NNS 2015 Abstract Book

fluid-filled cavities whose borders consisted of densely packed AQP4-

expressing astrocytes closely resembling the organization of normal

glia limitans externa,

in contrast to large cavities in control SCI rats

that lacked

glia-limitans

-like borders and contained reactive glial

cells. Given that we found that TMX affects both oligodendrocytes

and astrocytes in injured spinal cords, we used an

in vitro

model of

glia progenitor cells to test the hypothesis that TMX acts on glia

progenitors in injured spinal cords. By using rodent glia progenitors

in vitro

, and different experimental paradigms, we found that TMX

induces differentiation of glia progenitors towards both oligodendro-

cytes and astrocytes. In sum, our data strongly suggest that TMX is a

promising candidate for the therapeutic treatment of SCI, in part by

promoting differentiation of glia progenitors and by normalizing

functions of both oligodendrocytes and astrocytes in injured spinal

cords.

Keywords: rat spinal cord injury, motor recovery, tamoxifen, glia

progenitors

B3-06

CROSS-SECTIONAL DIFFERENCES IN FRACTIONAL ANI-

SOTROPY WITHOUT LONGITUDINAL EVIDENCE OF RE-

COVERY BY ONE MONTH POST-CONCUSSION

Timothy Meier

1,2

, Maurizio Bergamino

, Patrick Bellgowan

, Josef

Ling

Andrew Mayer

The Mind Research Network, LBERI, Albuquerque, USA

Laureate Institute for Brain Research, LIBR, Tulsa, USA

NINDS, NIH, North Bethesda, USA

Changes in white matter structure are hypothesized as one conse-

quence of sports-related concussion (SRC). However, the timeframe

for recovery of these deficits has not been established. We assessed

longitudinal changes in fractional anisotropy (FA) in 40 collegiate

athletes (20.1

–

1.4 year old) across acute and sub-acute timeframe

post-concussion. Concussed athletes completed serial scanning ses-

sions at one day (T1; n

33, 1.64 days post), one week (T2; n

30,

8.3 days post), and one month (T3; n

26, 32.2 days) post-concus-

sion. Forty-six healthy contact sport athletes served as controls (HC;

20.3

–

1.5 years old). Structured interviews for anxiety and depres-

sion were used to assess concussion symptoms. Diffusion tensor

imaging (30 non-collinear directions, b-value

1000 s/mm

) was

performed using a GE 3-T scanner. Both region-of-interest and

voxel-wise analyses were conducted to assess longitudinal and cross-

sectional differences in FA. Results demonstrated longitudinal evi-

dence of recovery for both anxiety and depression scores by one

month post-concussion (F’s

20, p’s

0.001). In contrast, no sig-

nificant differences in FA were observed across the acute and sub-

acute period post-concussion. However, cross-sectional comparisons

indicated increased FA for concussed athletes at T1 in the bilateral

superior longitudinal fasciculi, right sagittal stratum, right forceps

minor, right internal capsule, bilateral superior cerebellar peduncles,

and left corona radiata. Differences in FA persisted at T2 and T3

relative to HC in all regions (p’s

0.05). Exploratory analyses found

that return-to-play time was positively correlated with behavioral

scores at T1 (rho’s

0.42, p’s

0.05), and with FA at both T1 and T3

(rho’s

0.43, p’s

0.05). These results demonstrate that white matter

deficits following SRC extend beyond the typical period of symptom

resolution for most clinical symptoms (e.g., balance, cognitive

testing, and self-reported emotional sequelae). The relationship be-

tween FA, clinical measures, and plasma tau concentrations in a

subset of participants (19/19/12/18; T1/T2/T3/HC) will be explored

in the future.

Keywords: concussion, diffusion, athletes

B3-07

TRANSPLANTATION OF EMBRYONIC SPINAL CORD DE-

RIVED CELLS INTO TRANSECTED PERIPHERAL NERVE

TO PREVENT MUSCULAR ATROPHY

Carolin Ruven

, Wutian Wu

The University of Hong Kong, Department of Anatomy, Hong Kong,

Hong Kong

An average human body contains around 45 miles of nerves essential

for our life. So what happens when just a small part like one nerve

will be injured? In serious injury, the connection between spinal cord

and the target organ will be lost resulting in the muscle atrophy.

Luckily, regeneration in PNS is possible and many surgical ap-

proaches can be implied. However, most nerves in the human body

are too long for the slow regeneration and treatment methods to

prevent the muscle atrophy during the regeneration time should be

applied in addition to the surgical approach. In this project, cells

isolated from E14 rat embryos’ spinal cords were injected into the

distal side of transected musculocutaneous nerve in hope that they

are able to prevent the muscle atrophy. We tested cells isolated from

spinal cord different segments (cervical, thoracic and lumbar) as

well as directly isolated fetal cells that mostly contain neurons (P0

cells) and cultured neural progenitor cells (P2 cells). Our results

show that cells were able to survive and help to retain the muscle

fiber size that was 31%, 70% and 51% (p

0.001) of uninjured side

in control, P0 cell and P2 cell group, respectively. Furthermore,

motor endplates in control animals were smaller (205

–

m) and

had either shrunken or fragmented appearance while in cell treat-

ment groups endplates were bigger (278

–

m in P0 and

241

–

m in P2 cell group) and 20–40% of them showed normal

pretzel-like structure. In electromyographic studies, stimulation of

transected nerve with cell transplantation was able to induce the

response in biceps brachii while no response was seen in the control

group. Interestingly, P0 cells survived and were able to reduce

muscle atrophy more than P2 cells whereas the cells from lumbar

segment showed the best results. In conclusion, cells isolated from

embryonic spinal cord are able to reduce the muscle atrophy and

therefore they hold a great promise for the future of treatment of

peripheral nerve injuries.

Keywords: muscle atrophy, cell transplantation, neuron replace-

ment, fetal spinal cord cells, peripheral nerve injury

B3-08

STABILIZING MICROTUBULES AFTER TRAUMATIC AX-

ONAL INJURY MITIGATES ACCUMULATION OF TAU,

CALCIUM INFLUX AND AXONAL DEGENERATION

Jean-Pierre Dolle

, Andrew Jaye, Victoria Johnson, Douglas Smith

University of Pennsylvania, Neurosurgery, Philadelphia, USA

Introduction:

Traumatic axonal injury (TAI), a common conse-

quence of traumatic brain injury (TBI), can result in mechanical

damage of microtubules and influx of calcium, in concert with un-

binding of the microtubule-stabilizing protein, tau, in axons and its

accumulation in the neuronal soma. Here, we examined the effects

microtubule stabilization treatment using Taxol on outcome of TAI

using a well-characterized in-vitro model of dynamic axon stretch-

injury.

Methods:

Primary cortical neurons were grown on micropatterned

deformable silastic membranes, whereby a series of parallel 2 mm-

long lanes containing only axons spanned two populations of neuronal

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