Acetylcholine induces neurite outgrowth.
Iron chelator induces neurite outgrowth.
If one were to eat one of my maltol/ iron chelator caramel containing
vegetable lecithin / choline one could theoretically .. get .. up ..
and .. walk.
"Acetylcholine induces neurite outgrowth and promotes the formation
and strengthening of synapses, or connections between neurons"
Neurotransmitters in biopolymers stimulate nerve regeneration
December 11th, 2007 Fluorescence micrograph of a ganglion on a 70
percent acetylcholine polymer that shows neurites expressing an
established neuronal marker called synaptophysin. The bright red spots
on the neurites indicate the presence of synaptic vesicle proteins,
which are required for functional restoration after nerve injury.
Research reported December 11 in the journal Advanced Materials
describes a potentially promising strategy for encouraging the
regeneration of damaged central nervous system cells known as
neurons.
The technique would use a biodegradable polymer containing a chemical
group that mimics the neurotransmitter acetylcholine to spur the
growth of neurites, which are projections that form the connections
among neurons and between neurons and other cells. The biomimetic
polymers would then guide the growth of the regenerating nerve.
There is currently no treatment for recovering human nerve function
after injury to the brain or spinal cord because central nervous
system neurons have a very limited capability of self-repair and
regeneration.
“Regeneration in the central nervous system requires neural activity,
not just neuronal growth factors alone, so we thought a
neurotransmitter might send the necessary signals,” said Yadong Wang,
assistant professor in the Coulter Department of Biomedical
Engineering at Georgia Tech and Emory University, and principal
investigator of the study. The research was supported by Georgia Tech,
the National Science Foundation and the National Institute of
Biomedical Imaging and Bioengineering (NIBIB).
Chemical neurotransmitters relay, amplify and modulate signals between
a neuron and another cell. This new study shows that integrating
neurotransmitters into biodegradable polymers results in a biomaterial
that successfully promotes neurite growth, which is necessary for
victims of central nervous system injury, stroke or certain
neurodegenerative diseases to recover sensory, motor, cognitive or
autonomic functions.
Wang and graduate student Christiane Gumera developed novel
biodegradable polymers with a flexible backbone that allowed
neurotransmitters to be easily added as a side chain. In its current
form, the polymer would be implanted via surgery to repair damaged
central nerves.
“One of our ultimate goals is to create a conduit for nerve
regeneration that guides the neurons to regenerate, but gradually
degrades as the neurons regenerate so that it won’t constrict the
nerves permanently,” explained Wang.
For the experiments, the researchers tested polymers with different
concentrations of the acetylcholine-mimicking groups. Acetylcholine
was chosen because it is known to induce neurite outgrowth and promote
the formation and strengthening of synapses, or connections between
neurons. They isolated ganglia nervous tissue samples, placed them on
the polymers and observed new neurites extend from the ganglia.
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Since these neuron extensions must traverse a growth inhibiting
material in the body, Wang and Gumera tested the ability of the
biomaterial to enhance the extension of sprouted neurites. More
specifically, they assessed whether the ganglia sprouted at least 20
neurites and then measured neurite length and neurite length
distribution with an inverted phase contrast microscope.
“We found that adding 70 percent acetylcholine to the polymer induced
regenerative responses similar to laminin, a benchmark material for
nerve culture,” said Wang. Seventy percent acetylcholine also led to a
neurite growth rate of up to 0.7 millimeters per day, or approximately
half the thickness of a compact disc.
Laminin is a natural protein present in the nervous tissues, but it
dissolves in water, making it difficult to incorporate into a conduit
that needs to support nerves for months. A synthetic polymer with
acetylcholine functional groups, on the other hand, can be designed to
be insoluble in water, according to Wang.
Since functional restoration after nerve injury requires synapse
formation, the researchers also searched for the presence of synaptic
vesicle proteins on the newly formed neurites. With fluorescence
imaging, they found that neurons cultured on these acetylcholine
polymers expressed an established neuronal marker called
synaptophysin.
To provide insights to new approaches in functional nerve
regeneration, the researchers are currently investigating the
mechanisms by which the neurons interact with these polymers. Since
neurons that remain intact after severe injury have only a limited
capacity to penetrate the scar tissue, these new findings in nerve
regeneration could help compensate for the lost connections.
“This polymer and approach aren’t limited to nerve regeneration
though, they can probably be used for other neurodegenerative
disorders as well,” added Wang.
Source: Georgia Institute of Technology
————-
Deferoxamine-induced neurite outgrowth and synapse formation
in postnatal rat dorsal root ganglion (DRG) cell cultures
Marcin Nowickia, Joanna Kosackaa, Katharina Spanel-Borowskia and
Jürgen Borlakb, ,
aUniversity of Leipzig, Institute of Anatomy, Liebigstraße 13,
D-04103
Leipzig, Germany
bFraunhofer Institute of Toxicology and Experimental Medicine,
Nikolai-
Fuchs-Straße 1, D-30625 Hannover, Germany
Received 11 March 2009; revised 22 May 2009; accepted 25 May 2009.
Available online 5 July 2009.
Abstract
Deferoxamine (DFO) was granted orphan drug status for the
treatment of traumatic spinal cord injury but its
neuroprotective mechanism is not well understood.
We therefore investigated the mode of action of DFO in
serum-starved and/or iron-stressed cultures of rat dorsal
root ganglion (DRG) cells.
We probed for redox signaling by determining hemeoxygenase-1
activity and by measuring expression of intracellular iron
metabolism-related proteins under pro-oxidative conditions.
We also employed DNA microarrays to better understand the
genomic response of DRG cultures to treatment with DFO thereby
enabling the generation of hypotheses.
Essentially, DFO treatment resulted in outgrowth of
neurofilament 200-positive neurites and induction of synapse
formation as determined by immunoblotting, transmission
electron microscopy and immunofluorescence confocal microscopy.
Furthermore, DFO treatment of DRG cell cultures activated
neuroprotective and antioxidative programs such as matrix
metallopeptidase 2 and apolipoprotein D to promote neurite
regeneration.
Indeed, DFO reduced markedly reactive oxygen species formation,
increased the expression of hemeoxygenase-1 and improved iron
management through regulation of transferrin receptor and ferritin.
We propose DFO treatment of DRG cell cultures to completely
abolish the oxidative effect of ferrous iron (Fe2+).
Taken collectively, DFO reduced oxidative stress and induced
synthesis of neuroprotective and antioxidative molecules to foster
nerve repair and functional recovery.
Our findings help to better understand the therapeutic benefit
of DFO in the treatment of spinal cord injury.
Keywords: Deferoxamine; Dorsal root ganglion; Neurite outgrowth;
Nerve repair; Synapse formation; Oxidative stress
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