caa a22 4500 445376031 CHVBK 20180317143002.0 cr unu---uuuuu 170323e20110101xx s 000 0 eng 10.1007/s00702-010-0498-0 doi (NATIONALLICENCE)springer-10.1007/s00702-010-0498-0 Traumatic brain injury and recovery mechanisms: peptide modulation of periventricular neurogenic regions by the choroid plexus-CSF nexus [Elektronische Daten] [Conrad Johanson, Edward Stopa, Andrew Baird, Hari Sharma] In traumatic brain injury (TBI), severe disruptions occur in the choroid plexus (CP)-cerebrospinal fluid (CSF) nexus that destabilize the nearby hippocampal and subventricular neurogenic regions. Following invasive and non-invasive injuries to cortex, several adverse sequelae harm the brain interior: (i) structural damage to CP epithelium that opens the blood-CSF barrier (BCSFB) to protein, (ii) altered CSF dynamics and intracranial pressure (ICP), (iii) augmentation of leukocyte traffic across CP into the CSF-brain, (iv) reduction in CSF sink action and clearance of debris from ventricles, and (v) less efficient provision of micronutritional and hormonal support for the CNS. However, gradual post-TBI restitution of the injured CP epithelium and ependyma, and CSF homeostatic mechanisms, help to restore subventricular/subgranular neurogenesis and the cognitive abilities diminished by CNS damage. Recovery from TBI is faciltated by upregulated choroidal/ependymal growth factors and neurotrophins, and their secretion into ventricular CSF. There, by an endocrine-like mechanism, CSF bulk flow convects the neuropeptides to target cells in injured cortex for aiding repair processes; and to neurogenic niches for enhancing conversion of stem cells to new neurons. In the recovery from TBI and associated ischemia, the modulating neuropeptides include FGF2, EGF, VEGF, NGF, IGF, GDNF, BDNF, and PACAP. Homeostatic correction of TBI-induced neuropathology can be accelerated or amplified by exogenously boosting the CSF concentration of these growth factors and neurotrophins. Such intraventricular supplementation via the CSF route promotes neural restoration through enhanced neurogenesis, angiogenesis, and neuroprotective effects. CSF translational research presents opportunities that involve CP and ependymal manipulations to expedite recovery from TBI. The Author(s), 2010 CSF homeostasis nationallicence Subventricular zone nationallicence Blood-CSF barrier permeability nationallicence Periventricular lesions nationallicence Hydrocephalus nationallicence Leukocyte traffic nationallicence Neurogenesis nationallicence Intracranial pressure nationallicence Ischemia nationallicence Traumatic brain injury models nationallicence Dentate gyrus nationallicence Hippocampus nationallicence Cerebrospinal formation and drainage nationallicence CSF dynamics nationallicence Neuropeptides nationallicence ANP : Atrial natriuretic peptide nationallicence BBB : Blood-brain barrier nationallicence BCSFB : Blood-CSF barrier nationallicence BDNF : Brain-derived neurotrophic factor nationallicence CNS : Central nervous system nationallicence CP : Choroid plexus nationallicence CSF : Cerebrospinal fluid nationallicence DG : Dentate gyrus nationallicence FGF : Fibroblast growth factor nationallicence GDNF : Glial cell line-derived neurotrophic factor nationallicence ICP : Intracranial pressure nationallicence IGF : Insulin-like growth factor nationallicence ISF : Interstitial fluid nationallicence NGF : Nerve growth factor nationallicence OATS : Organic anion-transporting polypeptides nationallicence PACAP : Pituitary adenylate cyclase activating polypeptide nationallicence SAS : Subarachnoid space nationallicence SVZ : Subventricular zone nationallicence TBI : Traumatic brain injury nationallicence TFI : Transient forebrain ischemia nationallicence VEGF : Vascular endothelial growth factor nationallicence Johanson Conrad Department of Neurosurgery, Warren Alpert Medical School at Brown University, 02903, Providence, RI, USA aut Stopa Edward Department of Pathology, Warren Alpert Medical School at Brown University, 02903, Providence, RI, USA aut Baird Andrew Department of Surgery, UCSD School of Medicine, 92103, San Diego, CA, USA aut Sharma Hari Laboratory of Cerebrovascular Research, Institute of Surgical Sciences, Department of Anaesthesiology and Intensive Care, University Hospital, Uppsala University, 75185, Uppsala, Sweden aut Journal of Neural Transmission Springer Vienna 118/1(2011-01-01), 115-133 0300-9564 118:1<115 2011 118 702 https://doi.org/10.1007/s00702-010-0498-0 text/html Onlinezugriff via DOI 1 review-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s00702-010-0498-0 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Johanson Conrad Department of Neurosurgery, Warren Alpert Medical School at Brown University, 02903, Providence, RI, USA aut NATIONALLICENCE 700 1- Stopa Edward Department of Pathology, Warren Alpert Medical School at Brown University, 02903, Providence, RI, USA aut NATIONALLICENCE 700 1- Baird Andrew Department of Surgery, UCSD School of Medicine, 92103, San Diego, CA, USA aut NATIONALLICENCE 700 1- Sharma Hari Laboratory of Cerebrovascular Research, Institute of Surgical Sciences, Department of Anaesthesiology and Intensive Care, University Hospital, Uppsala University, 75185, Uppsala, Sweden aut NATIONALLICENCE 773 0- Journal of Neural Transmission Springer Vienna 118/1(2011-01-01), 115-133 0300-9564 118:1<115 2011 118 702 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer