Cerebellar granule neurons

Rossi AD, Viviani B, Zhivotovsky B, Manzo L, Orrenius S, Vahter M, Nicotera P. 1997. Inorganic mercury modifies Ca + signal, triggers apoptosis and potentiates NMDA toxicity in cerebellar granule neurons. Cell Death Differentiation 4 317-324. 

HGF serves as an attractant for developing spinal motor neurons and thalamic axons in vitro. HGF was shown to protect cerebellar granule neurons against excitotoxicity. 

Bakken, I. J., White, L. R., Aasly, J. etal. [U-13C] aspartate metabolism in cultured cortical astrocytes and cerebellar granule neurons studied by NMR spectroscopy. Glia 23 271-277,1998. 

Antidepressant treatment has, in recent studies, been shown to upregulate the cyclic adenosine monophosphate (cAMP) response element binding protein (CREB) cascade and expression of BDNF [59]. This upregulation of CREB and BDNF raises the possibility that antidepressant treatment could oppose the cell death pathway, possibly via increased expression of the oncogene Bcl-2. Studies are necessary to determine if antidepressant treatment increases Bcl-2 expression. Increased expression of Bcl-2 in brain and cultured cells, and inhibition of apoptosis of cultured cerebellar granule neurons have been reported with lithium treatment [57]. Mice lacking the BDNF TrkB receptor fail to show behavioral and neurogenic responses to antidepressants. 

Hansen, S. L Ebert, B., Fjalland, B., and Kristiansen, U. (2001) Effects of GABA(A) receptor partial agonists in primary cultures of cerebellar granule neurons and cerebral cortical neurons reflect different receptor subunit compositions. Br. J. Pharmacol. 133, 539-549. 

Tia, S., Wang, J. F., Kotchabhakdi, N and Vicini, S. (1996) Developmental changes of inhibitory synaptic currents in cerebellar granule neurons role of GABAa receptor a6 subunit.. /. Neurosci. 16, 3630-3640. 

By contrast, apoptosis studied in the model of potassium deprivation of cerebellar granule neurons (CGN) revealed an early drop in histone acetylation levels... 

Figure 3. The many ways to lose a HAT. Decreased amounts of functional CBP protein and subsequent CBP s loss of function has been observed in different contexts of neurological disorders and neuronal apoptosis. RTS (Rubinstein-Taybi Syndrome) results from a mutation on one cbp gene allele. In several cases of polyQ diseases, CBP can be sequestred by the mutated polyQ proteins, forming aggregates in the cytoplasm or the nucleus. CBP proteasomal degradation was also shown to be favored by polyQ proteins. CBP is a caspase-6 substrate in cerebellar granule neurons (CGN) deprived of potassium modeling caspase-dependent apoptosis. Finally, cbp gene repression has been observed in oxidative stress-induced death of a motomeuronal cell line. The mechanisms by which CBP levels are reduced in motomeurons of ALS mice is still unknown...

Memo M, Bovolin P, Costa E, Grayson DR. 1991. Antagonists of the NMDA sensitive glutamate receptor down regulate mRNAs encoding various GABA receptors in cerebellar granule neurons. Mol Pharmacol 39 599-603. 

Santi MR, Ikonomovic S, Wroblewski JT, Grayson DR. 1994. Temporal and depolarization-induced changes in the absolute amounts of mRNAs encoding metabotropic glutamate receptors in cerebellar granule neurons in vitro. J Neuro-... 

Lombardi G., Szekely A. M., Bristol L. A., Guidotti A., and Manev H. (1993). Induction of ornithine decarboxylase by N-methyl-D-aspartate receptor activation is unrelated to potentiation of glutamate excitotoxicity by polyamines in cerebellar granule neurons. J. Neurochem. 60 1317-1324. 

Verdaguer E., Garcia-Jorda E., Canudas A. M., Dominguez E., Jimenez A., Pubill D., Escubedo E., Camarasa Pallas Merce J., and Camins A. (2002). Kainic acid-induced apoptosis in cerebellar granule neurons an attempt at cell cycle re-entry. NeuroReport 13 413—416. 

