Posted by AndrewB on September 9, 2000, at 15:17:47
In reply to Re: Bromocriptine?, posted by Seamus2 on September 9, 2000, at 11:32:36
Just to correct some misinformation in an above post, bromocriptine is neuroprotective rather than neurotoxic. See the medical abstracts below for more information.
Bromo. can cause nausea, headaches, etc. in some individiuals. These side effects usually go away quickly. They can be minimized by taking bromo. with food and starting at a low dosage and moving up slowly.
Other rare but serious side effects can occur with bromo. that I don't know the specifics on.
Bromo. is effective in lowering prolactin. Raised prolactin can cause sexual dysfunction in men and swollen breasts, weight gain, and missed menses in women. If you experience these effects when taking amisulpride, it is safe to assume they are due to raised prolactin levels.
I am taking bromo now., 2.5mgs at twice a day, and will get a prolactin level test in 2 weeks to see if it is effective in lowering raised prolactin levels due to amisulpride. I do not know if I will continue taking bromo. though because I don't seem to be experiencing any effects due to my raised prolactin levels.
Perhaps the endocronologist I will see can tell me whether there is anything I should be concerned about.
AndrewB
---------------------------------------------------------------------------Title: Neuroprotection by bromocriptine against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicity in mice.
Source: FASEB J 1998 Jul;12(10):905-12
Authors: Muralikrishnan D; Mohanakumar KP
Address: Laboratory of Neurochemistry, Division of Pharmacology and Experimental Therapeutics, Indian Institute of Chemical Biology, Calcutta.Mice were treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP; 30 mg/kg i.p. twice, 16 h apart). This resulted in changes in motor performance and toxic insult of nigral neurons as evidenced by dopamine depletion in nucleus caudatus putamen. In vitro and in vivo treatment of MPTP caused the generation of hydroxyl radicals (.OH) as measured by a sensitive salicylate hydroxylation procedure. A dopamine agonist, bromocriptine (10 microM and 10 mg/kg i.p.), blocked .OH formation caused by MPTP in vitro (20 microM) and in vivo (30 mg/kg i.p.). An MPTP-induced increase in the activity of catalase and superoxide dismutase in substantia nigra on the seventh day was reduced by bromocriptine pretreatment. Bromocriptine blocked MPTP-induced behavioral dysfunction as well as glutathione and dopamine depletion, indicating its potent neuroprotective action. This study suggests that bromocriptine stimulates antioxidant mechanisms in the brain and acts as a free radical scavenger in addition to its action at dopamine receptors, thus indicating its strength as a valuable neuroprotectant.
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Title: Bromocriptine protects dopaminergic neurons from levodopa-induced toxicity by stimulating D(2)receptors.Source: Exp Neurol 1999 Sep;159(1):98-104
Authores: Takashima H; Tsujihata M; Kishikawa M; Freed WJ
Address: Section of Neurology, Nagasaki Kita Hospital, Nagasaki, 852-8061, Japan.Neuroprotective properties of bromocriptine, a D(2) receptor agonist, were investigated using the in vitro neurotoxicity of levodopa for dopaminergic neurons from rat embryonic ventral mesencephalon. Levodopa, when added to the culture medium, showed toxicity which was specific for dopaminergic neurons. Bromocriptine was found to protect dopaminergic neurons from levodopa toxicity. Another D(2) agonist, 2-(N-phenethyl-N-propyl-amino-5-hydroxytetralin, showed similar protective effects. The neuroprotective effect of bromocriptine was inhibited by supplementation of the culture medium with sulpiride, a D(2) antagonist, or by D(2) receptor knockdown with an antisense oligonucleotide. Dopaminergic neurons treated with levodopa showed an increase in free radicals. These data suggest that neuroprotective properties of bromocriptine seen in this cellular model of neurotoxicity are dependent on dopamine D(2) autoreceptor binding and that levodopa toxicity may be related to increased free radical generation in dopaminergic neurons.
poster:AndrewB
thread:44425
URL: http://www.dr-bob.org/babble/20000905/msgs/44523.html