Melatonin fails to protect against long-term MPTP-Induced dopamine depletion in mouse striatum

1999 ◽  
Vol 1 (4) ◽  
pp. 261-269 ◽  
Author(s):  
Cornelis J. van der Schyf ◽  
Kay Castagnoli ◽  
Sonya Palmer ◽  
Lisa Hazelwood ◽  
Neal Castagnoli
Keyword(s):  
Dopamine Depletion ◽  
Mouse Striatum

Dopamine depletion induces neuron‐specific alterations of GABAergic transmission in the mouse striatum

2020 ◽  
Vol 52 (5) ◽  
pp. 3353-3374
Author(s):  
Ida Luisa Boccalaro ◽  
Cornelia Schwerdel ◽  
Leonardo Cristiá‐Lara ◽  
Jean‐Marc Fritschy ◽  
Lena Rubi
Keyword(s):  
Dopamine Depletion ◽  
Gabaergic Transmission ◽  
Mouse Striatum

Author response for "Dopamine Depletion induces Neuron‐specific Alterations of GABAergic Transmission in the Mouse Striatum"

2020 ◽  
Author(s):  
Ida Luisa Boccalaro ◽  
Cornelia Schwerdel ◽  
Leonardo Cristiá‐Lara ◽  
Jean‐Marc Fritschy ◽  
Lena Rubi
Keyword(s):  
Author Response ◽  
Dopamine Depletion ◽  
Gabaergic Transmission ◽  
Mouse Striatum

Relationship between Methamphetamine-Induced Dopamine Release, Hyperthermia, Self-Injurious Behaviour and Long Term Dopamine Depletion in BALB/c and C57BL/6 Mice

2003 ◽  
Vol 93 (1) ◽  
pp. 33-41 ◽  
Author(s):  
Alycia K. Halladay ◽  
Alexander Kusnecov ◽  
Lauri Michna ◽  
Taizo Kita ◽  
Chiaki Hara ◽  
...  
Keyword(s):  
Dopamine Release ◽  
Dopamine Depletion

scholarly journals Changes in Striatal Medium Spiny Neuron Morphology Resulting from Dopamine Depletion Are Reversible

Cells ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 2441
Author(s):  
Victoria Sofie Witzig ◽  
Daniel Komnig ◽  
Björn H. Falkenburger
Keyword(s):  
Substantia Nigra ◽  
Dopaminergic Neurons ◽  
Morphological Changes ◽  
Medium Spiny Neuron ◽  
Motor Complications ◽  
Spine Density ◽  
Branch Points ◽  
Dopamine Depletion ◽  
Axon Terminals

The classical motor symptoms of Parkinson’s disease (PD) are caused by degeneration of dopaminergic neurons in the substantia nigra, which is followed by secondary dendritic pruning and spine loss at striatal medium spiny neurons (MSN). We hypothesize that these morphological changes at MSN underlie at least in part long-term motor complications in PD patients. In order to define the potential benefits and limitations of dopamine substitution, we tested in a mouse model whether dendritic pruning and spine loss can be reversible when dopaminergic axon terminals regenerate. In order to induce degeneration of nigrostriatal dopaminergic neurons we used the toxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in C57BL/6J mice; 30 mg/kg MPTP was applied i.p. on five consecutive days. In order to assess the consequences of dopamine depletion, mice were analyzed 21 days after the last injection. In order to test reversibility of MSN changes we exploited the property of this model that striatal axon terminals regenerate by sprouting within 90 days and analyzed a second cohort 90 days after MPTP. Degeneration of dopaminergic neurons was confirmed by counting TH-positive neurons in the substantia nigra and by analyzing striatal catecholamines. Striatal catecholamine recovered 90 days after MPTP. MSN morphology was visualized by Golgi staining and quantified as total dendritic length, number of dendritic branch points, and density of dendritic spines. All morphological parameters of striatal MSN were reduced 21 days after MPTP. Statistical analysis indicated that dendritic pruning and the reduction of spine density represent two distinct responses to dopamine depletion. Ninety days after MPTP, all morphological changes recovered. Our findings demonstrate that morphological changes in striatal MSN resulting from dopamine depletion are reversible. They suggest that under optimal conditions, symptomatic dopaminergic therapy might be able to prevent maladaptive plasticity and long-term motor complications in PD patients.

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