Neurosciences Neuron-Glia
Plasticity
HC 9
According to textbooks, glial cells are given the label of supportive cells, while actually their
functions appear to be way more diverse than previously figured. In a nutshell, their
functions include maintaining physical structure; repair tissue; phagocytose; provide
nutrients; and regulate the interstitial fluid composition. There are actually diverse glial cell
types, which are spread over the PNS and CNS alike. The cell-types discussed below are the
ones active in plasticity. We know two types of plasticity, both adherent to the given
phenomenon to be able to change their connections and functioning over time.
The first type of plasticity is myelin plasticity, so the ability of myelin to form and change
composition and appear and disappears, etc. The cells in the CNS actively contributing to
myelin formation and plasticity are glial cells, the oligodendrocytes. Myelinating glia sculpt
the structural and electrical properties of axons by controlling their diameter and clustering
ions channels at nodes. This myelination starts before birth and continues into adolescence,
encapsulating and changing continuously. Synaptogenesis and synaptic pruning on the other
hand, has several peaks of different areas which are more active; sensorimotor cortex first,
then parietal/association cortices and lastly the prefrontal cortex. The actual mechanism
behind the encapsulating of axons, in developmental myelination is as follows:
oligodendrocytes are generated by designated precursor cells, whereby axonal signals like
NRG1 type III cause dimerization of oligodendritic membrane proteins ErbB2/ErbB3. If this
signal is strong enough, crossing a certain threshold, they become promyelinating and
eventually myelinating cells. The same occurs for Schwann cells. If the NRG1 type III is too
low, a non-myelinating cell rather develops, which simply surrounds smaller axons. A signal
is typically low if the axon is smaller. The strength of the signal furthermore determines the
actual thickness of the myelin layer. Aside from these molecular signals, also action
potentials prove to induce myelination. In experiments using toxins that prevent synaptic
vesicle fusion and exocytosis, so indirectly prevent neurotransmitter release and
propagation of an action potential, the neurons are less myelinated. There is an intrinsic,
genetically programmed extent of myelination, but the adaptive myelination model kicks in
later which, depending on the further signaling and extent of action potential exposure,
myelinates further. The intrinsic myelination can be seen in experiments where
oligodendrocytes also wrap around random fibers roughly the size of an axon, without any
signals. This mechanism of myelination occurs both in development and during adulthood,
when learning new things or in memory.
This latter part is what confers learning and memory. Extensive piano practicing has
regionally specific effects on the amount of white matter, as does 6 weeks of juggling
influence and change the white matter structure. Experiments in mice show how learning
and performing tasks over and over again influences the myelination pattern; it increases
myelination. The importance of myelination is especially seen because of deficits and
improper white matter organization in psychiatric, cognitive and emotional disorders.
Myelination, aside from its apparent role in learning and memory, also aids in optimal
signaling between axons. A receiving neuron has several synapses it needs to integrate
Plasticity
HC 9
According to textbooks, glial cells are given the label of supportive cells, while actually their
functions appear to be way more diverse than previously figured. In a nutshell, their
functions include maintaining physical structure; repair tissue; phagocytose; provide
nutrients; and regulate the interstitial fluid composition. There are actually diverse glial cell
types, which are spread over the PNS and CNS alike. The cell-types discussed below are the
ones active in plasticity. We know two types of plasticity, both adherent to the given
phenomenon to be able to change their connections and functioning over time.
The first type of plasticity is myelin plasticity, so the ability of myelin to form and change
composition and appear and disappears, etc. The cells in the CNS actively contributing to
myelin formation and plasticity are glial cells, the oligodendrocytes. Myelinating glia sculpt
the structural and electrical properties of axons by controlling their diameter and clustering
ions channels at nodes. This myelination starts before birth and continues into adolescence,
encapsulating and changing continuously. Synaptogenesis and synaptic pruning on the other
hand, has several peaks of different areas which are more active; sensorimotor cortex first,
then parietal/association cortices and lastly the prefrontal cortex. The actual mechanism
behind the encapsulating of axons, in developmental myelination is as follows:
oligodendrocytes are generated by designated precursor cells, whereby axonal signals like
NRG1 type III cause dimerization of oligodendritic membrane proteins ErbB2/ErbB3. If this
signal is strong enough, crossing a certain threshold, they become promyelinating and
eventually myelinating cells. The same occurs for Schwann cells. If the NRG1 type III is too
low, a non-myelinating cell rather develops, which simply surrounds smaller axons. A signal
is typically low if the axon is smaller. The strength of the signal furthermore determines the
actual thickness of the myelin layer. Aside from these molecular signals, also action
potentials prove to induce myelination. In experiments using toxins that prevent synaptic
vesicle fusion and exocytosis, so indirectly prevent neurotransmitter release and
propagation of an action potential, the neurons are less myelinated. There is an intrinsic,
genetically programmed extent of myelination, but the adaptive myelination model kicks in
later which, depending on the further signaling and extent of action potential exposure,
myelinates further. The intrinsic myelination can be seen in experiments where
oligodendrocytes also wrap around random fibers roughly the size of an axon, without any
signals. This mechanism of myelination occurs both in development and during adulthood,
when learning new things or in memory.
This latter part is what confers learning and memory. Extensive piano practicing has
regionally specific effects on the amount of white matter, as does 6 weeks of juggling
influence and change the white matter structure. Experiments in mice show how learning
and performing tasks over and over again influences the myelination pattern; it increases
myelination. The importance of myelination is especially seen because of deficits and
improper white matter organization in psychiatric, cognitive and emotional disorders.
Myelination, aside from its apparent role in learning and memory, also aids in optimal
signaling between axons. A receiving neuron has several synapses it needs to integrate
