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Cerebellar cortex protein

Daniel H, Crepel F (2001) Control of Ca(2+) influx by cannabinoid and metabotropic glutamate receptors in rat cerebellar cortex requires K(+) channels. J Physiol 537(Pt 3) 793-800 Davis MI, Ronesi J, Lovinger DM (2003) A predominant role for inhibition of the adenylate cy-clase/protein kinase A pathway in ERK activation by cannabinoid receptor 1 in N1E-115 neuroblastoma cells. J Biol Chem 278(49) 48973-80 Devane WA, Hanus L, Breuer A, Pertwee RG, Stevenson LA, Griffin G, Gibson D, Mandelbaum A, Etinger A, Mechoulam R (1992) Isolation and structure of a brain constituent that binds to the cannabinoid receptor. Science 258 1946-9... [Pg.468]

The lack of correspondence between receptor protein and mRNA in some areas is likely to be due to the transport of the receptor from the site of synthesis into terminal areas. In the cerebellar cortex, for example, Di receptors synthesized in the granule cell layer are transported to the molecular layer (Mansour et al., 1992). [Pg.68]

Akimoto, Y., Comer, F.I., Cole, R.N., Kudo, A., Kawakami, H., Hirano, H. and Hart, G.W. (2003) Localization of the O-GlcNAc transferase and 0-GlcNAc-modified proteins in rat cerebellar cortex. Brain Res. 966, 194-205. [Pg.94]

Fig. 28. Developmental expression of protein kinase C (PKC) isoenzymes in rat cerebellum. Immunofluores-cent staining of cerebellar cortex by antibodies specific for PKC 1, corresponding to PKCr (panels A, B and C), PKC (panels D, E and F) and PKCa (panels G, H and I), Sagittal sections of cerebellum of 1-week-old (A, D and G), 2-week-old (B, E and H) and 3-week-old (C, F and I) rats were used. PKCr antibody stained mainly the Purkinje ceil bodies and dendrites throughout the development. PKC/8 antibody stained the cerebellar granule cells in the external germinal layer (EGL) of the 1- and 2-week-old rats and mainly the granular layer of the 3-week-old rats. PKCa antibody stained both granule cells and Purkinje cells throughout the development. Fluang et al. (1991). Fig. 28. Developmental expression of protein kinase C (PKC) isoenzymes in rat cerebellum. Immunofluores-cent staining of cerebellar cortex by antibodies specific for PKC 1, corresponding to PKCr (panels A, B and C), PKC (panels D, E and F) and PKCa (panels G, H and I), Sagittal sections of cerebellum of 1-week-old (A, D and G), 2-week-old (B, E and H) and 3-week-old (C, F and I) rats were used. PKCr antibody stained mainly the Purkinje ceil bodies and dendrites throughout the development. PKC/8 antibody stained the cerebellar granule cells in the external germinal layer (EGL) of the 1- and 2-week-old rats and mainly the granular layer of the 3-week-old rats. PKCa antibody stained both granule cells and Purkinje cells throughout the development. Fluang et al. (1991).
Chen S, Hillman DE (1993a) Compartmentation of the cerebellar cortex by protein kinase C delta. Neuroscience, 56, 177-188. [Pg.321]

Kadowaki K, McGowan E, Mock G, Chandler S, Emson PC (1993) Distribution of calcium binding protein mRNAs in rat cerebellar cortex. Neurosci. Lett., 153, 80-84. [Pg.337]

Shearman MS, Shinomura T, Oda T, Nishizuka Y (1991) Synaptosomal protein kinase C subspecies A. Dynamic changes in the hippocampus and cerebellar cortex concomitant with synaptogenesis. J. Neurochem.. 56. 1255-1262. [Pg.359]

