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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 6 of 6. This is the beginning of the thread.
Posted by JohnX2 on March 25, 2002, at 3:54:36
I wonder this explains my 1 hour Provigil (alpha-1) poop out?Bear with me as I learn about these dopamine sensitization pathways. Trying to come up with some explination on my super-duper quick poop out syndromes. May help others with the same problems.
Need to dig up more articles on this one.
Also I don't get Serzone poop-out (only AD to sustain). Serzone is a partial alpha-1 antagonist, so maybe it sorta acts as a mitigator of d1 receptor sensitization?
any thoughts are entertained..
John
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7931580&dopt=Abstract
: J Neurosci 1994 Oct;14(10):6280-8 Related Articles, Books, LinkOut
Accelerated resensitization of the D1 dopamine receptor-mediated response in cultured cortical and striatal neurons from the rat: respective role of alpha 1-adrenergic and N-methyl-D-aspartate receptors.Trovero F, Marin P, Tassin JP, Premont J, Glowinski J.
INSERM U 114, Chaire de Neuropharmacologie, College de France, Paris.
As previously shown in vivo, noradrenergic and glutamatergic neurons can regulate the denervation supersensitivity of D1 dopaminergic (DA) receptors in the rat prefrontal cortex and striatum respectively. Therefore, the effects of methoxamine (an alpha 1-adrenergic agonist) and glutamate on the resensitization of D1 DA receptors were investigated in cultured cortical and striatal neurons from the embryonic rat. In the presence of sulpiride and propranolol, DA stimulated the D1 DA receptor-mediated conversion of 3H-adenine into 3H-cAMP in both intact cortical and striatal cells and these responses were markedly desensitized in cells preexposed for 15 min to DA (50 microM). The complete recovery of the D1 DA response was more rapid in striatal (15 min) than in cortical (80 min) neurons. Methoxamine accelerated the resensitization of the D1 response in cortical but not in striatal neurons. The effect of the alpha 1-adrenergic agonist in cortical neurons was blocked by prazosin and chlorethylclonidine. In contrast, glutamate accelerated the resensitization of the D1 response in striatal but not in cortical neurons and the effect observed in striatal neurons was totally blocked by 2-amino-5-phosphonovaleric acid, an NMDA receptor antagonist. Protein kinase C was shown to be involved in the alpha 1-adrenergic-induced resensitization of the cortical D1 response but not in the glutamate-evoked resensitization of the striatal D1 response. Finally, for comparison, similar experiments were performed on beta-adrenergic receptors using isoproterenol (1 microM) as an agonist. Methoxamine did not modify the resensitization of the beta-adrenergic response in cortical neurons, but glutamate accelerated the resensitization of this response in striatal neurons.
PMID: 7931580 [PubMed - indexed for MEDLINE]
Posted by JohnX2 on March 25, 2002, at 5:54:31
In reply to resens d1 receptors by a1 agonists? (SLS,et,al), posted by JohnX2 on March 25, 2002, at 3:54:36
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9826228&dopt=Abstract: Synapse 1998 Dec;30(4):362-70 Related Articles, Books, LinkOut
Alpha1-adrenergic, D1, and D2 receptors interactions in the prefrontal cortex: implications for the modality of action of different types of neuroleptics.
Gioanni Y, Thierry AM, Glowinski J, Tassin JP.
INSERM U 114, Chaire de Neuropharmacologie, College de France, Paris.
The activation of rat mesocortical dopaminergic (DA) neurons evoked by the electrical stimulation of the ventral tegmental area (VTA) induces a marked inhibition of the spontaneous activity of prefrontocortical cells. In the present study, it was first shown that systemic administration of either clozapine (a mixed antagonist of D1, D2, and alpha1-adrenergic receptors) (3-5 mg/kg, i.v.), prazosin (an alpha1-adrenergic antagonist) (0.2 mg/kg, i.v.), or sulpiride (a D2 antagonist) (30 mg/kg, i.v.), but not SCH 23390 (a D1 antagonist) (0.2 mg/kg, i.v.), reversed this cortical inhibition. Second, it was found that following the systemic administration of prazosin, the VTA-induced cortical inhibition reappeared when either SCH 23390 or sulpiride was applied by iontophoresis into the prefrontal cortex. Third, it was seen that, whereas haloperidol (0.2 mg/kg, i.v.), a D2 antagonist which also blocks alpha1-adrenergic receptors, failed to reverse the VTA-induced inhibition, the systemic administration of haloperidol plus SCH 23390 (0.2 mg/kg, i.v.) blocked this inhibition. Finally, it was verified that the cortical inhibitions obtained following treatments with either "prazosin plus sulpiride" or "prazosin plus SCH 23390" were blocked by a superimposed administration of either SCH 23390 or sulpiride, respectively. These data indicate that complex interactions between cortical D2, D1, and alpha1-adrenergic receptors are involved in the regulation of the activity of prefrontocortical cells innervated by the VTA neurons. They confirm that the physiological stimulation of cortical alpha1-adrenergic receptors hampers the functional activity of cortical D1 receptors and suggest that the stimulations of cortical D1 and D2 receptors exert mutual inhibition on each other's transmission.
PMID: 9826228 [PubMed - indexed for MEDLINE]
Posted by JohnX2 on March 25, 2002, at 7:01:30
In reply to resens d1 receptors by a1 agonists? (SLS,et,al), posted by JohnX2 on March 25, 2002, at 3:54:36
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8097162&dopt=AbstractEur J Pharmacol 1993 Mar 16;233(1):79-84 Related Articles, Books, LinkOut
Prazosin modulates the firing pattern of dopamine neurons in rat ventral tegmental area.Grenhoff J, Svensson TH.
Department of Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Previous studies have indicated a noradrenergic modulation of midbrain dopamine cell activity. The effects of systemic administration of the alpha 1-adrenoceptor antagonist prazosin and the alpha 2-antagonist idazoxan on midbrain dopamine cell firing were now studied with extracellular recording from single dopamine neurons in the ventral tegmental area of chloral hydrate-anaesthetized male rats. Prazosin (0.15-0.6 mg/kg i.v.) dose dependently decreased burst firing and regularized the firing pattern of dopamine neurons, while the firing rate was unaffected. The prazosin-induced effects were abolished by pretreatment with reserpine. Idazoxan (0.5-2.0 mg/kg i.v.) increased firing rate and burst firing and made the firing pattern less regular, probably by increasing adrenergic transmission via blockade of presynaptic alpha 2-adrenoceptors. The effects of idazoxan were blocked by prazosin. The present results indicate that noradrenergic neurons modulate the dopamine cell firing pattern via excitatory postsynaptic alpha 1-adrenoceptors. This mechanism might be involved in the pathogenesis and pharmacological treatment of schizophrenia.
PMID: 8097162 [PubMed - indexed for MEDLINE]
Posted by Zo on March 26, 2002, at 3:17:29
In reply to Re: figure this one out??, posted by JohnX2 on March 25, 2002, at 5:54:31
Posted by JohnX2 on March 26, 2002, at 5:28:31
In reply to Re: are you trying to give me a headache? (nm) » JohnX2, posted by Zo on March 26, 2002, at 3:17:29
Posted by Zo on March 27, 2002, at 4:17:34
In reply to Re: are you trying to give me a headache? HERE » Zo, posted by JohnX2 on March 26, 2002, at 5:28:31
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