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Synaptic remodeling

FIGURE 1.7 Time course of neuronal and synaptic remodeling in the rodent cerebral cortex. Neurogenesis and pruning of cells, axon collaterals, and synapses are distinct processes with partially overlapping time courses. Data are compiled from Fraser Evan (1996) Vaux Strasser, (1996) Ferrer et al. (1990). [Pg.12]

Nonetheless, there is considerable cause for concern about the use of psychotropic medication in preschool-age children during a period of continued rapid neural maturation (including synaptic remodeling and construction). The cortical synaptic density reaches its maximum at the age of 3 years and is substantially modified by the pruning process during the next 7 years (Huttenlocher, 1990). At the same time, the cerebral metabolic rate peaks between 3 and 4 years of... [Pg.664]

Fong DK, Rao A, Crump FT, Craig AM. 2002. Rapid synaptic remodeling by protein kinase C reciprocal translocation of NMDA receptors and calcium/calmodulin-dependent kinase II. J. Neurosci. 22 2153-64... [Pg.354]

Beaudet A, Sotelo C (1981) Synaptic remodeling of serotonin axon terminals in rat agranular cerebellum. Brain Res., 206, 305-329. [Pg.315]

The neurotoxicological effects of lead have been suggested to be related to its ability to activate Ca-sensitive protein kinase responsible for synaptic remodeling, either by direct interaction with the enzyme or by activating calmodulin which in turn activates the enzyme [42-45]. [Pg.433]

Fig. 4.1 Hypothetical model of pathogenesis of pain in DSP. (1) Injury of peripheral nerve fibers due to multifocal inflammation and secreted macrophage activation products results in abnormal spontaneous activity of neighboring uninjured nociceptive fibers ( peripheral sensitization ). (2) Furthermore, the aberrant inflammatory response in DRG leads to alterations in neuronal sodium and calcium channel expression and ectopic impulse generation. (3) This results in central remodeling within the dorsal horn due to A-fiber sprouting and synaptic formation with pain fibers in lamina 11, and maintenance of neuropathic pain ( central sensitization ). Reproduced with permission from (Keswani et al. 2002)... Fig. 4.1 Hypothetical model of pathogenesis of pain in DSP. (1) Injury of peripheral nerve fibers due to multifocal inflammation and secreted macrophage activation products results in abnormal spontaneous activity of neighboring uninjured nociceptive fibers ( peripheral sensitization ). (2) Furthermore, the aberrant inflammatory response in DRG leads to alterations in neuronal sodium and calcium channel expression and ectopic impulse generation. (3) This results in central remodeling within the dorsal horn due to A-fiber sprouting and synaptic formation with pain fibers in lamina 11, and maintenance of neuropathic pain ( central sensitization ). Reproduced with permission from (Keswani et al. 2002)...
In the central nervous system (CNS) nitric oxide (NO) functions as a neurotransmitter (Bredt and Synder, 1992). NO has been implicated as a mediator of long-term potentiation (Haley et al., 1992 Schuman and Madison, 1994) and as a cellular correlate of memory, and it may also mediate synaptic plasticity and remodeling (Hess et al., 1993 Wu et al., 1994). Unlike conventional neurotransmitters, NO is not packaged into synaptic vesicles and then released in quantal packets. Indeed, its chemical instability in solution (Ignarro, 1990) and its membrane permeability would appear... [Pg.91]


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