A nicotinic antagonist used primarily as a ganglionic blocker in animal research. It has been used as an antihypertensive agent but has been supplanted by more specific drugs in most clinical applications.
Agents having as their major action the interruption of neural transmission at nicotinic receptors on postganglionic autonomic neurons. Because their actions are so broad, including blocking of sympathetic and parasympathetic systems, their therapeutic use has been largely supplanted by more specific drugs. They may still be used in the control of blood pressure in patients with acute dissecting aortic aneurysm and for the induction of hypotension in surgery.
Drugs that bind to nicotinic cholinergic receptors (RECEPTORS, NICOTINIC) and block the actions of acetylcholine or cholinergic agonists. Nicotinic antagonists block synaptic transmission at autonomic ganglia, the skeletal neuromuscular junction, and at central nervous system nicotinic synapses.
A nicotinic antagonist that is well absorbed from the gastrointestinal tract and crosses the blood-brain barrier. Mecamylamine has been used as a ganglionic blocker in treating hypertension, but, like most ganglionic blockers, is more often used now as a research tool.
Nicotine is highly toxic alkaloid. It is the prototypical agonist at nicotinic cholinergic receptors where it dramatically stimulates neurons and ultimately blocks synaptic transmission. Nicotine is also important medically because of its presence in tobacco smoke.
Clusters of neurons and their processes in the autonomic nervous system. In the autonomic ganglia, the preganglionic fibers from the central nervous system synapse onto the neurons whose axons are the postganglionic fibers innervating target organs. The ganglia also contain intrinsic neurons and supporting cells and preganglionic fibers passing through to other ganglia.
The d-form of AMPHETAMINE. It is a central nervous system stimulant and a sympathomimetic. It has also been used in the treatment of narcolepsy and of attention deficit disorders and hyperactivity in children. Dextroamphetamine has multiple mechanisms of action including blocking uptake of adrenergics and dopamine, stimulating release of monamines, and inhibiting monoamine oxidase. It is also a drug of abuse and a psychotomimetic.
Family of large marine CRUSTACEA, in the order DECAPODA. These are called clawed lobsters because they bear pincers on the first three pairs of legs. The American lobster and Cape lobster in the genus Homarus are commonly used for food.
Pinched-off nerve endings and their contents of vesicles and cytoplasm together with the attached subsynaptic area of the membrane of the post-synaptic cell. They are largely artificial structures produced by fractionation after selective centrifugation of nervous tissue homogenates.
One of the two major classes of cholinergic receptors. Nicotinic receptors were originally distinguished by their preference for NICOTINE over MUSCARINE. They are generally divided into muscle-type and neuronal-type (previously ganglionic) based on pharmacology, and subunit composition of the receptors.
The phylogenetically newer part of the CORPUS STRIATUM consisting of the CAUDATE NUCLEUS and PUTAMEN. It is often called simply the striatum.
Injections into the cerebral ventricles.
The largest and uppermost of the paravertebral sympathetic ganglia.
Changes in the amounts of various chemicals (neurotransmitters, receptors, enzymes, and other metabolites) specific to the area of the central nervous system contained within the head. These are monitored over time, during sensory stimulation, or under different disease states.
Drugs that bind to and activate nicotinic cholinergic receptors (RECEPTORS, NICOTINIC). Nicotinic agonists act at postganglionic nicotinic receptors, at neuroeffector junctions in the peripheral nervous system, and at nicotinic receptors in the central nervous system. Agents that function as neuromuscular depolarizing blocking agents are included here because they activate nicotinic receptors, although they are used clinically to block nicotinic transmission.
The restriction of the MOVEMENT of whole or part of the body by physical means (RESTRAINT, PHYSICAL) or chemically by ANALGESIA, or the use of TRANQUILIZING AGENTS or NEUROMUSCULAR NONDEPOLARIZING AGENTS. It includes experimental protocols used to evaluate the physiologic effects of immobility.

