User:Miniroovigilante/NMDA-Glutamatergic-Antagonists

anything capable of reducing Such activity

metapramine, PCP,

partial agonists/antagonists, M1+NMDA,

http://www.ncbi.nlm.nih.gov/pubmed/9580111 Melatonin interaction with magnesium and zinc in the response of the striatum to sensorimotor cortical stimulation in the rat.

http://www.ncbi.nlm.nih.gov/pubmed/16286679 http://www.ncbi.nlm.nih.gov/pubmed/16632895 http://www.ncbi.nlm.nih.gov/pubmed/15998291 http://www.ncbi.nlm.nih.gov/pubmed/16371010 Bromocriptine glutamate inhibition
 * 888888

-Memantine = alpha-7 nAChR, NMDA and 5-HT3 antagonist,  D2 agonist -Amantadine = -Ketamine= -Dextromethorphan (DXM) = -Dextrorphan= (DXM's active metabolite) -PCP

[B]Endegenous/Mineral/Vitamins [/B]

-Magnesium -Zinc -Kynurenic acid *** -Agmatine L-Arginine + NOS-inhibitor = Agmatine

[B] shady/unverified ones[/B]

-Acamprosate = -Tramadol     = Norepinephrine reuptake inhibitor, Serotonin releaser, alpha-7(5) Nicotinic antagonist,  Muscarinic M1/M3/M5 antagonist, 5-HT2C antagonist, mu- Opioid agonist -( through active metabolite, O-desmethyltramadol ) -Methadone -Huperzine A  = Acetylcholinesterase inhibititor, NMDA Antagonist -Carvedilol     = alpha/beta-blocker,  [URL="http://www.ncbi.nlm.nih.gov/pubmed/7916141"]http://www.ncbi.nlm.nih.gov/pubmed/7916141[/URL] -Procyclidine = -Orphenadrine = -Indantadol --- in clinical trials, ~ -Hodgkinsine - -Psychotridine -Rhynchophylline - [ Uncaria tomentosa also has compounds that are 5-HT2A antagonists ]

[B]Glutamate release inhibitors : =[/B]

- ( Various Sodium [Na+] and Calcium [Ca2+] channel blockers) - Riluzole - Lamotrigine - Carbamazapine, .....ect, ..... [ __________ ] - [B]Bromocriptine[/B]

[B]Glutamate reuptake enhancers : = [/B]

- Ceftriaxone [URL="http://www.jbc.org/content/283/19/13116.short"]http://www.jbc.org/content/283/19/13116.short[/URL]

---*** Kynurenic acid Miniroovigilante (talk) i just noted this cuz i think its really important, and deserves alot of research  [URL="http://www.nature.com/npp/journal/v30/n4/full/1300583a.html"]http://www.nature.com/npp/journal/v30/n4/full/1300583a.html[/URL]

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 * 1) NMDA, nicotinic a-7, ect. antags
 * memantine
 * ketamine
 * PCP ( phenylcyclidine)
 * DXM, dextorphan,
 * methadone
 * amantadine
 * tramadol
 * kyrenuric acid
 * 1) glutamate release inhibitors (calcium and sodium channel blockers)
 * Riluzole
 * Lamotrigine?
 * magnesium (bioavaliable)
 * Carvedilol
 * zinc
 * agmatine
 * 1) vesicular glutamate uptake inhibitors & synaptic glutamate reuptake enhancers
 * Bromocriptine
 * Ceftriaxone


 * 1) glutamate synthesis inhibitors


 * 1) Muscarinic ( M1, M2, M3 ? ) antagonists / (possible) NMDA/glutamate/AMPA/Kainate/other Antagonists?
 * Trihexyphenidyl
 * Orphenadrine
 * Scopolamine
 * Atropine
 * Bulleted list item
 * 1) glycine antagonists
 * kyrenuric acid
 * 1) Unspecified
 * Simvastatin
 * acamprosate


 * 1) presynaptic D2 antagonists?
 * 2) acetylcholine release inhibitors?
 * 3) histamine H1 antagonists ***
 * 4) estrogen antagonists?
 * 5) GABA-A/B agonists
 * 6) Metabotropic (subtype-specific) modulators?

