Neuronal Cell Death

Pettmann, Brigitte; Henderson, Chris

doi:10.1016/s0896-6273(00)81004-1

Cited by 539 publications

(358 citation statements)

References 172 publications

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“…Thus, neurotrophic factors are important signalling molecules for the development and maintenance of neurons, acting throughout development on many types of neuronal populations (Ibanez 1995;Mamounas et al 1995). They increase cell survival by providing necessary trophic support for growth, but also by exerting inhibitory effects on cell death cascades (Thoenen 1995;Pettmann and Henderson 1998;Riccio et al 1999).…”

Section: Neurotrophic Factorsmentioning

confidence: 99%

“…In addition, exposure to psychotropic drugs or stress regulates the rate of neurogenesis in adult brain by regulating the expression and function of growth factor cascades, suggesting a possible role for neurogenesis in the pathophysiology and treatment of depression and others illnesses (Smith et al 1995;Nibuya et al 1999;Duman et al 2001). Several neurotrophic factors (such as nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and glial-derived neurotrophic factor (GDNF)), as well as cytokines and insulin-like growth factor-1 (IGF-1), increase cell survival (Mamounas et al 1995;Pettmann and Henderson 1998). This occurs through binding of these factors to membrane receptors and regulation of intracellular signal transduction pathways that can control apoptosis, including regulation of Bcl-2 family members.…”

Section: Neurotrophic Factorsmentioning

confidence: 99%

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Consensus paper of the WFSBP Task Force on Biological Markers: Biological Markers in Depression

Mößner

Mikova

Koutsilieri

et al. 2007

The World Journal of Biological Psychiatry

227

126

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Biological markers for depression are of great interest to aid in elucidating the causes of major depression. We assess currently available biological markers to query their validity for aiding in the diagnosis of major depression. We specifically focus on neurotrophic factors, serotonergic markers, biochemical markers, immunological markers, neuroimaging, neurophysiological findings, and neuropsychological markers. We delineate the most robust biological markers of major depression. These include decreased platelet imipramine binding, decreased 5-HT1A receptor expression, increase of soluble interleukin-2 receptor and interleukin-6 in serum, decreased brain-derived neurotrophic factor in serum, hypocholesterolemia, low blood folate levels, and impaired suppression of the dexamethasone suppression test. To date, however, none of these markers are sufficiently specific to contribute to the diagnosis of major depression. Thus, with regard to new diagnostic manuals such as DSM-V and ICD-11 which are currently assessing whether biological markers may be included in diagnostic criteria, no biological markers for major depression are currently available for inclusion in the diagnostic criteria.

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Section: Neurotrophic Factorsmentioning

confidence: 99%

Section: Neurotrophic Factorsmentioning

confidence: 99%

Consensus paper of the WFSBP Task Force on Biological Markers: Biological Markers in Depression

Mößner

Mikova

Koutsilieri

et al. 2007

The World Journal of Biological Psychiatry

227

126

View full text Add to dashboard Cite

show abstract

“…The binding of trophic factors with their receptors triggers a variety of signaling responses that promote cell survival, in some cases through interactions with BCL-2-related proteins (Kaplan and Miller, 1997;Pettmann and Henderson, 1998). For example, NGF or IGF-1 can induce the phosphorylation of BAD, a non-membrane-bound BCL-2 relative, by activating Akt, a serine-threonine protein kinase.…”

Section: Granule Cell Survival and Olivary Neuron Deathmentioning

confidence: 99%

BaxInactivation in Lurcher Mutants Rescues Cerebellar Granule Cells But Not Purkinje Cells or Inferior Olivary Neurons

2000

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Lurcher is a gain-of-function mutation in the ␦2 glutamate receptor gene (Grid2) that turns the receptor into a leaky ion channel. The expression of the Lurcher gene in heterozygous (Grid2 Lc/ϩ ) mutants induces the death of almost all Purkinje cells starting from the second postnatal week. Ninety percent of the granule cells and 60-75% of the inferior olivary neurons die because of the loss of their target neurons, the Purkinje cells. The apoptotic nature of the neurodegeneration has been demonstrated previously by the presence of activated caspase-3 and DNA fragmentation. Bax, a pro-apoptotic gene of the Bcl-2 family, has been shown to be involved in developmental neuronal death. To study the role of Bax in Grid2 Lc/ϩ neurodegeneration, double mutants with Grid2 Lc/ϩ mice and Bax knock-out mice (BaxϪ/Ϫ) were generated. Bax deletion had no effect on the death of Purkinje cells and inferior olivary neurons, although a temporary rescue of some Purkinje cells could be detected in P15 Grid2 Lc/ϩ ;BaxϪ/Ϫ animals. From postnatal day 15 (P15) to P60, the number of granule cells in Grid2 Lc/ϩ ;BaxϪ/Ϫmice did not significantly change and was significantly increased compared with the number found in Grid2 Lc/ϩ ;Baxϩ/ϩ mice. Granule cell number in P60 Grid2 Lc/ϩ ;BaxϪ/Ϫ mice corresponded to 70% of the number found in wild-type mice. Our results show that Bax inactivation in Grid2 Lc/ϩ mice does not rescue intrinsic Purkinje cell death or the target-related cell death of olivary neurons, but Bax inactivation does inhibit persistently target-related cell death in cerebellar granule cells.

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“…Death has been described among proliferating neuroblasts, early postmitotic cells and in many populations of neurons at the time they form synaptic connections (reviewed by Davies, 2003;de la Rosa and de Pablo, 2000;Lossi and Merighi, 2003;Oppenheim, 1991;Pettmann and Henderson, 1998). A long established idea is that the survival of developing neurons depends on trophic factors produced in limited amounts, but recent studies have shown that neuronal death may also partly be due to the activation of cytotoxic signaling mechanisms, through cell receptors such as FasL, TNF-R and P75 (reviewed in Davies, 2003;Dechant and Barde, 2002;Raoul et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Neuronal death induced by endogenous extracellular ATP in retinal cholinergic neuron density control

et al. 2005

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The precise assembly of neuronal circuits requires that the correct number of pre- and postsynaptic neurons form synaptic connections. Neuronal cell number is thus tightly controlled by cell death during development. Investigating the regulation of cell number in the retina we found an ATP gated mechanism of neuronal death control. By degrading endogenous extracellular ATP or blocking the P2X7 ATP receptors we found that endogenous extracellular ATP triggers the death of retinal cholinergic neurons during normal development. ATP-induced death eliminates cholinergic cells too close to one another, thereby controlling the total number, the local density and the regular spacing of these neurons.

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Neuronal Cell Death

Cited by 539 publications

References 172 publications

Consensus paper of the WFSBP Task Force on Biological Markers: Biological Markers in Depression

Consensus paper of the WFSBP Task Force on Biological Markers: Biological Markers in Depression

BaxInactivation in Lurcher Mutants Rescues Cerebellar Granule Cells But Not Purkinje Cells or Inferior Olivary Neurons

Neuronal death induced by endogenous extracellular ATP in retinal cholinergic neuron density control

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