Pivotal role of nitric oxide in the control of blood pressure after leptin administration. (1/81)

Leptin administration has been shown to increase renal, adrenal, and lumbar sympathetic nerve activity. However, this generalized sympathoexcitatory activity is not always followed by an increase in arterial pressure. The present study tested the hypothesis that leptin induces a release of nitric oxide (NO) that opposes the pressor effect of sympathoexcitation. The effect of intravenous administration of leptin (10, 100, and 1,000 microg/kg body wt) or vehicle on blood pressure (BP), heart rate (HR), and serum nitrite/nitrate concentrations of anesthetized Wistar rats was examined. At 90 min after injection, the three leptin doses tested increased serum NO concentrations 20.5, 33.1, and 89.5%, respectively (P < 0.001 vs. baseline). The effect of leptin on NO concentrations was significantly dose-dependent on linear trend testing (P = 0.0001). In contrast, leptin did not change serum nitrite/nitrate concentrations of fa/fa rats. Leptin administration to Wistar rats under NO synthesis inhibition (N(omega)-nitro-L-arginine methyl ester [L-NAME]) produced a statistically significant increase (P < 0.05) in both systolic BP and mean arterial pressure as well as in HR (P < 0.01). Injection of leptin into rats with pharmacologically induced ganglionic blockade (chlorisondamine) was followed by a decrease in BP and HR to values significantly lower (P < 0.01) than those observed with chlorisondamine treatment alone. The leptin-induced hypotension observed in the setting of ganglionic blockade was blocked by L-NAME. These findings raise the possibility that the leptin-induced release of NO may contribute to the homeostasis of BP.  (+info)

Thermogenic effects of sibutramine and its metabolites. (2/81)

1. The thermogenic activity of the serotonin and noradrenaline reuptake inhibitor sibutramine (BTS 54524; Reductil) was investigated by measuring oxygen consumption (VO2) in rats treated with sibutramine or its two pharmacologically-active metabolites. 2. Sibutramine caused a dose-dependent rise in VO2, with a dose of 10 mg kg(-1) of sibutramine or its metabolites producing increases of up to 30% that were sustained for at least 6 h, and accompanied by significant increases (0.5-1.0 degrees C) in body temperature. 3. Based on the accumulation in vivo of radiolabelled 2-deoxy-[3H]-glucose, sibutramine had little or no effect on glucose utilization in most tissues, but caused an 18 fold increase in brown adipose tissue (BAT). 4. Combined high, non-selective doses (20 mg kg(-1)) of the beta-adrenoceptor antagonists, atenolol and ICI 118551, inhibited completely the VO2 response to sibutramine, but the response was unaffected by low, beta1-adrenoceptor-selective (atenolol) or beta2-adrenoceptor-selective (ICI 118551) doses (1 mg kg(-1)). 5. The ganglionic blocking agent, chlorisondamine (15 mg kg(-1)), inhibited completely the VO2 response to the metabolites of sibutramine, but had no effect on the thermogenic response to the beta3-adrenoceptor-selective agonist BRL 35135. 6. Similar thermogenic responses were produced by simultaneous injection of nisoxetine and fluoxetine at doses (30 mg kg(-1)) that had no effect on VO2 when injected individually. 7. It is concluded that stimulation of thermogenesis by sibutramine requires central reuptake inhibition of both serotonin and noradrenaline, resulting in increased efferent sympathetic activation of BAT thermogenesis via beta3-adrenoceptor, and that this contributes to the compound's activity as an anti-obesity agent.  (+info)

AV3V lesions attenuate the cardiovascular responses produced by blood-borne excitatory amino acid analogs. (3/81)

Systemic injections of the excitatory amino acid (EAA) analogs, kainic acid (KA) and N-methyl-D-aspartate (NMDA), produce a pressor response in conscious rats that is caused by a centrally mediated activation of sympathetic drive and the release of arginine vasopressin (AVP). This study tested the hypothesis that the tissue surrounding the anteroventral part of the third ventricle (AV3V) plays a role in the expression of the pressor responses produced by systemically injected EAA analogs. Specifically, we examined whether prior electrolytic ablation of the AV3V region would affect the pressor responses to KA and NMDA (1 mg/kg iv) in conscious rats. The KA-induced pressor response was smaller in AV3V-lesioned than in sham-lesioned rats (11 +/- 2 vs. 29 +/- 2 mmHg; P < 0.05). After ganglion blockade, KA produced a pressor response in sham-lesioned but not AV3V-lesioned rats (+27 +/- 3 vs. +1 +/- 2 mmHg; P < 0.05). The KA-induced pressor response in ganglion-blocked sham-lesioned rats was abolished by a vasopressin V1-receptor antagonist. Similar results were obtained with NMDA. The pressor response to AVP (10 ng/kg iv) was slightly smaller in AV3V-lesioned than in sham-lesioned ganglion-blocked rats (45 +/- 3 vs. 57 +/- 4 mmHg; P < 0.05). This study demonstrates that the pressor responses to systemically injected EAA analogs are smaller in AV3V-lesioned rats. The EAA analogs may produce pressor responses by stimulation of EAA receptors in the AV3V region, or the AV3V region may play an important role in the expression of these responses.  (+info)

