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Target Concepts:
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Query: UMLS:C0026838 (
spasticity
)
6,471
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The GABA-B receptor is densely expressed throughout the brain and has been implicated in many CNS functions and disorders, including addiction, epilepsy,
spasticity
, schizophrenia, anxiety, cognitive deficits, and depression, as well as various aspects of nervous system development. How one GABA-B receptor is involved in so many aspects of CNS function remains unanswered. Activation of GABA-B receptors is normally thought to produce inhibitory responses in the nervous system, but puzzling contradictory responses exist. Here we report that in rat mitral cells of the olfactory bulb, GABA-B receptor activation inhibits both the persistent sodium current (
INa
P
) and the sodium-activated potassium current (IK
Na
), which is coupled to it. We find that the primary effect of GABA-B activation is to inhibit
INa
P
, which has the secondary effect of inhibiting IK
Na
because of its dependence on persistent sodium entry for activation. This can have either a net excitatory or inhibitory effect depending on the balance of
INa
P
/IK
Na
currents in neurons. In the olfactory bulb, the cell bodies of mitral cells are densely packed with sodium-activated potassium channels. These channels produce a large IK
Na
which, if constitutively active, would shunt any synaptic potentials traversing the soma before reaching the spike initiation zone. However, GABA-B receptor activation might have the net effect of reducing the IK
Na
blocking effect, thus enhancing the effectiveness of synaptic potentials.
...
PMID:GABA-B Controls Persistent Na
+
Current and Coupled Na
+
-Activated K
+
Current. 2866 Feb 46
