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torsdag 5 maj 2011

Glysinerginen neuronaali signaalivälitys on sinkkiherkkää


November 24th, 2006, 15:12 GMT| By Stefan Anitei

German scientists have recently proved that zinc
plays an important role in the neuronal signaling.

Neurobiologists have been puzzled by the considerable
evels of free zinc ions among certain types of
neurons. For 50 years, studies were made in the
neurobiology field to understand the neuronal
role of the zinc. Many studies showed that zinc
can be toxic on transmission of neural impulses,
but none could conclusively display the metal's
function in normal neuronal transmission.

By eliminating a gene encoding a proteic
zinc sensitive receptor, called glycine receptor,
the researchers achieved mice with symptoms
similar to human hyperekplexia (or " startle
disease"), when children have an exaggerated
paralysis as a response to fright. In fact, the
same receptor is mutated in humans with
hyperekplexia. The receptor is a modulator of
neuron transmission in both motor and sensory
signaling pathways in the brain and spinal cord.

This approach was more specific; previous
ones just decreased overall neuronal zinc
amounts using chemicals called chelators
that absorb zinc ions. The mutant mice
presented tremors, delayed ability to
right themselves when turned over, odd
gait, altered transmission of visual signals,
and the specific enhanced startle response
to sudden noise.

Electrophysiological studies of the mutants'
neurons revealed significant zinc-related
abnormalities in signaling at the neuronal
synapses level. "The data presented disclose
a pivotal role of ambient synaptic [zinc ion]
for glycinergic neurotransmission
n the context of normal animal behavior."

Manipulating synaptic zinc levels could
shift the neuronal action of zinc, but
such manipulation "highlights the complexity
of potential therapeutic interventions,"
which could cause an imbalance between
the excitatory and inhibitory circuitry
in the central nervous system.

Alan R. Kay, Jacques Neyton, and Pierre
Paoletti wrote " This work provides a clear
demonstration that interfering with zinc
modulation of a synaptic pathway leads to
a significant alteration in the phenotype
of the animal."

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