Lithium increases Acetylcholine-excess-induced Toxicity GABA-activation oppossess Acetylcholinesterase-induced toxicity/symptoms

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Excitatory amino acid(s) comprise a vast majority of the excitatory neurotransmitter network.......... Aspartate, Aspartic acid, glutamic acid, glutamate, Serine, glycine, Ca2+............... [ and others, ....******* ] function to  sustains the form of awareness known as conciousness. Too much Excitatory acitivyy results in the formation and progression of Parkinsons disease, possibly alzheimers disease, and depression, fibromyalia, chronic fatigue, ADD/ADHD [in some cases], tolerance and addiction to reinforcing substances.

Glutamate transporter, vesicular glutamate transporter, GABA-glutamate, Calcium-channels,

http://www.nature.com/npp/journal/v29/n5/full/1300381a.html

In our ADE model, subchronic MPEP treatment also significantly reduced relapse-like drinking behavior in a dose-dependent manner without any observable side effects on body weight or total fluid intake. Although the ADE model has good predictive validity—pharmacological agents that have been shown to attenuate relapse rates in humans (acamprosate, naltrexone, and 5-HT3-antagonists) also attenuate the ADE (Spanagel and Hölter, 2000; Rodd-Henricks et al, 2000)—this model has certain limitations to mimic the human situation. Thus the drinking profile of an ADE does not closely reflect the profile of relapse drinking in alcoholics (Spanagel, 2000) and furthermore little is known about the neuronal circuits involved in the ADE. However, it has been repeatedly shown that noncompetitive NMDA receptor antagonists abolish the ADE (Hölter et al, 1996, 2000; Bienkowski et al, 2001), suggesting a crucial role of NMDA receptors in mediating the ADE. The fact that synaptic transmission at NMDA receptors is modulated by simultaneous activation of mGluR5 (Sorensen and Conn, 2003) could at least provide a clue for the effects of MPEP on the ADE. This functional coupling could result from the postsynaptic association of NMDA receptors with a complex of proteins, which includes different scaffolding proteins (eg PSD-95, Homer, Shank), but other receptors including mGluR5 are also linked to this complex (Kotecha et al, 2003), and activation of mGluR5 can lead to an enhancement of NMDA receptor function through phosphorylation by protein kinase C (Hermans and Challiss, 2001; Schoepp and Conn, 1993). The high affinity of MPEP for mGluR5 receptors, which is more than 1000-fold higher compared to NMDARs, makes it very unlikely that under the used conditions MPEP affects NMDARs directly (Oleary et al, 2000; Gubellini et al, 2001; Spooren et al, 2001; Kozela et al, 2003). In summary, the functional coupling of mGluR5 and NMDA receptor suggests that the blockade of mGluR5 by MPEP reduces glutamatergic signaling through NMDA receptors and thereby interacts with ethanol-seeking and relapse behavior.

'''Having the limitations of the animal models used in the present study in mind, it is proposed that pharmacological targeting of mGluR5 might be a promising therapeutic line to pursue in alcoholic patients. This assumption is supported by three other recent findings: (i) In a preliminary report it has been shown that MPEP decreases operant ethanol self-administration during periods of peak consumption in mice (Sharko et al, 2002). (ii) The finding that MPEP evokes anxiolytic- and antidepressant-like effects in rats (Tatarczynska et al, 2001; Pilc et al, 2002) also has implications for the treatment of alcoholism due to the high comorbidity with these psychiatric disorders. (iii) Furthermore, Harris et al (2002) showed that acamprosate exhibits binding and functional characteristics that are consistent with an mGluR5 antagonist. These authors further speculate that acamprosate's ability to reduce relapse rates in alcoholic patients may result from its alterations in glutamatergic neurotransmission through mGluR5s. '''

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http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T1J-401HHD6-4&_user=10&_origUdi=B6SYR-4835YY2-1RR&_fmt=high&_coverDate=04%2F14%2F2000&_rdoc=1&_orig=article&_origin=article&_zone=related_art&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=102d977217974cee5323c3031a977a49