A pharmacologic congener of serotonin that contracts smooth muscle and has actions similar to those of tricyclic antidepressants. It has been proposed as an oxytocic.
A psychedelic phenyl isopropylamine derivative, commonly called DOM, whose mood-altering effects and mechanism of action may be similar to those of LSD.
Endogenous compounds and drugs that bind to and activate SEROTONIN RECEPTORS. Many serotonin receptor agonists are used as ANTIDEPRESSANTS; ANXIOLYTICS; and in the treatment of MIGRAINE DISORDERS.
Cell-surface proteins that bind SEROTONIN and trigger intracellular changes which influence the behavior of cells. Several types of serotonin receptors have been recognized which differ in their pharmacology, molecular biology, and mode of action.
A selective and potent serotonin-2 antagonist that is effective in the treatment of a variety of syndromes related to anxiety and depression. The drug also improves the subjective quality of sleep and decreases portal pressure.
Drugs that bind to but do not activate serotonin receptors, thereby blocking the actions of serotonin or SEROTONIN RECEPTOR AGONISTS.
Benign and malignant neoplastic processes arising from or involving components of the central, peripheral, and autonomic nervous systems, cranial nerves, and meninges. Included in this category are primary and metastatic nervous system neoplasms.
Space between the dura mater and the walls of the vertebral canal.
Drugs used for their effects on serotonergic systems. Among these are drugs that affect serotonin receptors, the life cycle of serotonin, and the survival of serotonergic neurons.
An ergot derivative that is a congener of LYSERGIC ACID DIETHYLAMIDE. It antagonizes the effects of serotonin in blood vessels and gastrointestinal smooth muscle, but has few of the properties of other ergot alkaloids. Methysergide is used prophylactically in migraine and other vascular headaches and to antagonize serotonin in the carcinoid syndrome.

Recovery of locomotion after ventral and ventrolateral spinal lesions in the cat. II. Effects of noradrenergic and serotoninergic drugs. (1/54)

The effects of serotoninergic and noradrenergic drugs (applied intrathecally) on treadmill locomotion were evaluated in two adult cats subjected to a ventral and ventrolateral spinal lesion (T13). Despite the extensive spinal lesion, severely damaging important descending pathways such as the reticulo- and vestibulospinal tracts, both cats recovered quadrupedal voluntary locomotion. As detailed in a previous paper, the locomotor recovery occurred in three stages defined as early period, when the animal could not walk with its hindlimbs, recovery period, when progressive improvement occurred, and plateau period, when a more stable locomotor performance was observed. At this latter stage, the cats suffered from postural and locomotor deficits, such as poor lateral stability, irregular stepping of the hindlimbs, and inconsistent homolateral fore- and hindlimb coupling. The present study aimed at evaluating the potential of serotoninergic and/or noradrenergic drugs to improve the locomotor abilities in the early and late stages. Both cats were implanted chronically with an intrathecal cannula and electromyographic (EMG) electrodes, which allowed determination, under similar recording conditions, of the locomotor performance pre- and postlesion and comparisons of the effects of different drugs. EMG and kinematic analyses showed that norepinephrine (NE) injected in early and plateau periods improved the regularity of the hindlimb stepping and stabilized the interlimb coupling, permitting to maintain constant locomotion for longer periods of time. Methoxamine, the alpha1-agonist (tested only at the plateau period), had similar effects. In contrast, the alpha2-agonist, clonidine, deteriorated walking. Serotoninergic drugs, such as the neurotransmitter itself, serotonin (5HT), the precursor 5-hydroxytryptophan (5HTP), and the agonist quipazine improved the locomotion by increasing regularity of the hindlimb stepping and by increasing the step cycle duration. In contrast, the 5HT1A agonist 8-hydroxy-dipropylaminotetralin (DPAT) caused foot drag in one of the cats, resulting in frequent stumbling. Injection of combination of methoxamine and quipazine resulted in maintained, regular stepping with smooth movements and good lateral stability. Our results show that the effects of drugs can be integrated to the residual voluntary locomotion and improve some of its postural aspects. However, this work shows clearly that the effects of drugs (such as clonidine) may depend on whether or not the spinal lesion is complete. In a clinical context, this may suggest that different classes of drugs could be used in patients with different types of spinal cord injuries. Possible mechanisms underlying the effect of noradrenergic and serotoninergic drugs on the locomotion after partial spinal lesions are discussed.  (+info)

Direct agonists for serotonin receptors enhance locomotor function in rats that received neural transplants after neonatal spinal transection. (2/54)

