Serotonin methysergide

However, the specific serotonin uptake inhibitor fluoxetine failed to produce an MBDB-like cue and failed to block the stimulus effects of MBDB when it was given prior to a training dose of MBDB. Table 3 summarizes results of fluoxetine testing in MBDB-trained rats. In other exploratory studies, pretreatment of MDMA-trained rats with either methysergide or ketanserin failed to block completely the MDMA-discriminative stimulus. 

Methysergide is an ergotamine derivative that impacts central serotonin balance.51 It is reserved for use in migraineurs refractory to other agents, due to its significant adverse-effect profile. As an ergot compound, it is a vasoconstrictor that may worsen vascular dilatory reserves and precipitate cardiovascular events or ischemic stroke in those with... 

Figure 3 Putative model for the mechanism by which biogenic amines stimulate CE secretion across the rabbit corneal epithelium. Epn = epinephrine Nep = norepinephrine Tim = Timolol Ser = serotonin Msg = methysergide Dop = dopamine Hal = haloperi-dol (E = (E-adrenoceptor AC = adenylate cyclase. The scheme is consistent with the observation that epithelial responsiveness to serotonin and dopamine can be blocked by their receptor antagonists haloperidol and methysergide, respectively, and by both timolol treatment and sympathectomy. The probable source of serotonin or dopamine is the sympathetic fibers that innervate the cornea. (From Ref. 284.)...

Methysergide (Sansert ) is believed to alter the ability of serotonin to cause inflammation, platelet aggregation (blood clotting), and dilation of blood vessels. However, methysergide has some undesirable side effects, such as motor incoordination and dizziness and can cause heart problems. Usually, the drug is intentionally discontinued for 4-6 weeks twice a year because of these problems. Thus, methysergide is used only in special cases. 

In 1962, Sai-Halasz, who worked with Sz ra, reported that DMT was potentiated by pretreatment with serotonin antagonists like methysergide in 1963, he announced that such potentiation could be diminished by pretreatment with monoamine oxidase inhibitors. 

Serotonin (5-hydroxytryptamine, 5-HT) is synthesised in enterochromaffin cells, largely in the gut, and also extensively taken up into blood platelets from which it is released to have vascular effects. It has complex effects on the cardiovascular system, varying with the vascular bed and its physiological state it generally constricts arterioles and veins and induces blood platelet aggregation it stimulates intestinal and bronchial smooth muscle. Carcinoid tumours secrete serotonin and symptoms may be benefited by serotonin antagonists, e.g. cyproheptadine, methysergide and sometimes by octreotide (see Index). It is a neurotransmitter in the brain. 

The exact mechanism of mescaline has not been clearly defined. The central nervous system effects of mescaline appear to involve stimulation of both serotonin and dopamine receptors. In experimental studies, these effects can be blocked by either serotonin antagonists such as methysergide or dopamine antagonists such as haloperidol. Mescaline is structurally related to the amphetamines and cathine (khat). Sympathomimetic effects can occur and are thought to be centrally mediated. Mescaline does not appear to inhibit monoamine oxidase. 

Dopamine agonists (e.g., bromocriptine) GABA agonists (e.g., muscimol) Serotonin antagonists (e.g.. methysergide)... 

Serotonin agonists appear to be more potent presynaptically rather than postsynaptically. These analogs include lysergic acid diethylamide and di-methyltryptamine. Serotonin antagonists such as methysergide and cyproheptadine have little effect on central inhibitory receptors, but are quite effective on the few excitatory receptors that have been identified. No clear explanation for this apparent dichotomy has been put forth. 

---