Parkinson's and Potassium Channels

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Science  23 Dec 2005:
Vol. 310, Issue 5756, pp. 1871-1873
DOI: 10.1126/science.310.5756.1871d

Parkinson's disease (PD) results from the selective loss of dopaminergic neurons in the substantia nigra of the brain. However, dopaminergic neurons in nearby parts of the brain are not affected, even though the genes implicated in familial inherited PD, as well as toxins that can induce symptoms of PD, are not restricted in their effects. Why then is this small region targeted for destruction in PD? There are hints that substantia nigra neurons show disruptions in mitochondrial respiratory function. Diminished cellular metabolism, as well as oxidative stress, can in turn cause the potassium (K)-ATP channels of dopaminergic neurons to open. Liss et al. investigated the interaction between these channels, the signals that control their function, and the degeneration of neurons. The K-ATP channel mediates dopaminergic neuron degeneration in response to mitochondrial complex 1 inhibition, in response to PD-inducing treatment of susceptible mice, and also in the mutant weaver mouse, in which dopaminergic neuron degeneration is due to constitutive activation of another potassium channel. The inappropriate function of K-ATP channels is characteristic of substantia nigra neurons, but not of dopaminergic neurons in other nearby brain areas, in which the channels seem to be connected to cellular metabolism through different signaling networks. — PJH

Nat. Neuro 8, 1742 (2005).

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