We analyzed whether acute treatment with serotonergic agonists would improve motor function in rats with transected spinal cords (spinal rats) and in rats that received transplants of fetal spinal cord into the transection site (transplant rats). Neonates received midthoracic spinal transections within 48 hr of birth; transplant rats received fetal (embryonic day 14) spinal cord grafts at the time of transection. At 3 weeks, rats began 1-2 months of training in treadmill locomotion. Rats in the transplant group developed better weight-supported stepping than spinal rats. Systemic administration of two directly acting agonists for serotonergic 5-HT(2) receptor subtypes, quipazine and (+/-)-1-[2, 5]-dimethoxy-4-iodophenyl-2-aminopropane), further increased weight-supported stepping in transplant rats. The improvement was dose-dependent and greatest in rats with poor to moderate baseline weight support. In contrast, indirectly acting serotonergic agonists, which block reuptake of 5-HT (sertraline) or release 5-HT and block its reuptake (D-fenfluramine), failed to enhance motor function. Neither direct nor indirect agonists significantly improved locomotion in spinal rats as a group, despite equivalent upregulation of 5-HT(2) receptors in the lumbar ventral horn of lesioned rats with and without transplants. The distribution of immunoreactive serotonergic fibers within and caudal to the transplant did not appear to correspond to restoration of motor function. Our results confirm our previous demonstration that transplants improve motor performance in spinal rats. Additional stimulation with agonists at subtypes of 5-HT receptors produces a beneficial interaction with transplants that further improves motor competence.  (+info)

Evidence for a role for central 5-HT2B as well as 5-HT2A receptors in cardiovascular regulation in anaesthetized rats. (3/54)

1. The effects of injections i.c.v. of quipazine, (2 micromol kg-1) and 1-(2,5-di-methoxy-4-iodophenyl)-2-aminopropane (DOI; 2 micromol kg-1) on renal sympathetic and phrenic nerve activity, mean arterial blood pressure (MAP) and heart rate were investigated in alpha-chloralose anaesthetized rats pretreated with a peripherally acting 5-HT2 receptor antagonist. 2. Quipazine or DOI caused a rise in MAP which was associated with a tachycardia and renal sympathoinhibition in rats pretreated (i.c.v.) with the antagonist vehicle 10% PEG. These effects of quipazine were completely blocked by pretreatment with cinanserin (a 5-HT2 receptor antagonist) and attenuated by spiperone (a 5-HT2A receptor antagonist). However, pretreatment with SB200646A (a 5-HT2B/2C receptor antagonist) only blocked the sympathoinhibition, while pretreatment with SB204741 (a 5-HT2B receptor antagonist) reversed the sympathoinhibition to excitation as it also did for DOI. Quipazine also caused renal sympathoexcitation in the presence (i.v.) of a vasopressin V1 receptor antagonist. 3. Injection (i.v.) of the V1 receptor antagonist at the peak pressor response evoked by quipazine alone and in the presence of SB204741 caused an immediate fall in MAP. For quipazine alone the renal sympathoinhibition was slowly reversed to an excitation, while the renal sympathoexcitation observed in the presence of SB204741 was potentiated. In both, the quipazine-evoked tachycardia was unaffected. 4. The data indicate that cardiovascular responses caused by i.c.v. quipazine and DOI are primarily due to activation of central 5-HT2A receptors, which causes the release of vasopressin and a tachycardia. This released vasopressin appears to suppress a 5-HT2A receptor-evoked central increase in sympathetic outflow, which involves the activation of central 5-HT2B receptors indirectly by the released vasopressin.  (+info)

RNA-editing of the 5-HT(2C) receptor alters agonist-receptor-effector coupling specificity. (4/54)

1. The serotonin(2C) (5-HT(2C)) receptor couples to both phospholipase C (PLC)-inositol phosphate (IP) and phospholipase A(2) (PLA(2))-arachidonic acid (AA) signalling cascades. Agonists can differentially activate these effectors (i.e. agonist-directed trafficking of receptor stimulus) perhaps due to agonist-specific receptor conformations which differentially couple to/activate transducer molecules (e.g. G proteins). Since editing of RNA transcripts of the human 5-HT(2C) receptor leads to substitution of amino acids at positions 156, 158 and 160 of the putative second intracellular loop, a region important for G protein coupling, we examined the capacity of agonists to activate both the PLC-IP and PLA(2)-AA pathways in CHO cells stably expressing two major, fully RNA-edited isoforms (5-HT(2C-VSV), 5-HT(2C-VGV)) of the h5-HT(2C) receptor. 2. 5-HT increased AA release and IP accumulation in both 5-HT(2C-VSV) and 5-HT(2C-VGV) expressing cells. As expected, the potency of 5-HT for both RNA-edited isoforms for both responses was 10 fold lower relative to that of the non-edited receptor (5-HT(2C-INI)) when receptors were expressed at similar levels. 3. Consistent with our previous report, the efficacy order of two 5-HT receptor agonists (TFMPP and bufotenin) was reversed for AA release and IP accumulation at the non-edited receptor thus demonstrating agonist trafficking of receptor stimulus. However, with the RNA-edited receptor isoforms there was no difference in the relative efficacies of TFMPP or bufotenin for AA release and IP accumulation suggesting that the capacity for 5-HT(2C) agonists to traffic receptor stimulus is lost as a result of RNA editing. 4. These results suggest an important role for the second intracellular loop in transmitting agonist-specific information to signalling molecules.  (+info)

