Actin in Axons: Stable Scaffolds and Dynamic Filaments
... polymerization; (3) cap F-actin barbed ends to inhibit polymerization; (4) cap pointed ends to inhibit depolymerization; (5) bind barbed ends to inhibit capping; (6) bind pointed ends to promote depolymerization; (7) bundle, crosslink or stabilize F-actin; (8) sever actin filaments; (9) move cargo a ...
... polymerization; (3) cap F-actin barbed ends to inhibit polymerization; (4) cap pointed ends to inhibit depolymerization; (5) bind barbed ends to inhibit capping; (6) bind pointed ends to promote depolymerization; (7) bundle, crosslink or stabilize F-actin; (8) sever actin filaments; (9) move cargo a ...
Different neurotrophins are expressed and act in a developmental
... raised the issue of whether similar correlations between target field innervation, neurotrophin synthesis and neuronal responsiveness exist for these more recently identified neurotrophins. This is especially pertinent as these neurotrophins, in contrast to NGF, have additional roles in neuronal dev ...
... raised the issue of whether similar correlations between target field innervation, neurotrophin synthesis and neuronal responsiveness exist for these more recently identified neurotrophins. This is especially pertinent as these neurotrophins, in contrast to NGF, have additional roles in neuronal dev ...
INFUSION OF NERVE GROWTH FACTOR (NGF) INTO KITTEN
... or attenuate visual cortical plasticity in the rat. In cats and ferrets, the e¡ects of exogenous NGF on development and plasticity of visual cortex have been reported to be small or nonexistent. To determine whether locally delivered NGF a¡ects ocular dominance column formation or the plasticity pro ...
... or attenuate visual cortical plasticity in the rat. In cats and ferrets, the e¡ects of exogenous NGF on development and plasticity of visual cortex have been reported to be small or nonexistent. To determine whether locally delivered NGF a¡ects ocular dominance column formation or the plasticity pro ...
glial versus neuronal uptake of glutamate
... inputs to the hippocampus were shown in autoradiographic studies to be localized in the known target areas of these projections (Storm-Mathisen, 1977). Aspartate is taken up by a high-affinity transport system which appears to be the same as that for glutamate and therefore cannot be distinguished i ...
... inputs to the hippocampus were shown in autoradiographic studies to be localized in the known target areas of these projections (Storm-Mathisen, 1977). Aspartate is taken up by a high-affinity transport system which appears to be the same as that for glutamate and therefore cannot be distinguished i ...
Spatially and Functionally Distinct Roles of the PI3
... Akt (protein kinase B). Neurons were maintained under conditions in which cell bodies and proximal axons (hereafter referred to as the cell body compartment) were exposed to medium containing a neutralizing antibody directed against NGF (␣-NGF) while distal axons, which are ⬎1 mm away from cell bodi ...
... Akt (protein kinase B). Neurons were maintained under conditions in which cell bodies and proximal axons (hereafter referred to as the cell body compartment) were exposed to medium containing a neutralizing antibody directed against NGF (␣-NGF) while distal axons, which are ⬎1 mm away from cell bodi ...
Full Text
... Background: Since the discovery that mutations in the enzyme SOD1 are causative in human amyotrophic lateral sclerosis (ALS), many strategies have been employed to elucidate the toxic properties of this ubiquitously expressed mutant protein, including the generation of GFP-SOD1 chimaeric proteins fo ...
... Background: Since the discovery that mutations in the enzyme SOD1 are causative in human amyotrophic lateral sclerosis (ALS), many strategies have been employed to elucidate the toxic properties of this ubiquitously expressed mutant protein, including the generation of GFP-SOD1 chimaeric proteins fo ...
- Journal of Vestibular Research
... supersensitivity, receptor up-regulation, or increased neurotransmitter release. To date, none of these explanations can adequately account for static compensation in all mammalian species (Table 3). Reactive synaptogenesis has often been suggested as a possible explanation for vestibular compensati ...
... supersensitivity, receptor up-regulation, or increased neurotransmitter release. To date, none of these explanations can adequately account for static compensation in all mammalian species (Table 3). Reactive synaptogenesis has often been suggested as a possible explanation for vestibular compensati ...
