Parkinson's disease causes specific changes of neuronal properties within the substantia nigra

A team of electrophysiologists from Frankfurt and Freiburg, have shown how neuronal properties are altered in the substantia nigra (SN), a brain region that suffers from cell loss in Parkinson's disease (PD).

Parkinson's is a degenerative disorder of the central nervous system. It is one of the most common neural disorders, and its prevalence rises with age. As such, the search for remedies against PD is an increasing priority for societies confronted with aging populations. The research group, supervised by Professor Jochen Roeper, has made a big step forward in unravelling the mechanisms underlying PD pathology.

A hallmark of PD is the loss of neurons within a particular brain area, the SN. This loss appears to be associated with an intracellular accumulation of the protein α-synuclein. Although this was already known, it remained a mystery why SN neurons are vulnerable to degeneration whilst those from other brain areas are spared (even though they also accumulate α-synuclein).

The results published in the Journal of Neuroscience have begun to reveal the answers. Roeper and colleagues recorded in vivo and in vitro electrical properties of neurons in the SN and other brain areas in transgenic mice suffering from PD symptoms due to overexpression of α-synuclein.

Using an ELC-03M amplifier and other equipment from npi electronic (including a DPA-2FS), they registered the neurons' spiking activity and performed juxtacellular dye fillings of the recorded cells.

In vivo firing rates were found to be systematically elevated in dopaminergic neurons in SN, but not in other brain areas. These changes could be traced back to alterations in the properties of Kv4.3 potassium channels.

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Research paper:

Subramaniam M., Althof D., Gispert S., Schwenk J., Auburger G., Kulik A., Fakler B., Roeper J. (2014) Mutant α-synuclein enhances firing frequencies in dopamine substantia nigra neurons by oxidative impairment of A-type potassium channels Journal of Neuroscience 34:13586-99 doi: 10.1523/JNEUROSCI.5069-13.2014