Serotonergic attenuation of the reinforcing and neurochemical effects of cocaine in squirrel monkeys. (5/54)

Preclinical studies have documented that serotonin (5-HT) can modulate the behavioral effects of cocaine. The present study examined the ability of 5-HT to attenuate the reinforcing and neurochemical effects of cocaine in nonhuman primates. In squirrel monkeys trained to self-administer cocaine (0.1 and 0.3 mg/injection) under a second-order schedule of i.v. drug delivery, the 5-HT uptake inhibitor alaproclate (3.0 and 10.0 mg/kg) and the 5-HT direct agonist quipazine (0.3-1.0 mg/kg) decreased response rates at doses that had no significant effect on behavior maintained by an identical schedule of stimulus termination. The neurochemical bases of the observed drug interactions on behavior were investigated further using in vivo microdialysis techniques in a separate group of awake monkeys to monitor drug-induced changes in extracellular dopamine (DA). Cocaine (1.0 mg/kg) elevated the concentration of DA in the caudate nucleus to approximately 300% of basal levels. Pretreatment with alaproclate or quipazine attenuated cocaine-induced increases in extracellular DA at the same pretreatment doses that decreased cocaine self-administration. The results obtained suggest that increasing brain 5-HT activity can attenuate the reinforcing effects of cocaine, ostensibly by decreasing the ability of cocaine to elevate extracellular DA in brain areas that mediate the behavioral effects. These findings extend those reported previously for the behavioral-stimulant effects of cocaine and identify a potential neurochemical mechanism underlying drug interactions on behavior.  (+info)

Serotonin sets the day state in the neurons that control coupling between the optic lobe circadian pacemakers in the cricket Gryllus bimaculatus. (6/54)

The bilaterally paired optic lobe circadian pacemakers of the cricket Gryllus bimaculatus mutually exchange photic and circadian information to keep their activity synchronized. The information is mediated by a neural pathway, consisting of the so-called medulla bilateral neurons, connecting the medulla areas of the two optic lobes. We investigated the effects of serotonin on the neural activity in this coupling pathway. Spontaneous and light-induced electrical activity of the neurons in the coupling pathway showed daily variations, being more intense during the night than the day. Microinjection of serotonin or a serotonin-receptor agonist, quipazine, into the optic lobe caused a dose- and time-dependent inhibition of spontaneous and light-induced responses, mimicking the day state. The amount of suppression was greater and the recovery from the suppression occurred faster during the night. Application of metergoline, a non-selective serotonin-receptor antagonist, increased spontaneous activity and light-evoked responses during both the day and the night, with higher effect during the day. In addition, metergoline effectively attenuated the effects of serotonin. These facts suggest that in the cricket's optic lobe, serotonin is released during the daytime and sets the day state in the neurons regulating coupling between the bilaterally paired optic lobe circadian pacemakers.  (+info)

Metachlorophenylpiperazine (m-CPP) induced intracavernous pressure responses in anaesthetized rats. (7/54)

Here we have recorded the effects of metachlorophenylpiperazine (m-CPP) on intracavernous pressure (ICP) in anesthetized rats pretreated with various pharmacological agents in an attempt to determine the mechanism and relevance of the m-CPP induced ICP response to other models of erection. m-CPP elicited consistent and significantly greater increases in ICP (71.5+/-6.6 mmHg) compared with the mixed 5-HT(2a/2c) agonists trifluoromethylphenylpiperazine (3.4+/-1.3 mmHg) and quipazine (10.9+/-1.8 mmHg). Blockade of 5-HT(2a) receptors with ketanserin failed to unmask any stimulatory effect of quipazine (7.2+/-1.0 mmHg). m-CPP induced ICP responses (71+/-7.0 mmHg) were unaffected in the presence of mianserin (63+/-5 mmHg) and ketanserin (51+/-12 mmHg). Spiperone significantly reduced the m-CPP induced increase in ICP (8.0+/-1.0 mmHg). Naloxone, yohimbine and 8-hydroxy-2-(di-n-propylamino)tetralin (8-OHDPAT) failed to elicit increases in ICP on their own. All three drugs significantly reduced the latency to the first m-CPP induced ICP response compared to saline. Yohimbine increased the duration of m-CPP induced ICP responses whereas 8-OHDPAT increased the mean number of m-CPP induced ICP responses compared to saline. The effects of m-CPP on ICP in anesthetized rats may not be mediated by 5-HT(2c) receptors and appears to be similar to erection in copula, but not erection elicited by other drugs or penile sheath retraction.  (+info)