Opposing adrenergic actions of intravenous metformin on arterial pressure in female spontaneously hypertensive rats. (4/81)

OBJECTIVE: Intravenous (i.v.) injection of the antidiabetic drug metformin rapidly lowers mean arterial pressure (MAP) in spontaneously hypertensive rats (SHR). However, if autonomic ganglia or alpha-adrenoceptors are first blocked then metformin rapidly raises MAP in SHR. This study was conducted to further characterize the adrenergic mechanisms of these opposing i.v. actions of the drug. METHODS: Conscious, undisturbed female SHR with indwelling vascular catheters were used to measure acute effects of i.v. metformin (100 mg/kg; before and after sustained ganglionic blockade, GB, with chlorisondamine, 5 mg/kg) on: (1) circulating levels of catecholamines, (2) MAP after pharmacologic modulation of beta- as well as alpha-adrenoceptors and (3) all the above in the absence as well as presence of the adrenal medulla. RESULTS: Plasma norepinephrine (NE) and epinephrine (E) levels (pg/ml) were rapidly increased by i.v. metformin (8 SHR, p < 0.05) both before GB (delta NE = +146 +/- 41; delta E = +119 +/- 31) and after GB (delta NE = +79 +/- 24; delta E = +120 +/- 32). Similar increases in plasma NE (though not E) were seen in SHR without adrenal medullae. Blockade of beta-adrenoceptors with propranolol (pro; 3 mg/kg, 8 SHR) enhanced the rapid depressor response to i.v. metformin before GB (delta MAP, mmHg: -38 +/- 4 with pro vs -17 +/- 3 without pro; p < 0.05) and attenuated the rapid pressor response to i.v. metformin after GB (delta MAP, mmHg: +8 +/- 3 with pro vs +30 +/- 4 without pro; p < 0.05). Results were similar in SHR without adrenal medullae. Finally, if baseline MAP under GB was raised back to hypertensive levels with i.v. infusion of either NE or phenylephrine then i.v. metformin did not raise but rather reduced MAP in SHR. CONCLUSION(S): The acute depressor action of i.v. metformin in female SHR (1) is most likely due to a direct vasodilator action which includes inhibition of alpha-receptor-mediated vasoconstriction and (2) is buffered by an acute beta-receptor-mediated pressor action likely due to a direct metformin-induced release of NE from postganglionic sympathetic nerve endings.  (+info)

Reward and somatic changes during precipitated nicotine withdrawal in rats: centrally and peripherally mediated effects. (5/81)

The negative affective aspects of nicotine withdrawal have been hypothesized to contribute to tobacco dependence. In the present studies in rats, brain stimulation reward thresholds, conditioned place aversions, and somatic signs of withdrawal were used to investigate the role of central and peripheral nicotinic acetylcholine and opioid receptors in nicotine withdrawal. Rats prepared with s.c. osmotic mini-pumps delivering 9.0 mg/kg/day nicotine hydrogen tartrate or saline were administered various doses of the nicotinic antagonists mecamylamine (s.c.), chlorisondamine (s. c. or i.c.v.), dihydro-beta-erythroidine (s.c.), or the opiate antagonist naloxone (s.c.). Nicotine-treated rats receiving mecamylamine or i.c.v. chlorisondamine exhibited elevated thresholds and more somatic signs than saline-treated rats. Nicotine-treated rats receiving s.c. chlorisondamine, at doses that do not readily cross the blood-brain barrier, exhibited more somatic signs than saline-treated rats with no threshold elevations. Naloxone administration produced threshold elevations and somatic signs only at high doses that induced similar magnitude effects in both nicotine- and saline-treated subjects. Mecamylamine or dihydro-beta-erythroidine administration induced conditioned place aversions in nicotine-treated rats but required higher doses than those needed to precipitate threshold elevations. In contrast, naloxone administration induced conditioned place aversions at lower doses than those required to precipitate threshold elevations and somatic signs. These data provide evidence for a dissociation between centrally mediated elevations in reward thresholds and somatic signs that are both centrally and peripherally mediated. Furthermore, threshold elevations and somatic signs of withdrawal appear to be mediated by cholinergic neurotransmission, whereas conditioned place aversions appear to be primarily mediated by the opioid system.  (+info)

