Anterograde and transsynaptic degeneration ‘en cascade’ in basal ganglia induced by intrastriatal injection of kainic acid: an animal analogue of huntington's disease

Krammer, Eva B.

doi:10.1016/0006-8993(80)90727-1

Cited by 72 publications

(19 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…We have shown that a postnatal striatal axonsparing lesion will induce death of SN dopamine neurons through PND14, but thereafter it does not (Kelly and Burke 1996). In adult rats, an extensive striatal axonsparing lesion results in transneuronal degeneration of neurons within the SN pars reticulata, but not of the SNpc (Stefanis and Burke 1996;Krammer 1980;Pasinetti et al 1991;Saji and Reis 1987). Björklund and coinvestigators have shown that such a lesion leads to the atrophy, but not loss, of SN dopamine neurons (Lundberg et al 1994).…”

Section: Other Neurotrophic Factors Affecting the Development Of Sn Dmentioning

confidence: 97%

Ontogenic cell death in the nigrostriatal system

Burke

2004

Cell Tissue Res

View full text Add to dashboard Cite

Like most neural systems, dopamine neurons of the substantia nigra undergo apoptotic natural cell death during development. In rodents, this occurs largely postnatally and is biphasic with an initial major peak just after birth and a second minor peak on postnatal day 14. As envisioned by classic neurotrophic theory, this event is regulated by interactions with the target of these neurons, the striatum, because a developmental target lesion results in an augmented natural cell death event with fewer nigral dopamine neurons surviving into adulthood. Until recently, the striatal target-derived neurotrophic factors providing developmental support of dopamine neurons were unknown, but there is now growing evidence that glial-cell-line-derived neurotrophic factor (GDNF) serves as a physiologic limiting neurotrophic factor for these neurons during the first phase of natural cell death. During this phase, intrastriatal injection of GDNF diminishes the natural cell death event and neutralizing antibodies augment it. Sustained overexpression of GDNF in the striatum throughout development in a unique double transgenic mouse model results in an increased number of dopamine neurons surviving the first phase of natural cell death. However, this increase does not persist into adulthood. Therefore, other factors or mechanisms must play important roles in the determination of the mature number of nigral dopamine neurons. Further elucidation of these mechanisms will be important in the development of neuroprotective and cell replacement therapies for Parkinson's disease.

show abstract

Section: Other Neurotrophic Factors Affecting the Development Of Sn Dmentioning

confidence: 97%

Ontogenic cell death in the nigrostriatal system

Burke

2004

Cell Tissue Res

View full text Add to dashboard Cite

show abstract

“…For SN dopamine neurons, developmental target dependence lasts only 2 weeks (Kelly and Burke, 1996). Numerous studies have shown that following extensive striatal target lesion in adulthood, there is no loss of SN dopamine neurons (Krammer, 1980; Lundberg et al, 1994; Stefanis and Burke, 1996). …”

Section: Pcd In Dopamine Neurons: Is It the Default Mode?mentioning

confidence: 99%

Intracellular signalling pathways in dopamine cell death and axonal degeneration

Burke¹

2010

Progress in Brain Research

View full text Add to dashboard Cite

The pathways of programmed cell death (PCD) are now understood in extraordinary detail at the molecular level. Although much evidence suggests that they are likely to play a role in Parkinson’s disease (PD), the precise nature of that role remains unknown. Two pathways of cell death that are especially well characterized are cyclin-dependent kinase 5-mediated phosphorylation of myocyte enhancer factor 2 and the mitogen-activated protein kinase signalling cascade. Although blockade of these pathways in animals has achieved a truly remarkable degree of neuroprotection of the neuron cell soma, it has not achieved protection of axons. Thus, there is a need to explore beyond the canonical pathways of PCD and investigate mechanisms of axon destruction. We also need to move beyond the narrow classic concept that the mechanisms of PCD are activated exclusively ‘downstream’, following cellular injury. Studies in the genetics of PD suggest that in some forms of the disease, activation may be an early ‘upstream’ event. Additionally, recent observations suggest that cell death in some contexts may not be initiated by injury, but instead by a failure of intrinsic cell survival signalling. These new points of view offer new opportunities for molecular targeting.

show abstract

“…One example of anterograde transsynaptic degeneration is the death of neurons in the substantia nigra pars reticulata (SNr) after destruction by excitotoxins of neurons of the caudate nucleus (CN) (3,4). Excitotoxin treatment results in death of the neurons in the CN (5,6).…”

Section: Makoto Saji and Donald J Reismentioning

confidence: 99%

Delayed Transneuronal Death of Substantia Nigra Neurons Prevented by γ-Aminobutyric Acid Agonist

Saji

Reis

1987

Science

213

View full text Add to dashboard Cite

In an investigation of the mechanism by which brain lesions result in delayed degeneration of neurons remote from the site of injury, neurons within the caudate nucleus of rats were destroyed by local injection of the excitotoxin ibotenic acid. Treatment resulted in the rapid degeneration of the striatonigral pathway including projections containing the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) and delayed transneuronal death of neurons in the substantia nigra pars reticulata. The distribution of nigral cell loss corresponded to the loss of GABAergic terminals. Neuronal death was prevented by long-term intraventricular infusion of the GABA agonist muscimol. Delayed transneuronal degeneration may be produced by neuronal disinhibition consequent to loss of inhibitory inputs. Replacement of inhibitory transmitters by suitable drugs may prevent some forms of delayed neuronal death.

show abstract

Anterograde and transsynaptic degeneration ‘en cascade’ in basal ganglia induced by intrastriatal injection of kainic acid: an animal analogue of huntington's disease

Cited by 72 publications

References 43 publications

Ontogenic cell death in the nigrostriatal system

Ontogenic cell death in the nigrostriatal system

Intracellular signalling pathways in dopamine cell death and axonal degeneration

Delayed Transneuronal Death of Substantia Nigra Neurons Prevented by γ-Aminobutyric Acid Agonist

Contact Info

Product

Resources

About