Regulation of collagenase gene expression by serotonin and progesterone in rat uterine smooth muscle cells. (8/54)

The regulation of collagenase gene expression by serotonin and progesterone was investigated in primary cultures of rat uterine smooth muscle cells. Northern blot analysis demonstrates that serotonin (5-hydroxytryptamine (5-HT)), when administered to cells in serotonin-depleted medium, causes 6-8-fold increases in levels of collagenase mRNA. Selective serotonin 5-HT2 receptor agonists were able to mimic the effect of the natural hormone, while the induction by serotonin could be blocked by 5-HT2 receptor antagonists. Addition of phorbol ester (PMA) to 5-HT-depleted cultures fully mimicked the effect of 5-HT on collagenase mRNA induction. Treatment with progesterone analogs caused a decrease in collagenase mRNA, even in the presence of saturating levels of serotonin or PMA. In all experiments, levels of secreted collagenase were observed to correspond to levels of collagenase mRNA. Experiments with cycloheximide demonstrate that serotonin- and PMA-induced increases in collagenase mRNA are dependent on protein synthesis. Furthermore, nuclear run-on analysis shows that mRNA increases are accompanied by increases in initiation of transcripts. These data indicate that transcription of collagenase mRNA in myometrial smooth muscle cells is stimulated by serotonin, possibly via activation of protein kinase C, but is in some way prevented by the negative influence of progesterone.  (+info)

Quipazine is not generally considered a medical term, but it is a chemical compound that has been studied in the field of medicine and neuroscience. Quipazine is a type of drug known as a serotonin receptor agonist, which means it binds to and activates serotonin receptors in the brain.

Serotonin is a neurotransmitter, a chemical that transmits signals in the brain and nervous system, that plays a role in regulating mood, appetite, sleep, and other functions. Quipazine has been studied for its potential therapeutic uses in various conditions, including depression, anxiety, schizophrenia, and substance abuse disorders. However, it is not currently approved for use as a medication in any country.

It's important to note that while quipazine may have potential therapeutic benefits, it also has significant side effects, including seizures, changes in heart rate and blood pressure, and neuroleptic malignant syndrome, a potentially life-threatening condition characterized by muscle rigidity, fever, and autonomic dysfunction. As such, its use is generally limited to research settings.

2,5-Dimethoxy-4-Methylamphetamine (also known as DOM) is a psychoactive drug that belongs to the phenethylamine and amphetamine chemical classes. It is a synthetic compound that is not found naturally in any plant or animal sources.

DOM is a potent hallucinogen, with effects similar to those of LSD. It can cause profound changes in perception, thought, and mood, and may also cause physical symptoms such as increased heart rate, blood pressure, and body temperature. The effects of DOM can last up to 24 hours or more, and the drug is considered to have a high potential for abuse and psychological dependence.

It's important to note that the possession, sale, and use of DOM are illegal in many countries, including the United States, due to its potential for abuse and lack of accepted medical use. Therefore, it should only be used under the supervision of trained medical professionals in a controlled research setting.

Serotonin receptor agonists are a class of medications that bind to and activate serotonin receptors in the body, mimicking the effects of the neurotransmitter serotonin. These drugs can have various effects depending on which specific serotonin receptors they act upon. Some serotonin receptor agonists are used to treat conditions such as migraines, cluster headaches, and Parkinson's disease, while others may be used to stimulate appetite or reduce anxiety. It is important to note that some serotonin receptor agonists can have serious side effects, particularly when taken in combination with other medications that affect serotonin levels, such as selective serotonin reuptake inhibitors (SSRIs) or monoamine oxidase inhibitors (MAOIs). This can lead to a condition called serotonin syndrome, which is characterized by symptoms such as agitation, confusion, rapid heart rate, high blood pressure, and muscle stiffness.

Serotonin receptors are a type of cell surface receptor that bind to the neurotransmitter serotonin (5-hydroxytryptamine, 5-HT). They are widely distributed throughout the body, including the central and peripheral nervous systems, where they play important roles in regulating various physiological processes such as mood, appetite, sleep, memory, learning, and cognition.

There are seven different classes of serotonin receptors (5-HT1 to 5-HT7), each with multiple subtypes, that exhibit distinct pharmacological properties and signaling mechanisms. These receptors are G protein-coupled receptors (GPCRs) or ligand-gated ion channels, which activate intracellular signaling pathways upon serotonin binding.

Serotonin receptors have been implicated in various neurological and psychiatric disorders, including depression, anxiety, schizophrenia, and migraine. Therefore, selective serotonin receptor agonists or antagonists are used as therapeutic agents for the treatment of these conditions.

