Disease relevance of Red Nucleus

• CONCLUSION: Activation (hyperoxia and blood volume increase) of the red nucleus and substantia nigra in association with visually triggered symptoms of migraine suggest that these brainstem structures are a part of a neuronal network activated during an attack [1].
• The width of the superior cerebellar peduncles also correlated with the diameter of the dentate or red nucleus in patients with MJD, but not in controls or in patients with sporadic olivopontocerebellar atrophy [2].
• These effects are thought to be mediated through the red nucleus because significantly more torticollis was observed when histamine was injected into the red nucleus rather than surrounding mid-brain areas, the substantia nigra, or the lateral ventricle [3].
• We have examined the expression of the multifunctional protein clusterin in the axotomized red nucleus, at the lesion site in the lateral funiculus of C3, as well as along the Wallerian degeneration in the lateral funiculus of T1 [4].
• 3. In a limited series of patients with Parkinson's disease post mortem analysis indicated lower values of MHPG in caudate n., putamen, s. nigra, red nucleus and n. accumbens [5].

High impact information on Red Nucleus

• In order to localize a particular site of memory formation within the brain, the rabbit eyeblink response was classically conditioned while regions of the cerebellum or red nucleus were temporarily inactivated by microinfusions of the gamma-aminobutyric acid agonist muscimol [6].
• We tested the relationship of the medial arc to oculomotor complex and red nucleus development by perturbing arc pattern formation in Sonic Hedgehog and FGF8 misexpression experiments [7].
• We further found that FGF8 manipulations that push the medial arc rostrally coordinately move both the red nucleus and oculomotor complex anlagen [7].
• Three months later the corticofugal projections to the red nucleus and the pons were analyzed; a relatively large number of corticorubral and corticopontine fibers from the lesioned side had crossed the midline and established an additional contralateral innervation of the red nucleus and the pons [8].
• These results suggest that glutamatergic afferent input contributes significantly to the death of axotomized red nucleus and Clarke's nucleus neurons via NMDA receptors located on these neurons [9].

Biological context of Red Nucleus

• The cerebellum and red nucleus, which only express BZ1 binding sites, appear to be areas significantly modified by ethanol and its withdrawal [10].
• Improved choline acetyltransferase immunohistochemistry in the red nucleus by blocking the axonal transport [11].
• 3-acetylpyridine (3-AP) given in one single dose near to LD50 causes hydropic-vacuolic degeneration and cellular necrosis of varying degree and extension in the red nucleus of white rats in more than 50 percent of the cases [12].

Anatomical context of Red Nucleus

• Intranigral injection of 1.3 microliters 1 microM muscimol (0.15 ng) induced increases in glucose consumption locally in the substantia nigra reticulata (by 87%), distally in the contralateral reticulata, red nucleus, nucleus accumbens, and prefrontal cortex, and bilaterally in the pyriform cortex, as compared to values in control animals [13].
• In the corpus callosum, basal ganglia, corpus pineale, colliculi, corpus geniculatum mediale, nucleus ruber, pons, medulla oblongata, and medulla spinalis, receptor binding of NPY was detectable but less than 0.5 pmol/mg of protein [14].
• Following injection of HRP into the LRN, labelled cells were found mainly within Rexed's laminae VII and VIII of the spinal cord, the contralateral red nucleus, the ventro-rostral aspect of the contralateral fastigial nucleus and the contralateral anterior sigmoid and coronal gyri of the cerebral cortex [15].
• Doses of drug that affected performance on the rotating cylinder (18 and 60 mg/kg) reduced glucose utilization in brain regions involved with motor performance, including the red nucleus, vestibular nucleus, substantia nigra, and deep layers of the superior colliculus, whereas cerebral cortical regions were not altered significantly [16].
• Stimulation of cutaneous and of flexor muscle nerves of the brain stem reticular formation, the red nucleus, and the pyramidal tract all produced PAD of the group Ib GS fibers.(ABSTRACT TRUNCATED AT 400 WORDS)[17]

Associations of Red Nucleus with chemical compounds

• 1,3-Di-o-tolylguanidine (DTG), a highly selective ligand for the haloperidol-sensitive sigma-receptor, produced marked dystonia in rats after microinjection into the red nucleus, a motor area rich in this receptor [18].
• Phencyclidine was also without effect, as were injections of the active compounds in sites distant to the red nucleus [18].
• Six days after the injection, Nissl-stained sections through the lesion site showed that the majority of neurons in the red nucleus ipsilateral to the kainic acid injection were destroyed [19].
• The experiments were performed on cats decerebrated rostral to the red nucleus under halothane anaesthesia [20].
• Immunocytochemical methods were used to examine the ultrastructural features and cellular interrelationships of GABA and serotonin afferent fibers to the rat red nucleus [21].

Gene context of Red Nucleus

• Specific regions most influenced by NT-3 and BDNF were the reticular formation and red nucleus [22].
• The NFL null mice displayed enzymatic activity alterations in numerous hindbrain regions, mainly the cerebellum, connected regions of the brainstem (red nucleus, vestibular nuclei, and reticular formation), and cranial nerve nuclei [23].
• In particular, CB is the most abundant CaBP in this portion of the red nucleus [24].
• Heterogeneous distribution of neurons containing calbindin D-28k and/or parvalbumin in the rat red nucleus [25].
• Additionally, some large and medium-sized neurons displaying immunoreactivity for both PV and CB were encountered in the ventromedial sector of the red nucleus [25].

Analytical, diagnostic and therapeutic context of Red Nucleus

• Unoperated control groups showed a marked retrograde death of Red nucleus neurons contralateral to the lesion; Fb/BDNF recipients showed a significant rescue effect [26].
• In situ hybridizations revealed TIP39 expression in seminiferous tubuli and several brain regions, including nucleus ruber, nucleus centralis pontis, and nucleus subparafascicularis thalami [27].
• GABA nerve endings in the rat red nucleus combined detection with serotonin terminals using dual immunocytochemistry [21].
• These data suggest that testosterone both delays and reduces the astrocytic reaction in the red nucleus following rubrospinal tract axotomy, and confirms a difference between peripheral and central glial responses to axotomy and steroid administration [28].
• Experiment 2 showed that microinfusion of local anesthetic procaine hydrochloride into the medial septum resulted in a reversible blockade of theta field activity elicited by electrical stimulation of the red nucleus [29].

References