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Old 12-18-2007, 09:47 PM
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reverett123 reverett123 is offline
In Remembrance
 
Join Date: Aug 2006
Posts: 3,772
15 yr Member
reverett123 reverett123 is offline
In Remembrance
reverett123's Avatar
 
Join Date: Aug 2006
Posts: 3,772
15 yr Member
Default A pretty good explanation about what may be going on

at least with the dextromethorphan. What about naloxene (sp?) Is it an NMDA blocker too, or is there two different things going on?

And has anyone besides myself had major motor problems from MSG ingestion? Such an encounter should set the NMDA receptors firing like the Fourth of July and it sure does ruin a good half a day when it happens.


1: Pharmacol Ther. 2004 May;102(2):155-74.

Rationale for and use of NMDA receptor antagonists in Parkinson's disease.

Hallett PJ, Standaert DG.

MassGeneral Institute for Neurodegenerative Disease, Massachusetts General
Hospital, Harvard Medical School, 114 16th Street, Charlestown, MA 02129, USA.

N-Methyl-d-aspartate (NMDA) glutamate receptors are a class of excitatory amino
acid receptors, which have several important functions in the motor circuits of
the basal ganglia, and are viewed as important targets for the development of new
drugs to prevent or treat Parkinson's disease (PD). NMDA receptors are
ligand-gated ion channels composed of multiple subunits, each of which has
distinct cellular and regional patterns of expression. They have complex
regulatory properties, with both agonist and co-agonist binding sites and
regulation by phosphorylation and protein-protein interactions. They are found in
all of the structures of the basal ganglia, although the subunit composition in
the various structures is different. NMDA receptors present in the striatum are
crucial for dopamine-glutamate interactions. The abundance, structure, and
function of striatal receptors are altered by the dopamine depletion and further
modified by the pharmacological treatments used in PD. In animal models, NMDA
receptor antagonists are effective antiparkinsonian agents and can reduce the
complications of chronic dopaminergic therapy (wearing off and dyskinesias). Use
of these agents in humans has been limited because of the adverse effects
associated with nonselective blockade of NMDA receptor function, but the
development of more potent and selective pharmaceuticals holds the promise of an
important new therapeutic approach for PD.

PMID: 15163596 [PubMed - indexed for MEDLINE]
__________________
Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000.
Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well.
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