Ritanserin is a medication that belongs to the class of drugs known as serotonin antagonists. It works by blocking the action of serotonin, a neurotransmitter in the brain, which helps to reduce anxiety and improve mood. Ritanserin was initially developed for the treatment of depression and schizophrenia, but its development was discontinued due to its side effects.

The medical definition of Ritanserin is:

A piperazine derivative and a serotonin antagonist that has been used in the treatment of depression and schizophrenia. Its therapeutic effect is thought to be related to its ability to block the action of serotonin at 5HT2 receptors. However, development of ritanserin was discontinued due to its side effects, including orthostatic hypotension, dizziness, and sedation. It has also been studied for its potential in treating cocaine addiction and alcohol withdrawal syndrome.

Serotonin antagonists are a class of drugs that block the action of serotonin, a neurotransmitter, at specific receptor sites in the brain and elsewhere in the body. They work by binding to the serotonin receptors without activating them, thereby preventing the natural serotonin from binding and transmitting signals.

Serotonin antagonists are used in the treatment of various conditions such as psychiatric disorders, migraines, and nausea and vomiting associated with cancer chemotherapy. They can have varying degrees of affinity for different types of serotonin receptors (e.g., 5-HT2A, 5-HT3, etc.), which contributes to their specific therapeutic effects and side effect profiles.

Examples of serotonin antagonists include ondansetron (used to treat nausea and vomiting), risperidone and olanzapine (used to treat psychiatric disorders), and methysergide (used to prevent migraines). It's important to note that these medications should be used under the supervision of a healthcare provider, as they can have potential risks and interactions with other drugs.

Nervous system neoplasms are abnormal growths or tumors that occur within the nervous system, which includes the brain, spinal cord, and peripheral nerves. These tumors can be benign (non-cancerous) or malignant (cancerous), and their growth can compress or infiltrate surrounding tissues, leading to various neurological symptoms. The causes of nervous system neoplasms are not fully understood but may involve genetic factors, exposure to certain chemicals or radiation, and certain viral infections. Treatment options depend on the type, location, and size of the tumor and can include surgery, radiation therapy, chemotherapy, or a combination of these approaches.

The epidural space is the potential space located outside the dura mater, which is the outermost of the three membranes covering the brain and spinal cord (the meninges). This space runs the entire length of the spinal canal and contains fatty tissue, blood vessels, and nerve roots. It is often used as a route for administering anesthesia during childbirth or surgery, as well as for pain management in certain medical conditions. The injection of medications into this space is called an epidural block.

Serotonin agents are a class of drugs that work on the neurotransmitter serotonin (5-hydroxytryptamine, 5-HT) in the brain and elsewhere in the body. They include several types of medications such as:

1. Selective Serotonin Reuptake Inhibitors (SSRIs): These drugs block the reabsorption (reuptake) of serotonin into the presynaptic neuron, increasing the availability of serotonin in the synapse to interact with postsynaptic receptors. SSRIs are commonly used as antidepressants and include medications such as fluoxetine, sertraline, and citalopram.
2. Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs): These drugs block the reabsorption of both serotonin and norepinephrine into the presynaptic neuron, increasing the availability of these neurotransmitters in the synapse. SNRIs are also used as antidepressants and include medications such as venlafaxine and duloxetine.
3. Serotonin Receptor Agonists: These drugs bind to and activate serotonin receptors, mimicking the effects of serotonin. They are used for various indications, including migraine prevention (e.g., sumatriptan) and Parkinson's disease (e.g., pramipexole).
4. Serotonin Receptor Antagonists: These drugs block serotonin receptors, preventing the effects of serotonin. They are used for various indications, including nausea and vomiting (e.g., ondansetron) and as mood stabilizers in bipolar disorder (e.g., olanzapine).
5. Serotonin Synthesis Inhibitors: These drugs block the enzymatic synthesis of serotonin, reducing its availability in the brain. They are used as antidepressants and include medications such as monoamine oxidase inhibitors (MAOIs) like phenelzine and tranylcypromine.

It's important to note that while these drugs all affect serotonin, they have different mechanisms of action and are used for various indications. It's essential to consult a healthcare professional before starting any new medication.

Methysergide is a medication that belongs to a class of drugs called ergot alkaloids. It is primarily used for the prophylaxis (prevention) of migraine headaches. Methysergide works by narrowing blood vessels around the brain, which is thought to help prevent migraines.

The medical definition of Methysergide is:
A semisynthetic ergot alkaloid derivative used in the prophylaxis of migraine and cluster headaches. It has both agonist and antagonist properties at serotonin receptors, and its therapeutic effects are thought to be related to its ability to block the binding of serotonin to its receptors. However, methysergide can have serious side effects, including fibrotic reactions in various organs, such as the heart, lungs, and kidneys, so it is usually used only for short periods of time and under close medical supervision.

