·nə′sel·yə·lər]
(cell and molecular biology)
Having large cell bodies; said of various nuclei of the central nervous system.
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The association between PD and RBD can be explained as neurodegeneration in certain brainstem structures at Braak stage 1-2.[10] The pathogenesis of RBD in PD includes degeneration of laterodorsal tegmental nuclei, which is associated with the inhibition of locomotor generators in REM sleep, as well as magnocellular reticular formation, pedunculopontine nucleus, pontine reticular formation, and decreased numbers of nigrostriatal dopamine transporters.[3] RBD in PD can be diagnosed by video-PSG, RBD-SQ, and RBD-SS.
Sensitivity to the catecholamines is enhanced by TCAs, which may result in arrhythmias and hypertension when indirect- or direct-acting sympathomimetic drugs are used.[1] Similarly, anesthetics known to increase endogenous circulating catecholamines such as ketamine-, pancuronium-, and epinephrine-containing solution should be avoided.[4] Vasopressin is a nonapeptide hormone synthesized in the magnocellular neurons of the paraventricular and supraoptic nuclei of the hypothalamus.[5] The vasoconstrictive effect of vasopressin is independent of catecholamine and angiotensin receptors.
Magnocellular Neuron Activity and Inflammatory Pain Processing.
Magnocellular axons in passage through the median eminence release vasopressin.
Magnocellular neurons of the PVN and supraoptic nucleus of the hypothalamus also produce a number of anorexigenic neuropeptides, including CART, pituitary adenylate cyclase-activating polypeptide, cholecystokinin (CCK), and nesfatin-1 (51), and are activated during feeding and by satiety peptides such as CCK and GLP1.
In particular, the increase of the visual component P1 has been studied, with event-related potentials (ERP), by filtering low spatial frequencies, thus evidencing the rapid activation of the magnocellular system against stimuli that trigger emotions of high agitation [4].
Apelin and APJ gene expression was observed in the hypothalamic supraoptic nucleus and in the magnocellular and parvocellular parts of the paraventricular nucleus (PVN) in rats [43].
In this regard, a reduction in the number of parvocellular neurons and magnocellular gliosis was found [101].
In addition, conspicuous Lewy body pathology is present in H&E sections within dorsal nucleus of X in the medulla (D) and in cholinergic, magnocellular neurons of basal forebrain (E) (black arrows in [D and E] indicate Lewy bodies).
Chondroitin sulfate proteoglycan phosphacan/ RPTP beta in the hypothalamic magnocellular nuclei.
It is produced by two kinds of oxytocinergic neurons: The magnocellular neurons sending their projections to the neurohypophysis releasing OT into blood circulation, and the parvocellular neurons sending their projections mainly to the campus, ventral tegmental area, frontal cortex, brainstem, pons, medulla, and spinal cord [16].