question about parkinson's desease

Shamim Khaliq shamimkhaliq at hotmail.com
Mon Jan 15 08:48:38 EST 2001


my lecturer replied to me on this one with:
"The main point is GABA = inhibitory and glutamate excitatory.
Upset the balance in PD and reduce the thalamocortico activation."

Shamim Khaliq <shamimkhaliq at hotmail.com> wrote in message
news:3a619036$1_4 at news.intensive.net...
> The way I understand it, the substantia nigra pars compacta has a lot of
> dopaminergic neurons that go to the striatum (caudate and putamen) that
have
> a lot of GABAergic neurons that go to the globus pallidus interna that has
a
> load of GABAergic neuron that go to the thalamus which goes to the motor
> cortex, so exiting the substantia nigra pars compacta has an inhibitory
> effect on the cerebral motor cortex. So, if the substantia nigra pars
> compacta degenerates, as in Parkinson's, the striatum is less excited and
> sends less inhibition to the motor cortex.
>
> NOT TRUE! Parkinson's is too much inhibition of the cortex, rigidity and
> slowness of movement, not too much movement (as is caused by giving them
> levodopa). So somehow, killing the dopaminergic projections from the
> substantia nigra pars compacta to the striatum must INCREASE striatal
> inhibition of the motor cortex. Where is my logic failing me?
>
>
>







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