Effects of nicotine and chlorisondamine on cerebral glucose utilization in immobilized and freely-moving rats. (6/81)

Chlorisondamine blocks central nicotinic receptors for many weeks via an unknown mechanism. Intracerebroventricular administration of [(3)H]-chlorisondamine in rats results in an anatomically restricted and persistent intracellular accumulation of radioactivity. The initial aim of the present study was to test whether nicotinic receptor antagonism by chlorisondamine is also anatomically restricted. Male adult rats were pretreated several times with nicotine to avoid the disruptive effects of the drug seen in drug-naive animals. They then received chlorisondamine (10 microg i. c.v.) or saline, and local cerebral glucose utilization (LCGU) was measured 4 weeks later after acute nicotine (0.4 mg kg(-1) s.c.) or saline administration. During testing, rats were partially immobilized. Nicotine significantly increased LCGU in the anteroventral thalamus and in superior colliculus. Chlorisondamine completely blocked the first of these effects. Chlorisondamine significantly reduced LCGU in the lateral habenula, substantia nigra pars compacta, ventral tegmental area, and cerebellar granular layer. The second experiment was of similar design, but the rats were not pre-exposed to nicotine, and were tested whilst freely-moving. Acute nicotine significantly increased LCGU in anteroventral thalamus, superior colliculus, medial habenula and dorsal lateral geniculate. Overall, however, nicotine significantly decreased LCGU. Most or all of the central effects of nicotine on LCGU were reversed by chlorisondamine given 4 weeks beforehand. These findings suggest that chlorisondamine blocks nicotinic effects widely within the brain. They also indicate that in freely-moving rats, nicotine can reduce or stimulate cerebral glucose utilization, depending on the brain area. British Journal of Pharmacology (2000) 129, 147 - 155  (+info)

Activation of antigen-specific CD4+ Th2 cells and B cells in vivo increases norepinephrine release in the spleen and bone marrow. (7/81)

The neurotransmitter norepinephrine (NE) binds to the beta 2-adrenergic receptor (beta 2AR) expressed on various immune cells to influence cell homing, proliferation, and function. Previous reports showed that NE stimulation of the B cell beta 2AR is necessary for the maintenance of an optimal primary and secondary Th2 cell-dependent Ab response in vivo. In the present study we investigated the mechanism by which activation of Ag-specific CD4+ Th2 cells and B cells in vivo by a soluble protein Ag increases NE release in the spleen and bone marrow. Our model system used scid mice that were reconstituted with a clone of keyhole limpet hemocyanin-specific Th2 cells and trinitrophenyl-specific B cells. Following immunization, the rate of NE release in the spleen and bone marrow was determined using [3H]NE turnover analysis. Immunization of reconstituted scid mice with a cognate Ag increased the rate of NE release in the spleen and bone marrow 18-25 h, but not 1-8 h, following immunization. In contrast, immunization of mice with a noncognate Ag had no effect on the rate of NE release at any time. The cognate Ag-induced increase in NE release was partially blocked by ganglionic blockade with chlorisondamine, suggesting a role for both pre- and postganglionic signals in regulating NE release. Thus, activation of Ag-specific Th2 cells and B cells in vivo by a soluble protein Ag increases the rate of NE release and turnover in the spleen and bone marrow 18-25 h after immunization.  (+info)

Possible contribution of central gamma-aminobutyric acid receptors to resting vascular tone in freely moving rats. (8/81)

Previous studies have shown that central administration of GABA (gamma -aminobutyric acid), an inhibitory neurotransmitter, preferentially reduces hindquarters and carotid vascular resistances but not renal and coeliac vascular resistances in conscious rats. This study tested the hypothesis that these preferential actions of central GABA receptors are related to differences between vessels in resting autonomic vascular tone in freely moving rats. Rats were chronically implanted with intracisternal cannulas and/or electromagnetic probes to measure regional blood flows. In response to GABA administration, the changes in vascular resistance (arterial blood pressure/regional blood flow) of the hindquarters (n = 23) and carotid (n = 12) vascular beds were significantly and negatively correlated with basal vascular resistance. No such relationship was found for the renal (n = 21), coeliac (n = 13) and superior mesenteric (n = 23) vascular beds. This finding indicates that the responsiveness to GABA of brainstem pathways controlling the hindquarters and carotid vascular beds co-varies with resting resistance in hindquarters and carotid vessels. A similar analysis was performed, correlating the ongoing vascular resistance of each vessel with its response to ganglionic blockade by chlorisondamine. In this case, a significant negative correlation was also found for the hindquarters (n = 26) and carotid (n = 15) vascular beds, but not for the coeliac (n = 17) or superior mesenteric (n = 19) vessels. Together, these findings suggest that central GABA receptors accessible from the cisterna magna preferentially affect two vascular beds which, in the freely moving rat, show resting autonomic vascular tone.  (+info)

