This cross section of the brain shows the Limbic
System and focuses in on the amydgdala the area most
responsible for feelings of fear and anxiety.
If enough excitatory action potentials arrive at the axon
terminal simultaneously, the membrane potential will rise
above threshold, and a the nerve will fire. The presence of
inhibitory signals (from a nerve releasing GABA
for example) will lower the membrane potential. If enough
inhibitory nerves have fired, they will stop the neuron from
firing. In this video the neuron in the middle is an
inhibitory neuron, stopping the firing in the output neuron
generated by the other two excitatory neurons.
The action potential in the inhibitory interneuron travels
to the end of the axon, Here we find vesicles containing the
neurotransmitter GABA, waiting to be released. The vesicles
fuse with the presynaptic membrane, and release
the GABA molecules into the synaptic cleft, where they
can diffuse to the GABA receptors on the postsynaptic side.
When two molecules of GABA bind to the receptor, the channel
in the middle opens up, and chloride
ions rush into the receiving neuron. The chloride has an
inhibiting effect on the firing of the nerve.
The GABAa receptor has a second recognition site at which
can Benzodiazepines can bind. These drugs such as Librium
Valium and Xanax, are tranquilizers
which work to reduce fear and anxiety.
The Benzodiazepines do not bind directly to the GABA
recognition site, instead they alter the GABAreceptor in
such a way as to allow GABA to bind more easily to its own
binding site increasing its effectiveness.
effector that binds the diazepam site has the opposite
effect of the drugs it decreases the effectiveness of GABA,
and acts as an anxiogenic
receptor works in a very different way. When dopamine
binds to the receptor changes in the receptpr initiate a
series of reactions leading to cAMP formation (similar to
what happens with adrenaline). cAMP triggers
phosphorylations that among other things changes the
sensitivity of the neuron to stimuli.