Role of the Indirect Pathway of the Basal Ganglia
... Ogura and Kita, 2000; Cragg et al., 2004; Shen and Johnson, 2005; Kita, 2007; Fan et al., 2012; Wilson, 2013). These and other changes in values were chosen to reproduce key effects qualitatively rather than quantitatively. They amount to a substantial increase of the excitatory–inhibitory interplay ...
... Ogura and Kita, 2000; Cragg et al., 2004; Shen and Johnson, 2005; Kita, 2007; Fan et al., 2012; Wilson, 2013). These and other changes in values were chosen to reproduce key effects qualitatively rather than quantitatively. They amount to a substantial increase of the excitatory–inhibitory interplay ...
Kir2 potassium channels in rat striatum are strategically
... Kir4 is known to control K+ homeostasis in glial cells and the inner ear11. ATP-sensitive Kir6 (KATP) channels play an important role in the pancreas; they influence the control of insulin secretion12 in interaction with SUR (sulphonylurea receptor) subunits. Moreover, this channel may contribute to ...
... Kir4 is known to control K+ homeostasis in glial cells and the inner ear11. ATP-sensitive Kir6 (KATP) channels play an important role in the pancreas; they influence the control of insulin secretion12 in interaction with SUR (sulphonylurea receptor) subunits. Moreover, this channel may contribute to ...
GnRH Protein Levels in Atrazine-Treated Axolotls
... It is important to understand the mechanisms by which chemicals such as atrazine act as endocrine disruptors, so that newly developed chemicals may be designed to minimize endocrine disruption. GnRH is an important target to examine as a possible site of endocrine disruption, since endocrine disrupt ...
... It is important to understand the mechanisms by which chemicals such as atrazine act as endocrine disruptors, so that newly developed chemicals may be designed to minimize endocrine disruption. GnRH is an important target to examine as a possible site of endocrine disruption, since endocrine disrupt ...
Biochemistry of Alzheimer's disease
The biochemistry of Alzheimer's disease (AD), one of the most common causes of adult dementia, is as yet not well understood. AD has been identified as a protein misfolding disease due to the accumulation of abnormally folded amyloid beta protein in the brains of Alzheimer's patients. Amyloid beta, also written Aβ, is a short peptide that is an abnormal proteolytic byproduct of the transmembrane protein amyloid precursor protein (APP), whose function is unclear but thought to be involved in neuronal development. The presenilins are components of proteolytic complex involved in APP processing and degradation.Amyloid beta monomers are soluble and contain short regions of beta sheet and polyproline II helix secondary structures in solution, though they are largely alpha helical in membranes; however, at sufficiently high concentration, they undergo a dramatic conformational change to form a beta sheet-rich tertiary structure that aggregates to form amyloid fibrils. These fibrils deposit outside neurons in dense formations known as senile plaques or neuritic plaques, in less dense aggregates as diffuse plaques, and sometimes in the walls of small blood vessels in the brain in a process called amyloid angiopathy or congophilic angiopathy.AD is also considered a tauopathy due to abnormal aggregation of the tau protein, a microtubule-associated protein expressed in neurons that normally acts to stabilize microtubules in the cell cytoskeleton. Like most microtubule-associated proteins, tau is normally regulated by phosphorylation; however, in AD patients, hyperphosphorylated tau accumulates as paired helical filaments that in turn aggregate into masses inside nerve cell bodies known as neurofibrillary tangles and as dystrophic neurites associated with amyloid plaques. Although little is known about the process of filament assembly, it has recently been shown that a depletion of a prolyl isomerase protein in the parvulin family accelerates the accumulation of abnormal tau.Neuroinflammation is also involved in the complex cascade leading to AD pathology and symptoms. Considerable pathological and clinical evidence documents immunological changes associated with AD, including increased pro-inflammatory cytokine concentrations in the blood and cerebrospinal fluid. Whether these changes may be a cause or consequence of AD remains to be fully understood, but inflammation within the brain, including increased reactivity of the resident microglia towards amyloid deposits, has been implicated in the pathogenesis and progression of AD.