More on neuron oscillations
It’s not a direct tie-in to today’s topic, but I found an article on oscillating neuron activity that might interest some of you. The article was titled Oscillating purkinje neuron activity causing involuntary eye movement in a mutant mouse deficient in the glutamate receptor delta-2 subunit by Yoshida, et al. (2004). While experimenting with motor coordination in mice, it was found that mice deficient in the delta-2 subunit of glutamate receptors lacked the ability to stay perched on a rotating rod. This ability was, however, exhibited by lurcher mice completely lacking the purkinje neurons affected in the delta-2 deficient mouse. Why would a complete lack of output neurons from the cerebellar cortex aid in motor function? The answer lies in neuronal oscillations.
Transient firings of wild type mouse purkinje neurons (in an oscillating pattern, though no power curve was shown) did not hinder the acrobatic ability of the mice, nor did a lack of firing from lurcher mice. Glutamate receptor deficient mice still had the same pattern of oscillating neuron depolarization as the wild type mice, but they also experienced cluster fires. These firings were from purkinje neurons not in sync with each other. They all fired at a similar time, but did not together (this also happened in an oscillating pattern, and is where the paper gets its title). As explained in the paper, these cluster firings signaled for an eye twitch that interfered with motor control.
Though no glial cells were mentioned, I found it interesting how glutamate receptors were once again a central issue in a paper dealing with oscillations of neuronal firing. More intriguing was the fact that lesioning the purkinje fibers completely in deficient mice (so that they would operate more like lurcher mice) actually helped in motor and learning function. This may have interesting, but scary, applications in the medical community… (Almost reminds me of lobotomies being a cure-all for the mentally ill.)
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