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Isolation, Culture and Long-Term Maintenance of Primary Mesencephalic Dopaminergic Neurons From Embryonic Rodent Brains
Published on: February 19, 2015
Brief ischemia causes long-term depression in midbrain dopamine neurons
Vineeta Singh1, Melissa Carman, Jochen Roeper
1Department of Neurology, University of California, San Francisco, Ernest Gallo Clinic and Research Center, Emeryville, CA 94608, USA.
The European Journal of Neuroscience
|September 21, 2007
Summary
Brief oxygen and glucose deprivation causes long-term depression (LTD) in excitatory synapses of dopamine neurons. This ischemic LTD may protect neurons from excitotoxicity during conditions like Parkinsonism.
Area of Science:
- Neuroscience
- Neurophysiology
- Synaptic Plasticity
Background:
- Dopamine neuron degeneration in the substantia nigra pars compacta (SNc) is key in Parkinsonism and vascular dementia.
- SNc dopamine neurons are vulnerable to hypoxic/ischemic conditions, leading to degeneration.
- The role of SNc excitatory synapses in this degeneration is unclear.
Purpose of the Study:
- To investigate the effect of oxygen/glucose deprivation (OGD) on glutamatergic synaptic transmission in the SNc.
- To understand the mechanisms underlying OGD-induced synaptic changes.
- To determine if these changes offer neuroprotection.
Main Methods:
- Used a rat midbrain slice preparation.
- Applied 5-minute OGD to examine synaptic currents.
- Conducted pharmacological studies to identify receptor and channel involvement.
Main Results:
- OGD induced pre-synaptic ischemic long-term depression (iLTD) of glutamate transmission.
- Both AMPA and NMDA receptor-mediated currents were similarly depressed.
- iLTD was triggered by intracellular calcium rise and mediated by adenosine A(1) receptors and K(ATP) channels.
- iLTD did not occlude tetanic LTD, indicating distinct pathways.
Conclusions:
- Brief hypoxia/hypoglycemia causes LTD at glutamatergic synapses onto SNc neurons.
- This iLTD may serve as a protective mechanism against ischemia-induced excitotoxic injury.
- Findings shed light on neuroprotective strategies for dopamine neurons.
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