Stability of Conducting Polymer-Coated Carbon Microfibers for Long-Term Electrical Stimulation of Injured Neural Tissue.

Electroactive microfiber-based scaffolds aid neural tissue repair. Carbon microfibers (CMFs) coated with the conducting polymer poly(3,4-ethylenedioxythiophene) doped with poly[(4-styrenesulfonic acid)--(maleic acid)] (PEDOT:PSS--MA) provide efficient support and guidance to regrowing axons across spinal cord lesions in rodents and pigs. We investigated the electrical and structural performance of PEDOT:PSS--MA-coated carbon MFs (PCMFs) for long-term, biphasic electrical stimulation (ES).

[Translated article] Effects of duroplasty with bovine pericardium on fibrosis and extent of spinal cord injury: An experimental study in pigs.

Introduction: Traumatic spinal cord injury (SCI) leads to increased intraspinal pressure that can be prevented by durotomy and duroplasty. The aim of the study was to evaluate fibrosis and neural damage in a porcine model of SCI after duroplasty and application of hyaluronic acid (HA) in the tissue cavity.

Materials And Methods: Experimental study.

Effects of duroplasty with bovine pericardium on fibrosis and extent of spinal cord injury: An experimental study in pigs.

Introduction: Traumatic spinal cord injury (SCI) leads to increased intraspinal pressure that can be prevented by durotomy and duroplasty. The aim of the study was to evaluate fibrosis and neural damage in a porcine model of SCI after duroplasty and application of hyaluronic acid (HA) in the tissue cavity.

Materials And Methods: Experimental study.

Composite Fibrin/Carbon Microfiber Implants for Bridging Spinal Cord Injury: A Translational Approach in Pigs.

Biomaterials may enhance neural repair after spinal cord injury (SCI) and testing their functionality in large animals is essential to achieve successful clinical translation. This work developed a porcine contusion/compression SCI model to investigate the consequences of myelotomy and implantation of fibrin gel containing biofunctionalized carbon microfibers (MFs). Fourteen pigs were distributed in SCI, SCI/myelotomy, and SCI/myelotomy/implant groups.

CPEB1 is overexpressed in neurons derived from Down syndrome IPSCs and in the hippocampus of the mouse model Ts1Cje.

Trisomy 21, also known as Down syndrome (DS), is the most frequent genetic cause of intellectual impairment. In mouse models of DS, deficits in hippocampal synaptic plasticity have been observed, in conjunction with alterations to local dendritic translation that are likely to influence plasticity, learning and memory. Here we show that expression of a local translational regulator, the Cytoplasmic Polyadenylation Element Binding Protein 1 (CPEB1), is enhanced in hippocampal neurons from the Ts1Cje DS mouse model.

Biofunctionalized PEDOT-coated microfibers for the treatment of spinal cord injury.

Poly(3, 4-ethylenedioxythiophene)-coated carbon microfibers (PEDOT-MFs) hold promise for developing advanced neuroprostheses and neural repair devices. We investigated the chronic cellular responses to PEDOT-MFs implanted into the uninjured and the transected rat spinal cord, and compared the effects of polymer surface biofunctionalization with covalently attached polylysine (PLL) or a multimolecular complex of PLL, heparin, basic fibroblast growth factor (bFGF), and fibronectin. An alginate gel was used to facilitate microfiber implantation and reduce connective tissue scarring after spinal cord injury (SCI).

Glial progenitor cell migration promotes CNS axon growth on functionalized electroconducting microfibers.

Unlabelled: Electroactive systems that promote directional axonal growth and migration of glial progenitor cells (GPC) are needed for the treatment of neurological injuries. We report the functionalization of electroconducting microfibers with multiple biomolecules that synergistically stimulate the proliferation and migration of GPC, which in turn induce axonal elongation from embryonic cerebral cortex neurons. PEDOT doped with poly[(4-styrenesulfonic acid)-co-(maleic acid)] was synthesized on carbon microfibers and used for covalent attachment of molecules to the electroactive surface.

Deregulated mTOR-mediated translation in intellectual disability.

Local translation of dendritic mRNAs is a key aspect of dendrite and spine morphogenesis and synaptic plasticity, two phenomena generally compromised in intellectual disability disorders. Mammalian target of rapamycin (mTOR) is a protein kinase involved in a plethora of functions including dendritogenesis, plasticity and the regulation of local translation. Hence, this kinase may well be implicated in intellectual disability.

An increase in basal BDNF provokes hyperactivation of the Akt-mammalian target of rapamycin pathway and deregulation of local dendritic translation in a mouse model of Down's syndrome.

As in other diseases associated with mental retardation, dendrite morphology and synaptic plasticity are impaired in Down's syndrome (DS). Both these features of neurons are critically influenced by BDNF, which regulates local dendritic translation through phosphatidylinositol 3-kinase-Akt-mammalian target of rapamycin (mTOR) and Ras-ERK signaling cascades. Here we show that the levels of BDNF and phosphorylated Akt-mTOR (but not Ras-ERK) pathway proteins are augmented in hippocampal dendrites of Ts1Cje mice, a DS model.

NMDA-mediated regulation of DSCAM dendritic local translation is lost in a mouse model of Down's syndrome.

Down's syndrome cell adhesion molecule (DSCAM) belongs to the Down's syndrome critical region of human chromosome 21, and it encodes a cell adhesion molecule involved in dendrite morphology and neuronal wiring. Although the function of DSCAM in the adult brain is unknown, its expression pattern suggests a role in synaptic plasticity. Local mRNA translation is a key process in axonal growth, dendritogenesis, and synaptogenesis during development, and in synaptic plasticity in adulthood.

Local translation of dendritic RhoA revealed by an improved synaptoneurosome preparation.

Changes in dendritic spine morphology, a hallmark of synaptic plasticity, involve remodeling of the actin cytoskeleton, a process that is regulated by Rho GTPases. RhoA, a member of this GTPase family, segregates to dendrites in differentiated neurons. Given the emerging role of dendritic mRNA local translation in synaptic plasticity, we have assessed the possible localization and translation of RhoA mRNA at dendrites.