Chlorisondamine is a type of drug called an anticholinergic, which works by blocking the action of a neurotransmitter called acetylcholine in the body. It is a type of ganglionic blocker, which means that it blocks the activity of the ganglia, clusters of nerve cells that help transmit signals throughout the nervous system. Chlorisondamine has been used in the past to treat conditions such as hypertension (high blood pressure) and certain types of muscle spasms. However, it is not commonly used today due to the availability of safer and more effective treatment options.

Chlorisondamine is a synthetic compound that was first synthesized in the 1940s. It has a number of effects on the body, including decreasing heart rate and reducing the force of heart contractions. It also causes relaxation of smooth muscle tissue, which can lead to decreased blood pressure and reduced secretions from glands such as the sweat glands and salivary glands.

Like other anticholinergic drugs, chlorisondamine can cause a number of side effects, including dry mouth, blurred vision, constipation, difficulty urinating, and dizziness. It can also cause more serious side effects such as rapid heartbeat, confusion, hallucinations, and seizures. Chlorisondamine should be used with caution and only under the close supervision of a healthcare professional.

Ganglionic blockers are a type of medication that blocks the activity of the ganglia, which are clusters of nerve cells located outside the central nervous system. These medications work by blocking the transmission of nerve impulses between the ganglia and the effector organs they innervate, such as muscles or glands.

Ganglionic blockers were once used in the treatment of various conditions, including hypertension (high blood pressure), peptic ulcers, and certain types of pain. However, their use has largely been abandoned due to their significant side effects, which can include dry mouth, blurred vision, constipation, difficulty urinating, and dizziness or lightheadedness upon standing.

There are two main types of ganglionic blockers: nicotinic and muscarinic. Nicotinic ganglionic blockers block the action of acetylcholine at nicotinic receptors in the ganglia, while muscarinic ganglionic blockers block the action of acetylcholine at muscarinic receptors in the ganglia.

Examples of ganglionic blockers include trimethaphan, hexamethonium, and pentolinium. These medications are typically administered intravenously in a hospital setting due to their short duration of action and potential for serious side effects.

Nicotinic antagonists are a class of drugs that block the action of nicotine at nicotinic acetylcholine receptors (nAChRs). These receptors are found in the nervous system and are activated by the neurotransmitter acetylcholine, as well as by nicotine. When nicotine binds to these receptors, it can cause the release of various neurotransmitters, including dopamine, which can lead to rewarding effects and addiction.

Nicotinic antagonists work by binding to nAChRs and preventing nicotine from activating them. This can help to reduce the rewarding effects of nicotine and may be useful in treating nicotine addiction. Examples of nicotinic antagonists include mecamylamine, varenicline, and cytisine.

It's important to note that while nicotinic antagonists can help with nicotine addiction, they can also have side effects, such as nausea, vomiting, and abnormal dreams. Additionally, some people may experience more serious side effects, such as seizures or cardiovascular problems, so it's important to use these medications under the close supervision of a healthcare provider.

Mecamylamine is a non-competitive antagonist at nicotinic acetylcholine receptors. It is primarily used in the treatment of hypertension (high blood pressure) that is resistant to other medications, although it has been largely replaced by newer drugs with fewer side effects.

Mecamylamine works by blocking the action of acetylcholine, a neurotransmitter that activates nicotinic receptors and plays a role in regulating blood pressure. By blocking these receptors, mecamylamine can help to reduce blood vessel constriction and lower blood pressure.

It is important to note that mecamylamine can have significant side effects, including dry mouth, dizziness, blurred vision, constipation, and difficulty urinating. It may also cause orthostatic hypotension (a sudden drop in blood pressure when standing up), which can increase the risk of falls and fractures in older adults. As a result, mecamylamine is typically used as a last resort in patients with severe hypertension who have not responded to other treatments.

