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Top Abstracts
T1 Poster Session I - VIII - Finalists:
Student Competition Finalists
T1-01
EARLY HINDLIMB UNLOADING PRODUCES CHRONIC
BIOMECHANICAL, PHYSIOLOGICAL AND MOLECULAR
SIGNATURES OF MALADAPTIVE PLASTICITY IN SCI
Kazuhito Morioka
1,2
, Toshiki Tazoe
2,3
, J. Russell Huie
1
, Cristian F.
Guandique
1
, Xiaokui Ma
1
, Jeffrey A. Sacramento
1
, Sakae Tanaka
4
,
Jacqueline C. Bresnahan
1
, Michael S. Beattie
1
, Toru Ogata
2
, Adam R.
Ferguson
1
1
Brain and Spinal Injury Center (BASIC), University of California,
San Francisco, Department of Neurological Surgery, San Francisco,
USA
2
Research Institute, National Rehabilitation Center for the Persons
With Disabilities, Department of Rehabilitation for the Movement
Functions, Saitama, Japan
3
University of Pittsburgh, Department of Physical Medicine and Re-
habilitation, Pittsburgh, USA
4
Faculty of Medicine, The University of Tokyo, Department of Or-
thopaedic Surgery, Tokyo, Japan
Appropriate limb loading is essential for neurorehabilitation after
SCI, in part, because it guides spinal cord neuroplasticity. Complete
unloading such as prolonged bed rest may interfere with functional
recovery, whereas appropriate afferent information through reha-
bilitation may improve function by modulating spinal plasticity.
The impact of limb loading on synaptic plasticity in SCI remains
poorly understood. We investigated long-term biological, biome-
chanical and physiological consequence of hindlimb unloading
(HU) in the acute phase of SCI. Adult female SD rats received a
mild SCI (T9; 50 kdyn, IH). Three days post-injury, subjects were
randomized to two experimental groups: 1) HU by tail suspension,
or 2) normal-loading control. After two weeks, the HU group was
returned to normal loading condition. Animals were monitored until
8 weeks post-injury. Assessments included: 1) BBB locomotor re-
covery; 2) kinematic gait analysis; 3) electrophysiological H-reflex
testing at 8 weeks-post injury; 4) spinal cord tissue analysis using
biomolecular and robotic confocal microscopy assessments of
plasticity-related changes in ventral motorneurons. Results indi-
cated that: 1) HU early after SCI impaired recovery of coordinated
gait characteristics and produced excessive excitation of spinal re-
flex circuits; 2) Chronically increased synaptic glutamate AMPA
receptors on the plasma membrane of spinal motor neurons pro-
viding a cellular mechanism. Our findings suggest that limb un-
loading early after SCI induces maladaptive spinal cord plasticity
that persists to impair functional recovery in chronic phase, pro-
viding a novel mechanistic target for early intervention after SCI to
enhance the effect of rehabilitation in the chronic phase following
injury.
This works was supported by NS088475, NS067092, Wings for
Life Spinal Cord Research Foundation, Craig H. Neilsen Founda-
tion.
Keywords: AMPA, Synaptic Plasticity, Loading, Rehabilitation
T1-02
DENDRITIC MORPHOLOGY AND NEUROTRANSMITTER
TYPE OF THORACIC DESCENDING PROPRIOSPINAL
NEURONS IN SHAM, AXOTOMY, AND GDNF TREATMENT
Lingxiao Deng
1
, Yiwen Ruan
1
, Chen Chen
1
, Christian Corbin Frye
1
,
Dale Sengelaub
1
, Wenhui Xiong
1
, Xiaoming Jin
1
, Xiao-Ming Xu
1
1
Indiana University, Neurosurgery Department, Indianapolis, USA
2
Indiana University, Department of Psychological and Brain Sci-
ences, Bloomington, USA
After spinal cord injury, descending propriospinal neurons (DPSNs)
greatly contributed to spontaneous functional recoveries. However, little
is known regarding their normal dendritic morphology and plasticity
after injury. We applied a G-mutated rabies virus (G-Rabies virus) co-
expressing green fluorescence protein (GFP) to reveal Golgi-like
dendritic morphology of DPSNs, and their response to axotomy and
glial derived neurotrophic factor (GDNF) treatment. We also in-
vestigated their neurotransmitter type. The animals were divided into
three groups: sham or spinal transection injuries (with or without
GDNF). Each group was further divided into injection subgroup A
(Fluorescence Gold, FG) and B (G-Rabies virus), with injection into
the 2
nd
lumbar cord. Three days post-injection, transection was
performed at the 11
th
thoracic level, with gelfoam containing saline
or GDNF transplanted into the lesion gap. Four days post-injury, the
rats were sacrificed. The GFP signal of dendrites in the T7-T9 cord
was visualized via two-photon microscopy, then traced and ana-
lyzed. Our results indicated that the majority of FG labeled DPSNs
in T7-T9 spinal cords were located in the Rexed Lamina VII, with
greater than 90 percent glutamatergic neurons and the remaining 10
percent comprised of choline acetyltransferase, glycine, and GABA.
Uninjured DPSNs had a predominantly dorsal-ventral distribution of
dendrites. However, transection altered this dendritic distribution,
with dorsal-ventral retraction and lateral-medial extension, and in-
creased the density of spine-like structures. Transection caused
cellular death closest to the lesion. Short-term GDNF treatment did
not increase the number of surviving DPSNs but increased the ter-
minal dendritic length and enhanced the transection effect on spine-
like density. To our knowledge this is the first report describing the
neurotransmitter expression and morphologic characteristics of
DPSNs, as well as the dendritic response after transection injury and
GDNF treatment.
Keywords: Descending propriospinal neuron, dendrite, spine, rabies
virus, neurotransmitter, glial derived neurotrophic factor
A-2