We have known for a long time that neurons have a certain unchanging
specificity for the neurotransmitter they release. We have dopaminergic neurons
releasing dopamine, serotonergic neurons releasing serotonin, cholinergic
neurons releasing acetylcholine, and so on.
Neural plasticity is the idea that our brains can change in
many different ways to adjust to physiological and behavioral changes that our
bodies have. Frequently, this plasticity is expressed by a general change of
pace within the neuron. This can be a varying rate of firing of action
potentials, differing quantal release of neurotransmitter, or other similar changes
within the cell. It was not until recently that we began to think that a cell
could completely change which neurotransmitter it expressed, not just simply
how much of a given neurotransmitter is released. This idea is labeled
neurotransmitter respecification.
Spitzer’s fascinating research, outlined in the article linked below, found that this neuronal plasticity may go further than we had ever imagined; that neurotransmitter respecification can happen secondary to certain stimuli. Studies using primates showed that when eyelids were sutured shut, blocking visual input, the number of GABAergic neurons were reduced and later reappeared when vision was returned (opening of the eyelids). The mechanism was not that less GABA was released from those neurons, it was that those previously GABAergic neurons were no longer useful and reassigned themselves to a new neurotransmitter that would be beneficial to the system.
The potential clinical implications of this study are numerous. There are countless central nervous system diseases that result from altered levels of a neurotransmitter-take Parkinson’s Disease and dopamine for example. Parkinson’s is caused by the depletion of dopamine in a part of the substantia nigra. Current drug therapies attempt to restore some dopamine by administering the precursor, L-dopa, to a patient in order to synthesize and make up for some lost dopamine. Scientists are developing an additional type of therapy where certain stimuli can morph other neurons into dopaminergic ones to compensate for the disease-related loss. One therapy, already in use for many patients suffering from seasonal affective disorder, is the use of bright white lights, which can induce new dopaminergic neuron formation in the brain. Other disorders that this technique could targeted include Alzheimer’s and fragile X syndrome.
Spitzer’s fascinating research, outlined in the article linked below, found that this neuronal plasticity may go further than we had ever imagined; that neurotransmitter respecification can happen secondary to certain stimuli. Studies using primates showed that when eyelids were sutured shut, blocking visual input, the number of GABAergic neurons were reduced and later reappeared when vision was returned (opening of the eyelids). The mechanism was not that less GABA was released from those neurons, it was that those previously GABAergic neurons were no longer useful and reassigned themselves to a new neurotransmitter that would be beneficial to the system.
The potential clinical implications of this study are numerous. There are countless central nervous system diseases that result from altered levels of a neurotransmitter-take Parkinson’s Disease and dopamine for example. Parkinson’s is caused by the depletion of dopamine in a part of the substantia nigra. Current drug therapies attempt to restore some dopamine by administering the precursor, L-dopa, to a patient in order to synthesize and make up for some lost dopamine. Scientists are developing an additional type of therapy where certain stimuli can morph other neurons into dopaminergic ones to compensate for the disease-related loss. One therapy, already in use for many patients suffering from seasonal affective disorder, is the use of bright white lights, which can induce new dopaminergic neuron formation in the brain. Other disorders that this technique could targeted include Alzheimer’s and fragile X syndrome.
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