Granule cells death

Bachis A, Colangelo AM, Vicini S, Doe PP, De Bernardi MA, Brooker G, Mocchetti I (2001) Interleukin-10 prevents glutamate-mediated cerebellar granule cell death by blocking caspase-3-like activity. J Neurosci 21 3104—3112. 

Bachis A, Major EO, Mocchetti I (2003) Brain-derived neurotrophic factor inhibits human immunodeficiency virus-l/gpl20-mediated cerebellar granule cell death by preventing gpl20 internalization. J Neurosci 23 5715-5722. 

From a cell biological perspective, PrPc expressed from a neuron-specific enolase promoter could rescue granule cell degeneration but not a Dpl-specified leukoencephalopathy. In a reverse fashion, PrP expressed in trans from a myelin basic protein promoter could rescue leukoencephalopathy but not granule cell death [127]. 

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. 

Pannunzio, P., Hazell, A. S., Pannunzio, M., Rama Rao, K. V. and Butterworth, R. F. Thiamine deficiency results in metabolic acidosis and energy failure in cerebellar granule cells an in vitro model for the study of cell death mechanisms in Wernicke s encephalopathy. /. Neurosci. Res. 62 286-292, 2000. 

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. 

Figure 17.29 Organisation of granules within the cytotoxic T-cell prior to release. The organisation ensures that the released enzymes plus perforin are very close to the infected cell so that killing is restricted to the infected cell. This minimises damage to neighbouring non-intected cells. Death is due to either lysis or apoptosis.

The granules contain two types of proteins that result in death. First, compounds that produce holes (pores) in the membrane of the cells these are the proteins, perforin and granulysin. Both insert into the membrane to produce the pores. These were once considered to result in death by lysis (i.e. exchange of ions with extracellular space and entry of water into the cell). However, it is now considered that the role of the pores is to enable enzymes in the granules, known as granzymes, to enter the cell. These granzymes contain proteolytic enzymes. They result in death of the cell by proteolysis but, more importantly, activation of specific proteolytic enzymes, known as caspases. These enzymes initiate reactions that result in programmed cell death , i.e. apoptosis (Chapter 20). 

Gasull T., DeGregorio-Rocasolano N., Enguita M., Hurtan J. M., and Trullas R. (2002). Inhibition of phosphatidylcholine synthesis is associated with excitotoxic cell death in cerebellar granule cell cultures. Amino Acids 23 19-25. 

Suh YS, Oda S, Kang YH, Kim H, Rhyu IJ (2002) Apoptotic cell death of cerebellar granule cells in rolling mouse Nagoya. Neurosci Lett 325 1—4. 

Apoptosis is induced by various intra- and extracellular stimuli, and recently nitric oxide was reported to induce apoptosis in cultured cerebellar granule cells and cultured cortical neurons. The toxicity of nitric oxide is mainly ascribed to peroxynitrite, a reaction product of nitric oxide with superoxide (Figure 13.8). Cells producing an increased amount of SOD (superoxide, superoxide oxidoreductase EC 1.15.1.1) are resistant to nitric oxide-mediated apoptosis. In contrast, superoxide levels that have been increased by downregulation of Cu,Zn-SOD lead to apoptotic cell death in PC 12 cells, which required the reaction with nitric oxide to generate peroxynitrite. Peroxynitrite itself was found to induce apoptosis in PC12 cells and in cultured cortical neurons. 

Heneka, M. T., Feinstein, D., Galea, E., Gleichmann, M., Wullner, U., and Klockgether, T. (1999). Peroxisome proliferator-activated receptor gamma agonists protect cerebellar granule cells from cytokine-induced apoptotic cell death by inhibition of inducible nitric oxide synthase. J. Neuroim-munol. 100, 156-168. 

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

The discovery of apoptosis sheds a new light on the role of cell death in myocardial infarction and other cardiovascular diseases. There is mounting evidence that apoptosis plays an important role at multiple points in the evolution of myocardial infarction, and comprises not only cardiomyocytes but also inflammatory cells, as well as cells of granulation tissue and... 

Wei H, Leeds PR, Qian Y, Wei W, Chen R, Chuang D. Beta-amyloid peptide-induce death of PC12 cells and cerebellar granule cell neurons is inhibited by long-term lithium treatment. Eur J Pharmacol 2000 392 117-23. 

---