... is a serotonergic drug of the piperazine group which is used in scientific research. It was originally intended as an ... Quipazine produces a head-twitch response and other psychedelic-consistent effects in animal studies including in mice, rats, ... Quipazine is synthesized by reacting 2-chloroquinoline with piperazine. 2C-B-PP 6-Nitroquipazine Naphthylpiperazine ORG-37684 ... 2010). "The interactions of the 5-HT3 receptor with quipazine-like arylpiperazine ligands: the journey track at the end of the ...
ORG-12962 Quipazine Adams D, Duncton M (2001). "Efficient Synthesis of the 5-Ht2C Receptor Agonist, Org 37684". Synthetic ...
Schmidt AW, Hurt SD, Peroutka SJ (1989). "'[3H]quipazine' degradation products label 5-HT uptake sites". Eur. J. Pharmacol. 171 ...
Schmidt AW, Hurt SD, Peroutka SJ (November 1989). "'[3H]quipazine' degradation products label 5-HT uptake sites". European ...
Schmidt AW, Hurt SD, Peroutka SJ (1989). "'[3H]quipazine' degradation products label 5-HT uptake sites". Eur. J. Pharmacol. 171 ...
Schmidt AW, Hurt SD, Peroutka SJ (November 1989). "'[3H]quipazine' degradation products label 5-HT uptake sites". European ...
2C-B-PP mCPP ORG-12962 Quipazine Clineschidmt BV (1979). "MK-212: a serotonin-like agonist in the CNS". General Pharmacology. ...
Quipazine Vaatstra WJ, Deiman-Van Aalst WM, Eigeman L (March 1981). "Du 24565, a quipazine derivative, a potent selective ... on serotoninergic and noradrenergic neurones of the rat brain and comparison with the effects of quipazine". Naunyn- ...
Substituted piperazine Diphenylpiperazine Phenylpiperazine Quipazine Schoeffter P, Hoyer D (June 1989). "Interaction of ...
OSU-6162 acts as a partial agonist at both 5-HT2A and dopamine D2 receptors Quipazine, 5-HT2A agonist but also potent 5-HT3 ... March 2021). "Psychedelic-like Properties of Quipazine and Its Structural Analogues in Mice". ACS Chemical Neuroscience. 12 (5 ...
Dall'Olio R, Vaccheri A, Montanaro N (1985). "Reduced head-twitch response to quipazine of rats previously treated with ...
2-Methyl-5-hydroxytryptamine (2-methylserotonin) and quipazine are moderately selective agonists of the 5-HT3 receptor that are ...
867-868 2C-B-aminorex 2C-B-BZP 3-Chloro-4-fluorophenylpiperazine CPD-1 ORG-12962 Quipazine Substituted piperazine Lyon RA, ...
... quipazine MeSH D03.438.810.900 - saquinavir MeSH D03.438.834.700 - 2h-benzo(a)quinolizin-2-ol, 2-ethyl-1,3,4,6,7,11b-hexahydro- ... quipazine MeSH D03.383.606.845 - razoxane MeSH D03.383.606.880 - thiethylperazine MeSH D03.383.606.900 - trazodone MeSH D03.383 ...
Quiphile quipazine (INN) quisultazine (INN) quitiapine (INN) Quixin (Vistakon Pharmaceuticals) quizartinib (USAN, INN) Qvar ( ...
Some additional analogues include quipazine, ORG-12962, and 3C-PEP. mCPP is illegal in Belgium. mCPP is illegal in Brazil. mCPP ...
2C-B-PP 2,3-Dichlorophenylpiperazine 3-Chloro-4-fluorophenylpiperazine CPD-1 ORG-37684 Quipazine Porter RH, Benwell KR, Lamb H ...
Cereulide 2-methyl-5-HT Alpha-Methyltryptamine Bufotenin Chlorophenylbiguanide Ethanol Ibogaine Phenylbiguanide Quipazine RS- ...
Quipazine Sunifiram (nootropic) Tolpiprazole (tranquilizer) Most of these agents can be classified as either phenylpiperazines ...
Quipazine (2-piperazin-1-ylquinoline) Many azapirones such as buspirone, gepirone, and tandospirone produce 1-PP as a ...
Quipazine is a serotonergic drug of the piperazine group which is used in scientific research. It was originally intended as an ... Quipazine produces a head-twitch response and other psychedelic-consistent effects in animal studies including in mice, rats, ... Quipazine is synthesized by reacting 2-chloroquinoline with piperazine. 2C-B-PP 6-Nitroquipazine Naphthylpiperazine ORG-37684 ... 2010). "The interactions of the 5-HT3 receptor with quipazine-like arylpiperazine ligands: the journey track at the end of the ...
Kuhn DM Discriminative stimulus properties of quipazine: direct serotonergic mediation Neuropharmacology 1979 18:143-51 ... "Discriminative stimulus properties of quipazine: direct serotonergic mediation" Neuropharmacology. 1979;18:143-51. ...
"Drug-induced stimulus control and the concept of breaking point: LSD and quipazine". ... "Drug-induced stimulus control and the concept of breaking point: LSD and quipazine" Psychopharmacology. 1981;72:217-8. ...
