0will be to favor the release of glutamate from the nervous system. Astrocytes are glial
cells which make up 80% of the mass of the brain and communicate with neurons
via changes in Ca2+. Intracellular Ca2+ mediates changes in membrane proteins
to initiate transmitter release and ion channel opening; it also activates enzymes
to allow neurons to cover or uncover receptor sites that alter neuronal sensitivity.
Several studies indicate that following the rise of calcium, astrocytes release the
amino acid glutamate, which helps them talk to the neurons. The communication
flows both ways, with neurons also being able to talk to the astrocytes through
their own glutamate release. Signaling molecules, such as ATP, prostaglandins and
eicosanoids also appear to promote the cell-to-cell communication.
Communication between astrocytes and neurons may aid memory. Adding
glutamate to cell samples of astrocytes prompts them to produce special molecules
that nourish neurons, known as neurotrophins, that are key to memory function.
In one recent study, injections of trophic factors into the brains of rats boosted
the biological mechanisms known to relate to memory and improved the rats’
performance in a memory task. This all may mean that glutamate release from
neurons triggers astrocytes to produce neurotrophic factors, which then help
neurons process information for memory.
High blood sugar (hyperglycemia) is implicated in increasing the likelihood of
seizure. Ordinarily, insulin prods the liver to decrease its production of glucose. It
also helps the body’s fat and muscle tissues use glucose in the blood for energy. Insulin
has many roles including stimulating and balancing immune function, stimulating
revascularization, stimulating neuron and oligodendrocyte growth, reducing
cell death, stimulating myelination and re-myelination of neurons, stimulating
differentiation and proliferation of neural stem cells, increasing permeability and
transport of nutrients and wastes across cell membranes and the blood-brain barrie
r. (Oligodendrocyctes are the structures responsible for myelination. The presence
of NMDA receptors in oligodendrocyte processes presents a mechanism by which
demyelination might occur under excessive glutamate/Ca2+ conditions.)
lacK oF GlUtamate clearinG
Patients suffering from temporal lobe epilepsy (TLE), experienced increased
extracellular glutamate levels in the hippocampus both during and after clinical
seizures. These increased glutamate levels could be the result of malfunctioning
and/or downregulation of glutamate transporters, indicating impaired clearance
of glutamate released by neurons. Glutamate is predominantly cleared by glial
cells through the excitatory amino acid transporter 2 (EAAT2) and its subsequent
conversion to glutamine by the glial enzyme glutamine synthetase.
Cerebrospinal Fluid, limbic, temporal and striatum glutamine concentrations
are implicated in schizophrenia, bipolar disorder and major depression. The
answer, it appears, is by cleaning up their synapses. For ltP to occur, a presynaptic
neuron must release the glutamate in a continuous manner. Normally, glutamate
is removed from the synaptic cleft by housekeeping proteins, known as glutamate
transporters, in the postsynaptic neuron. Suspecting that this glutamate-removal
system might play a role in maintaining input specificity,