Nicotine is defined as a highly addictive psychoactive alkaloid and stimulant found in the nightshade family of plants, primarily in tobacco leaves. It is the primary component responsible for the addiction to cigarettes and other forms of tobacco. Nicotine can also be produced synthetically.

When nicotine enters the body, it activates the release of several neurotransmitters such as dopamine, norepinephrine, and serotonin, leading to feelings of pleasure, stimulation, and relaxation. However, with regular use, tolerance develops, requiring higher doses to achieve the same effects, which can contribute to the development of nicotine dependence.

Nicotine has both short-term and long-term health effects. Short-term effects include increased heart rate and blood pressure, increased alertness and concentration, and arousal. Long-term use can lead to addiction, lung disease, cardiovascular disease, and reproductive problems. It is important to note that nicotine itself is not the primary cause of many tobacco-related diseases, but rather the result of other harmful chemicals found in tobacco smoke.

Autonomic ganglia are collections of neurons located outside the central nervous system (CNS) that are a part of the autonomic nervous system (ANS). The ANS is responsible for controlling various involuntary physiological functions such as heart rate, digestion, respiratory rate, pupillary response, urination, and sexual arousal.

Autonomic ganglia receive inputs from preganglionic neurons, whose cell bodies are located in the CNS, and send outputs to effector organs through postganglionic neurons. The autonomic ganglia can be divided into two main subsystems: the sympathetic and parasympathetic systems.

Sympathetic ganglia are typically located close to the spinal cord and receive inputs from preganglionic neurons whose cell bodies are located in the thoracic and lumbar regions of the spinal cord. The postganglionic neurons of the sympathetic system release noradrenaline (also known as norepinephrine) as their primary neurotransmitter, which acts on effector organs to produce a range of responses such as increasing heart rate and blood pressure, dilating pupils, and promoting glucose mobilization.

Parasympathetic ganglia are typically located closer to the target organs and receive inputs from preganglionic neurons whose cell bodies are located in the brainstem and sacral regions of the spinal cord. The postganglionic neurons of the parasympathetic system release acetylcholine as their primary neurotransmitter, which acts on effector organs to produce a range of responses such as decreasing heart rate and blood pressure, constricting pupils, and promoting digestion and urination.

Overall, autonomic ganglia play a critical role in regulating various physiological functions that are essential for maintaining homeostasis in the body.

Dextroamphetamine is a central nervous system stimulant that is used in the treatment of attention deficit hyperactivity disorder (ADHD) and narcolepsy. It works by increasing the levels of certain neurotransmitters, such as dopamine and norepinephrine, in the brain. Dextroamphetamine is available as a prescription medication and is sold under various brand names, including Adderall and Dexedrine. It is important to use this medication only as directed by a healthcare professional, as it can have potentially serious side effects if used improperly.

I'm sorry for any confusion, but "Nephropidae" is not a medical term. It is actually a taxonomic category in zoology, specifically a family of decapod crustaceans that includes lobsters and crayfish. If you have a question related to biology or veterinary medicine, I'd be happy to try to help with that.

Synaptosomes are subcellular structures that can be isolated from the brain tissue. They are formed during the fractionation process of brain homogenates and consist of intact presynaptic terminals, including the synaptic vesicles, mitochondria, and cytoskeletal elements. Synaptosomes are often used in neuroscience research to study the biochemical properties and functions of neuronal synapses, such as neurotransmitter release, uptake, and metabolism.

Nicotinic receptors are a type of ligand-gated ion channel receptor that are activated by the neurotransmitter acetylcholine and the alkaloid nicotine. They are widely distributed throughout the nervous system and play important roles in various physiological processes, including neuronal excitability, neurotransmitter release, and cognitive functions such as learning and memory. Nicotinic receptors are composed of five subunits that form a ion channel pore, which opens to allow the flow of cations (positively charged ions) when the receptor is activated by acetylcholine or nicotine. There are several subtypes of nicotinic receptors, which differ in their subunit composition and functional properties. These receptors have been implicated in various neurological disorders, including Alzheimer's disease, Parkinson's disease, and schizophrenia.