Quipazine dimaleate, 5-HT receptor agonist (ab120540) Description:. 5-HT receptor agonist ...
Assessing the effects of fenfluramine, quipazine and d-amphetamine on self-control in pigeons. / Woods, J. H.; Reilly, Mark P. ... Woods, J. H., & Reilly, M. P. (1998, May). Assessing the effects of fenfluramine, quipazine and d-amphetamine on self-control ... Woods, JH & Reilly, MP 1998, Assessing the effects of fenfluramine, quipazine and d-amphetamine on self-control in pigeons.. ... Dive into the research topics of Assessing the effects of fenfluramine, quipazine and d-amphetamine on self-control in pigeons ...
Evidence for the role of noradrenaline in some effects of quipazine Psychopharmacology (.... 1980. ...
2014) A combination therapy of neural and glial restricted precursor cells and chronic quipazine treatment paired with passive ... A Combination Therapy Promotes Quipazine-induced Weight-supported Stepping in Spinalized Adult Rats.). ... cycling promotes quipazine-induced stepping in adult spinalized rats. The Journal of Spinal Cord Medicine. ...
Examples include efavirenz and quipazine, which both activate serotonin 5-HT2A receptors and change rodent behavior in the same ...
Stimulation of serotonin receptors with quipazine inhibited suckling in deprived pups, and this effect was prevented by ...
Piperazines (e.g., aripiprazole, BZP, mCPP, quipazine, TFMPP). *PNU-22394. *PNU-181731 ...
quipazine, phencyclidine and SKF-10017). In human healthy volunteers, low doses of the extracts administered in a double-blind ...
1uM quipazine was used as a control. Results reported an IC50 of 0.50 mM for cytisinicline and 0.25 ┬ÁM for varenicline, ...
2. Quipazine or DOI caused a rise in MAP which was associated with a tachycardia and renal sympathoinhibition in rats ... In both, the quipazine-evoked tachycardia was unaffected. 4. The data indicate that cardiovascular responses caused by i.c.v. ... Quipazine also caused renal sympathoexcitation in the presence (i.v.) of a vasopressin V1 receptor antagonist. 3. Injection (i. ... These effects of quipazine were completely blocked by pretreatment with cinanserin (a 5-HT2 receptor antagonist) and attenuated ...
... given 15 min after quipazine produced significant. No minimum dosage has been identified as necessary to cause ad- verse ...
DOl and quipazine is surely an in vitro and in vivo agonist action at S HT receptors. for which COS 12066B has incredibly ... On this review, we demonstrated that TFMPP and mCPP, in addition to DOI and quipazine, potentiate tail flicks elicited by 5 HT ... Further, CGS 12066B, TFMPP, mCPP, DOI and quipazine all failed Factor Xa to elicit tail flicks when did not substantially ... TFMPP and mCPP are usually described as mixed 5 HTib/, and quipazine possesses mixed agonist/antagonist properties at 5 HT,b ...
Dose dependence of the 5-HT agonist quipazine in facilitating spinal stepping in the rat with epidural stimulation, Neurosci ... Spinal cord-transected mice learn to step in response to quipazine treatment and robotic training, J Neurosci, 2005; 25(50): ... Epidural spinal cord stimulation plus quipazine administration enable stepping in complete spinal adult rats, J Neurophysiol, ...
Rats have been pretreated 20 min before 8 OH DPAT with CGS 12066B, TFMPP, mCPP, DOI or quipazine. During the initial experiment ... Additional, CGS 12066B, TFMPP, mCPP, DOI and quipazine all failed to elicit tail flicks when did not appreciably potentiate the ...
Connectivity map have identified five drugs (levobunolol, NU-1025, quipazine, anisomycin and sulfathiazole) for CAHM targeted ...
Kulkarni S, Arzi A, Kaul P. Modification of drug-induced catatonia and tremors by quipazine in rats and mice. The Japanese ...
Alhaider, A.A. 1987: Novel congeners related to quipazine and trazodone as selective serotonin uptake inhibitors. Federation ...
Quipazine D3.438.810.850 D3.633.100.810.850 Quorum Sensing G4.299.122.700 G4.85.700 G6.590.580.700 G6.550.700 Rabeprazole ...
Quipazine D3.438.810.850 D3.633.100.810.850 Quorum Sensing G4.299.122.700 G4.85.700 G6.590.580.700 G6.550.700 Rabeprazole ...
Quipazine D3.438.810.850 D3.633.100.810.850 Quorum Sensing G4.299.122.700 G4.85.700 G6.590.580.700 G6.550.700 Rabeprazole ...
Quipazine D3.438.810.850 D3.633.100.810.850 Quorum Sensing G4.299.122.700 G4.85.700 G6.590.580.700 G6.550.700 Rabeprazole ...