In primary cultures of neonatal cerebellar granule neurons, all Ca2+ sensors, calmodulin, protein kinases C (PKC), and the p21(ras)/phosphatidylinositol 3 -kinase (Ptdlns-3K)/Akt pathway, converge towards NF-kB at the levels of nuclear translocation as well as transcription. The duration of NF-kB activation is a critical determinant for sensitivity toward excitotoxic stress and is dependent on the different upstream and downstream signaling associated with various kinases. This is in contrast to studies in non-neuronal cells, which either do not respond to Ca2+ or do not simultaneously activate all three cascades (Lilienbaum and Israel, 2003). Collective evidence suggests that brain inflammatory processes differ from systemic inflammation not only in the involvement of various types of neural cells but also in differences in response to second messengers. 

Berman F. W. and Murray T. F. (1997). Domoic acid neurotoxicity in cultured cerebellar granule neurons is mediated predominantly by NMDA receptors that are activated as a consequence of excitatory amino acid release. J. Neurochem. 69 693-703. 

See, V., Boutillier, A. L., Bito, H. and Loeffler, J. P., 2001, Calcium/calmodulin-dependent protein kinase type TV (CaMKIV) inhibits apoptosis induced by potassium deprivation in cerebellar granule neurons, Faseb J, 15, pp 134-144. 

Price, S. A., Held, B., and Pearson, H. A. (1998). Amyloid beta protein increases Ca2+ currents in rat cerebellar granule neurones. Neuroreport 9, 539-545. 

Qin N, Platano D, Olcese R, Stefani E, Birnbaumer L (1997) Direct interaction of gbetagamma with a C-terminal gbetagamma-binding domain of the Ca2+ channel alphal subunit is responsible for channel inhibition by G protein-coupled receptors. Proc Natl Acad Sci U S A 94 8866-71 Randall A, Tsien RW (1995) Pharmacological dissection of multiple types of Ca2+ channel currents in rat cerebellar granule neurons. J Neurosci 15 2995-3012 Reid CA, Bekkers JM, Clements JD (2003) Presynaptic Ca2+ channels a functional patchwork. Trends Neurosci 26 683-7... 

Koulich, E., Nguyen, T., Johnson, K., Giardina, C., and D mello, S. (2001). NF-kappaB is involved in the survival of cerebellar granule neurons Association of IkappaBbeta [correction of Ikappabeta] phosphorylation with cell survival.. Neurochem. 76, 1188-1198. 

Daily, D., Vlamis-Gardikas, A., Offen, D., Mittelman, L., Melamed, E., Holmgren, A., and Barzilai, A. 2001a. Glutaredoxin protects cerebellar granule neurons from dopamine-induced apoptosis by dual activation of the ras-phosphoinositide 3-kinase and jun N-terminal kinase pathways. J. Biol. Chem. 276 21618-21626. 

Protect against cell death of cerebellar granule neurons and the increase in ROS induced by 3-nitropropionic acid [132]... 

Greenlee JE, Parks TN, Jaeckle KA. Type Ha ( anti-Hu ) antineuronal antibodies produce destruction of rat cerebellar granule neurons in vitro. Neurology 1993 43(10) 2049-2054. 

Kovacs AD, Chakraborty-Sett S, Ramirez SH, Sniderhan LF, Willitimson AL et al (2004) Mechanism of NF-kappaB inactivation induced by survival signed withdrawal in cerebellar granule neurons. Eur J Neurosd 20 345-352... 

Berman, F.W., and Murray, TF 1999. Brevetoxins cause acute excitotoxicity in primary cultures of rat cerebellar granule neurons. Journal of Pharmacology and Experimental Therapeutics 290, 439-444. 

In agreement with previous reports on palytoxin cytotoxicity, we have recently found that in cultured cerebellar granule neurons palytoxin at 10 and 50 nM killed about 40% of cells after five minutes exposure of cultured neurons to the toxin as assessed with the MTT assay, while four hours exposure of neuroblastoma cells to 1 nM palytoxin decreased cell viability by about 100% (Fig. 6.5). 

Berman, F.W, LeEage, K.T., and Murray, TE 2002. Domoic acid neurotoxicity in cultured cerebellar granule neurons is controlled preferentially by the NMDA receptor Ca(2+) influx pathway. Brain Res 924, 20—29. 

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