The neostriatum is a component of the basal ganglia, a group of subcortical nuclei in the brain that are involved in motor control, procedural learning, and other cognitive functions. It is composed primarily of two types of neurons: medium spiny neurons and aspiny interneurons. The neostriatum receives input from various regions of the cerebral cortex and projects to other parts of the basal ganglia, forming an important part of the cortico-basal ganglia-thalamo-cortical loop.

In medical terminology, the neostriatum is often used interchangeably with the term "striatum," although some sources reserve the term "neostriatum" for the caudate nucleus and putamen specifically, while using "striatum" to refer to the entire structure including the ventral striatum (also known as the nucleus accumbens).

Damage to the neostriatum has been implicated in various neurological conditions, such as Huntington's disease and Parkinson's disease.

Intraventricular injections are a type of medical procedure where medication is administered directly into the cerebral ventricles of the brain. The cerebral ventricles are fluid-filled spaces within the brain that contain cerebrospinal fluid (CSF). This procedure is typically used to deliver drugs that target conditions affecting the central nervous system, such as infections or tumors.

Intraventricular injections are usually performed using a thin, hollow needle that is inserted through a small hole drilled into the skull. The medication is then injected directly into the ventricles, allowing it to circulate throughout the CSF and reach the brain tissue more efficiently than other routes of administration.

This type of injection is typically reserved for situations where other methods of drug delivery are not effective or feasible. It carries a higher risk of complications, such as bleeding, infection, or damage to surrounding tissues, compared to other routes of administration. Therefore, it is usually performed by trained medical professionals in a controlled clinical setting.

The superior cervical ganglion is a part of the autonomic nervous system, specifically the sympathetic division. It is a collection of nerve cell bodies (ganglion) that are located in the neck region (cervical) and is formed by the fusion of several smaller ganglia.

This ganglion is responsible for providing innervation to various structures in the head and neck, including the eyes, scalp, face muscles, meninges (membranes surrounding the brain and spinal cord), and certain glands such as the salivary and sweat glands. It does this through the postganglionic fibers that branch off from the ganglion and synapse with target organs or tissues.

The superior cervical ganglion is an essential component of the autonomic nervous system, which controls involuntary physiological functions such as heart rate, blood pressure, digestion, and respiration.

Brain chemistry refers to the chemical processes that occur within the brain, particularly those involving neurotransmitters, neuromodulators, and neuropeptides. These chemicals are responsible for transmitting signals between neurons (nerve cells) in the brain, allowing for various cognitive, emotional, and physical functions.

Neurotransmitters are chemical messengers that transmit signals across the synapse (the tiny gap between two neurons). Examples of neurotransmitters include dopamine, serotonin, norepinephrine, GABA (gamma-aminobutyric acid), and glutamate. Each neurotransmitter has a specific role in brain function, such as regulating mood, motivation, attention, memory, and movement.

Neuromodulators are chemicals that modify the effects of neurotransmitters on neurons. They can enhance or inhibit the transmission of signals between neurons, thereby modulating brain activity. Examples of neuromodulators include acetylcholine, histamine, and substance P.

Neuropeptides are small protein-like molecules that act as neurotransmitters or neuromodulators. They play a role in various physiological functions, such as pain perception, stress response, and reward processing. Examples of neuropeptides include endorphins, enkephalins, and oxytocin.

Abnormalities in brain chemistry can lead to various neurological and psychiatric conditions, such as depression, anxiety disorders, schizophrenia, Parkinson's disease, and Alzheimer's disease. Understanding brain chemistry is crucial for developing effective treatments for these conditions.

Nicotinic agonists are substances that bind to and activate nicotinic acetylcholine receptors (nAChRs), which are ligand-gated ion channels found in the nervous system of many organisms, including humans. These receptors are activated by the endogenous neurotransmitter acetylcholine and the exogenous compound nicotine.

When a nicotinic agonist binds to the receptor, it triggers a conformational change that leads to the opening of an ion channel, allowing the influx of cations such as calcium, sodium, and potassium. This ion flux can depolarize the postsynaptic membrane and generate or modulate electrical signals in excitable tissues, such as neurons and muscles.