Cyclic AMP has been implicated in synaptic transmission due to its actions on a number of important synaptic and neuronal events, such as membrane permeability, synaptic membrane phosphorylation, neurotransmitter synthesis, and cell growth and differentiation. As pointed out earlier, neurotransmitter-receptor interactions can result in direct physical perturbations of the membrane with consequent alterations in membrane permeability to specific ions. This effect is particularly the case when the ionophore is located near the receptor. However, if the ionic channel is distant from the receptor, mechanisms such as phosphorylation can result in an alteration of channel permeability. Cyclic AMP is known to lead to a hyperpolarization of neurons in a number of brain regions such as the cerebral cortex, the caudate nucleus, the peripheral paravertebral sympathetic ganglia, the cerebellar cortex, and the hippocampus. Although it has been hypothesized that this hyperpolarization is the consequence of the phosphorylation of specific neuronal membrane proteins, the relatively short duration of hyperpolarization... [Pg.144]

Transgenic mice overexpressing the mutant human SODl gene also show nitrated and oxidized proteins in the motor cortex, the cerebellar cortex, and the nucleus of hypoglossal nerves (regions related with movement). Significantly elevated protein nitration and nitric oxide synthesis have also been observed in brain tissues and CSF of mutant SODl mice. This study correlates mutation of the SODl gene to increased nitric oxide, nitration, and oxidation of proteins in ALS (Liu et al., 2007). [Pg.282]

Fig. 155. Staining with cyclic 3, 5 -guanosine monophosphate dependent protein kinase (cGK) antisera of sections of cerebellum of rat fetuses of embryonic day E17, E19 and a neonate (PO) cut in the frontal plane. A,B- E17. Cluster I is composed of a medial sheet (arrow in B) lying against the germinative neuroepithelium. Close to the midline this sheet bends dorsally and reaches the cortex. The central cluster (CC) is located at the center of the hemicerebellum. C. E19. In this section four of the five cGK-positive clusters I-V are present. The labelled fiber-like material, which tails the labelled clusters ( and o) indicates the migration pathways followed by the Purkinje cells of the clusters I and III from the subventricular plate and the central cluster at El7 to their present, superficial position. D. PO rat pup. Fiber bundles linking the clusters I and III with the cerebellar nuclei intersect at the former position of the central cluster. It is suggested that the bundle from cluster III ( ) terminates in the dorsolateral protuberance. In the adult this connection corresponds to the projection of the lateral extension of the A zone of Buisseret-Delmas (1988a, compare Figs. 142 and 144). Bar in A = 100 /tm, in B, C and D = 500 fxm. Wassef and Sotelo (1984). Fig. 155. Staining with cyclic 3, 5 -guanosine monophosphate dependent protein kinase (cGK) antisera of sections of cerebellum of rat fetuses of embryonic day E17, E19 and a neonate (PO) cut in the frontal plane. A,B- E17. Cluster I is composed of a medial sheet (arrow in B) lying against the germinative neuroepithelium. Close to the midline this sheet bends dorsally and reaches the cortex. The central cluster (CC) is located at the center of the hemicerebellum. C. E19. In this section four of the five cGK-positive clusters I-V are present. The labelled fiber-like material, which tails the labelled clusters ( and o) indicates the migration pathways followed by the Purkinje cells of the clusters I and III from the subventricular plate and the central cluster at El7 to their present, superficial position. D. PO rat pup. Fiber bundles linking the clusters I and III with the cerebellar nuclei intersect at the former position of the central cluster. It is suggested that the bundle from cluster III ( ) terminates in the dorsolateral protuberance. In the adult this connection corresponds to the projection of the lateral extension of the A zone of Buisseret-Delmas (1988a, compare Figs. 142 and 144). Bar in A = 100 /tm, in B, C and D = 500 fxm. Wassef and Sotelo (1984).
The first general biochemical study of the effects of lead on cerebral cortex and cerebellum, using 4% lead carbonate in the maternal diet from birth, was made by Michaelson (1973). He found a transient postnatal growth retardation and reduction of cerebral and cerebellar wet weights. The cerebellum showed increased water and reduced DNA content, suggesting a 15-20% deficit in cell numbers. DNA in the cerebrum and RNA and protein in both areas differed only marginally from controls, although all were consistently... [Pg.75]


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