Quipazine D3.438.810.850 D3.633.100.810.850 Quorum Sensing G4.299.122.700 G4.85.700 G6.590.580.700 G6.550.700 Rabeprazole ...
It ought to be additional that FLU, offered chronically, decreases the quipazine mduced head shakes which are also mediated by ...
... a dose that inhibited serotonin agonist quipazine induced GH rise, or 5) control. No drug altered mean GH or prolactin levels ... a dose that inhibited serotonin agonist quipazine induced GH rise, or 5) control. No drug altered mean GH or prolactin levels ... a dose that inhibited serotonin agonist quipazine induced GH rise, or 5) control. No drug altered mean GH or prolactin levels ... a dose that inhibited serotonin agonist quipazine induced GH rise, or 5) control. No drug altered mean GH or prolactin levels ...
Kohler, M.; Kalkowski, A.; Wollnik, F. 1999: Serotonin agonist quipazine induces photic-like phase shifts of the circadian ...
Quipazine Quisqualate Receptors use Receptors, AMPA Quisqualic Acid Quokkas use Macropodidae Quorum Quenching use Quorum ...
Quipazine Quisqualate Receptors use Receptors, AMPA Quisqualic Acid Quokkas use Macropodidae Quorum Quenching use Quorum ...
  • citation needed] Quipazine is a serotonin reuptake inhibitor, and also a moderately selective serotonin receptor agonist, binding to a range of different serotonin receptors, but particularly to the 5-HT2A and 5-HT3 subtypes. (wikipedia.org)
  • Structure-affinity relationship studies on arylpiperazine derivatives related to quipazine as serotonin transporter ligands. (wikipedia.org)
  • Examples include efavirenz and quipazine, which both activate serotonin 5-HT 2A receptors and change rodent behavior in the same way that other psychedelic drugs do. (bipolarnews.org)
  • Stimulation of serotonin receptors with quipazine inhibited suckling in deprived pups, and this effect was prevented by methysergide pretreatment. (duke.edu)
  • Quipazine is a serotonergic drug of the piperazine group which is used in scientific research. (wikipedia.org)
  • Quipazine produces a head-twitch response and other psychedelic-consistent effects in animal studies including in mice, rats, and monkeys. (wikipedia.org)
  • A Combination Therapy Promotes Quipazine-induced Weight-supported Stepping in Spinalized Adult Rats. (neurotree.org)
  • 2014 ) A combination therapy of neural and glial restricted precursor cells and chronic quipazine treatment paired with passive cycling promotes quipazine-induced stepping in adult spinalized rats. (neurotree.org)
  • citation needed] Quipazine is a serotonin reuptake inhibitor, and also a moderately selective serotonin receptor agonist, binding to a range of different serotonin receptors, but particularly to the 5-HT2A and 5-HT3 subtypes. (wikipedia.org)
  • Quipazine [nonselective agonist of 5-hydroxytryptamine (serotonin) (5-HT) receptors] can be administered at a dose that facilitates, but does not induce, locomotor activity in adult spinal cats ( Barbeau and Rossignol, 1991 ). (jneurosci.org)
  • To test this, adult rats received a complete spinal transection (T9-T10) followed by daily locomotor training performed under ES with administration of quipazine (a serotonin (5-HT) agonist) starting 7 days post-injury (dpi). (ucl.ac.uk)
  • Here we examined the effects of the 5-HT 1A/7 agonist 8-OH-DPAT and the 5-HT 1/2 agonist quipazine on the circadian system in mice, with some parallel experiments conducted with hamsters for comparative purposes. (nebraska.edu)
  • Here we examined the effects of the 5-HT1A/7 agonist 8-OH-DPAT and the 5-HT1/2 agonist quipazine on the circadian system in mice, with some parallel experiments conducted with hamsters for comparative purposes. (nebraska.edu)
  • Chronic testosterone propionatetreatment decreases the concentration of quipazine binding at 5 HT, receptors in theamygdala of the castrated male rat. (envirocleanmc.com)
  • Quipazine produces a head-twitch response and other psychedelic-consistent effects in animal studies including in mice, rats, and monkeys. (wikipedia.org)
  • In mice, quipazine modestly increased c-Fos expression in the SCN (site of the circadian pacemaker) during the subjective day, whereas 8-OH-DPAT did not affect SCN c-Fos. (nebraska.edu)
  • Epidural spinal cord stimulation plus quipazine administration enable stepping in complete spinal adult rats. (nature.com)