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question about parkinson's desease

et_al at my-deja.com et_al at my-deja.com
Tue Jan 16 02:35:06 EST 2001

On Mon, 15 Jan 2001 13:48:38 -0000, "Shamim Khaliq"
<shamimkhaliq at hotmail.com> wrote:

>my lecturer replied to me on this one with:
>"The main point is GABA = inhibitory and glutamate excitatory.

Your lecturer is only partly right. GABA is mostly inhibitory, and
glutamate is mostly excitatory. But in some circumstances they can
be the reverse.


>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
>> a lot of GABAergic neurons that go to the globus pallidus interna that has
>> 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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