Adhesion Molecules-28

Advances and Experimental-3

Aging-9

Agricultural Biotechnology-37

Angiogenesis-29

Antisense-4

Apoptosis-49

Atherosclerosis-12

Autoimmunity-69

Bacterial Virulence-18

Bioinformatics-13

BioMaterials-18

Biosurfactants-1

Biotechnology-99

Cancer Genetics-25

Cancer Metastasis-19

Cell Biology-16

Cell Cycle-34

Cell Metabolism-327

Channels and Transporters-79

Chaperones-11

Circadian Rhythms-13

Coagulation-14

Cytokines/Growth Factors-52

Development-223

DNA-56

DNA Surveillance and Repair-42

Drug Design-17

Endocrine-66

Evolution-33

Extracellular Matrix-30

Gastroenterology-52

Gene Expression-178

Gene Therapy-53

Heart-61

Heat Shock Proteins-19

Hematology-11

Immunology-93

Infectious Disease-71

Ischemia-Reperfusion-33

Leptin and Leptin Antagonists-1

Medical-20

MHC-17

Mitochondria-17

Molecular Biology-15

Molecular Complexes and Signaling-1

Nanomedicine-30

Neurodegenerative Disease-72

Neuropharmacology-112

Neuroscience-38

Nucleus-15

Oncogenes-8

Oncology-87

Parasitic Disease-12

Pharmacogenomics-14

Prebiotic Evolution-2

Protein-12

Reproductive Biology-59

RNA-152

Signal Transduction-186

Stem Cells-80

Surgery-37

T-Cell Activation-12

Tissue Engineering-116

Transplant-51

Vaccines-82

Viruses-85

Chapter category: Neurodegenerative Disease

Lesion-Induced Axonal Sprouting in the Central Nervous System

Chapter authors:
Thomas Deller, Carola A. Haas, Thomas M. Freiman, Amie Phinney, Mathias Jucker and Michael Frotscher

Injury or neuronal death often come about as a result of brain disorders. Inasmuch as the damaged nerve cells are interconnected via projections to other regions of the brain, such lesions lead to axonal loss in distal target areas. The central nervous system responds to deafferentation by means of plastic remodeling processes, in particular by inducing outgrowth of new axon collaterals from surviving neurons (collateral sprouting). These sprouting processes result in a partial reinnervation, new circuitry, and functional changes within the deafferented brain regions. Lesioning of the entorhinal cortex is an established model system for studying the phenomenon of axonal sprouting. Using this model system, it could be shown that the sprouting process respects the pre-existing lamination pattern of the deafferented fascia dentata, i. e., it is layer-specific. A variety of different molecules are involved in regulating this reorganization process (extracellular matrix molecules, cell adhesion molecules, transcription factors, neurotrophic factors, growth-associated proteins). It is proposed here that molecules of the extracellular matrix define the boundaries of the laminae following entorhinal lesioning and in so doing limit the sprouting process to the deafferented zone. To illustrate the role of axonal sprouting in disease processes, special attention is given to its significance for neurodegenerative disorders, particularly Alzheimer’s disease (AD), and temporal lobe epilepsy. Finally, we discuss both the beneficial as well as disadvantageous functional implications of axonal sprouting for the injured organism in question.

» Access chapter for $19

Additional chapters from this book: