Effect of Ser-129 phosphorylation on interaction of α-synuclein with synaptic and cellular membranes.

In the healthy brain, less than 5% of α-synuclein (α-syn) is phosphorylated at serine 129 (Ser(P)-129). However, within Parkinson disease (PD) Lewy bodies, 89% of α-syn is Ser(P)-129. The effects of Ser(P)-129 modification on α-syn distribution and solubility are poorly understood.

Expression of Semaphorin3C in axotomized rodent facial and rubrospinal neurons.

Semaphorins are a family of axonal guidance molecules that, by virtue of their chemorepulsive or chemoattractive actions, may be the important factors in determining the success or failure of axonal regeneration in the mature nervous system after injury. Here, we have used two adult mouse models of nervous system injury to evaluate the neuronal expression of Semaphorin3C (Sema3C) in regenerating (facial motoneurons) and non-regenerating (rubrospinal) neurons following axonal injury. Using in situ hybridization (ISH), we observed that uninjured facial motoneurons express Sema3C mRNA and, following axonal injury, there is a transient up-regulation in Sema3C mRNA expression in injured motoneurons.

Brain-derived neurotrophic factor gene transfer with adeno-associated viral and lentiviral vectors prevents rubrospinal neuronal atrophy and stimulates regeneration-associated gene expression after acute cervical spinal cord injury.

Study Design: Experimental animal study.

Objective: To determine if viral vectors carrying the gene for brain-derived neurotrophic factor (BDNF) could be used to promote an axonal regenerative response in rubrospinal neurons after an acute cervical spinal cord injury.

Summary Of Background Data: Following axotomy in the cervical spinal cord, rubrospinal neurons undergo severe atrophy and fail to up-regulate important genes for regeneration.

Dose-dependent beneficial and detrimental effects of ROCK inhibitor Y27632 on axonal sprouting and functional recovery after rat spinal cord injury.

Axonal regeneration within the injured central nervous system (CNS) is hampered by multiple inhibitory molecules in the glial scar and the surrounding disrupted myelin. Many of these inhibitors stimulate, either directly or indirectly, the Rho intracellular signaling pathway, providing a strong rationale to target it following spinal cord injuries. In this study, we infused either control (PBS) or a ROCK inhibitor, Y27632 (2 mM or 20 mM, 12 microl/day for 14 days) into the intrathecal space of adult rats starting immediately after a cervical 4/5 dorsal column transection.

Both positive and negative factors regulate gene expression following chronic facial nerve resection.

Previously, we reported that following a chronic nerve resection, removal of the neuroma reversed the atrophy, increased the number of countable motoneurons and resulted in the re-expression of GAP-43 and alpha tubulin mRNA. In the present study, we questioned whether this response was due to the removal of the neuroma, or a result of factors such as neurotrophins, produced at the injury site. To test this hypothesis, 10 weeks after axotomy, the axonal transport blocker colchicine or, glial derived neurotrophic factor (GDNF) was injected proximal to the neuroma.