Rapid dendritic and axonal responses to neuronal insults

TY - JOUR

T1 - Rapid dendritic and axonal responses to neuronal insults

A1 - Mizielinska,Sarah M.

A1 - Greenwood,Sam M.

A1 - Tummala,Hemanth

A1 - Connolly,Christopher N.

AU - Mizielinska,Sarah M.

AU - Greenwood,Sam M.

AU - Tummala,Hemanth

AU - Connolly,Christopher N.

PY - 2009/12

Y1 - 2009/12

N2 - <p>Glutamate is the major excitatory neurotransmitter in the mammalian central nervous system playing critical roles in basal synaptic transmission and mechanisms of learning and memory. Under normal conditions, glutamate is sequestered within synaptic vesicles (similar to 100 mm) with extracellular glutamate concentrations being limited (&lt;1 mu M), via retrieval by plasma-membrane transporters on neuronal and glial cells. in the case of central nervous system trauma, stroke, epilepsy, and in certain neurodegenerative diseases, increased concentrations of extracellular glutamate (by vesicular release, cell lysis and/or decreased glutamate transporter uptake/feversal) stimulate the overactivation of local ionotropic glutamate receptors that trigger neuronal cell death (excitotoxicity). Other natural agonists, such as domoic acid, alcohol and auto-antibodies, have also been reported to induce excitotoxicity.</p>

AB - <p>Glutamate is the major excitatory neurotransmitter in the mammalian central nervous system playing critical roles in basal synaptic transmission and mechanisms of learning and memory. Under normal conditions, glutamate is sequestered within synaptic vesicles (similar to 100 mm) with extracellular glutamate concentrations being limited (&lt;1 mu M), via retrieval by plasma-membrane transporters on neuronal and glial cells. in the case of central nervous system trauma, stroke, epilepsy, and in certain neurodegenerative diseases, increased concentrations of extracellular glutamate (by vesicular release, cell lysis and/or decreased glutamate transporter uptake/feversal) stimulate the overactivation of local ionotropic glutamate receptors that trigger neuronal cell death (excitotoxicity). Other natural agonists, such as domoic acid, alcohol and auto-antibodies, have also been reported to induce excitotoxicity.</p>

KW - dendrite

KW - dendritic bead

KW - excitotoxicity

KW - glutamate

KW - mitochondrion

KW - spine

KW - GLUTAMATE-RECEPTOR ACTIVATION

KW - ACUTE HIPPOCAMPAL SLICES

KW - MITOCHONDRIAL TRANSPORT

KW - NEURITIC DEGENERATION

KW - MORPHOLOGICAL-CHANGES

KW - EXCITOTOXIC INJURY

KW - FOREBRAIN NEURONS

KW - CULTURED NEURONS

KW - TRANSGENIC MICE

KW - KAINIC ACID

U2 - 10.1042/BST0371389

DO - 10.1042/BST0371389

M1 - Article

JO - Biochemical Society Transactions

JF - Biochemical Society Transactions

SN - 0300-5127

VL - 37

SP - 1389

EP - 1393

ER -