Nicotinic agonists have various therapeutic and recreational uses, but they can also produce harmful effects, depending on the dose, duration of exposure, and individual sensitivity. Some examples of nicotinic agonists include:

1. Nicotine: A highly addictive alkaloid found in tobacco plants, which is the prototypical nicotinic agonist. It is used in smoking cessation therapies, such as nicotine gum and patches, but it can also lead to dependence and various health issues when consumed through smoking or vaping.
2. Varenicline: A medication approved for smoking cessation that acts as a partial agonist of nAChRs. It reduces the rewarding effects of nicotine and alleviates withdrawal symptoms, helping smokers quit.
3. Rivastigmine: A cholinesterase inhibitor used to treat Alzheimer's disease and other forms of dementia. It increases the concentration of acetylcholine in the synaptic cleft, enhancing its activity at nicotinic receptors and improving cognitive function.
4. Succinylcholine: A neuromuscular blocking agent used during surgical procedures to induce paralysis and facilitate intubation. It acts as a depolarizing nicotinic agonist, causing transient muscle fasciculations followed by prolonged relaxation.
5. Curare and related compounds: Plant-derived alkaloids that act as competitive antagonists of nicotinic receptors. They are used in anesthesia to induce paralysis and facilitate mechanical ventilation during surgery.

In summary, nicotinic agonists are substances that bind to and activate nicotinic acetylcholine receptors, leading to various physiological responses. These compounds have diverse applications in medicine, from smoking cessation therapies to treatments for neurodegenerative disorders and anesthesia. However, they can also pose risks when misused or abused, as seen with nicotine addiction and the potential side effects of certain medications.

Immobilization is a medical term that refers to the restriction of normal mobility or motion of a body part, usually to promote healing and prevent further injury. This is often achieved through the use of devices such as casts, splints, braces, slings, or traction. The goal of immobilization is to keep the injured area in a fixed position so that it can heal properly without additional damage. It may be used for various medical conditions, including fractures, dislocations, sprains, strains, and soft tissue injuries. Immobilization helps reduce pain, minimize swelling, and protect the injured site from movement that could worsen the injury or impair healing.

... has been shown to form noncovalent complexes with various biomolecules including sphingomyelin and other ... Chlorisondamine is a nicotinic acetylcholine receptor antagonist that produces both neuronal and ganglionic blockade. ... Woods AS, Moyer SC, Wang HY, Wise RA (2003). "Interaction of chlorisondamine with the neuronal nicotinic acetylcholine receptor ...
... chlorisondamine chloride (INN) chlormadinone (INN) chlormerodrin (197 Hg) (INN) chlormerodrin (INN) chlormethine (INN) ...
... chlorisondamine MeSH D03.438.473.231 - cytochalasins MeSH D03.438.473.231.370 - cytochalasin b MeSH D03.438.473.231.450 - ...
... chlorisondamine MeSH D02.092.877.883.277 - chlormequat MeSH D02.092.877.883.333 - choline MeSH D02.092.877.883.333.100 - ... chlorisondamine MeSH D02.675.276.207 - chlormequat MeSH D02.675.276.210 - (4-(m-chlorophenylcarbamoyloxy)-2-butynyl) ...
... hexamethonium pentolinium mecamylamine trimetaphan tubocurarine pempidine benzohexonium chlorisondamine pentamine Nicotinic ...
Chlorisondamine has been shown to form noncovalent complexes with various biomolecules including sphingomyelin and other ... Chlorisondamine is a nicotinic acetylcholine receptor antagonist that produces both neuronal and ganglionic blockade. ... Woods AS, Moyer SC, Wang HY, Wise RA (2003). "Interaction of chlorisondamine with the neuronal nicotinic acetylcholine receptor ...
... chlorisondamine). Dexamethasone did not alter neural input to the myocardium (its actions were not reversed by ganglionic ...
Treatment of the animals with a nicotinic (chlorisondamine) or a muscarinic (atropine) receptor antagonist did not change the ... The capsaicin-induced elevation of junB mRNA levels was not influenced by chlorisondamine or atropine alone, whereas both ... Pretreatment of the rats with chlorisondamine alone or in combination with atropine diminished the capsaicin-induced increase ...
Chlorisondamine D3.438.473.193 D3.438.513.249. Chlorthalidone D3.438.513.750.500. Cholangiopancreatography, Magnetic Resonance ...
Chlorisondamine D3.438.473.193 D3.438.513.249. Chlorthalidone D3.438.513.750.500. Cholangiopancreatography, Magnetic Resonance ...
Chlorisondamine, Mecamyamine, and Pentolinium Tartrate Digital Record ...
... ganglionic blockade with chlorisondamine. In conclusion, intrauterine L-NAME exposure is followed by the impaired development ...
Chlorisondamine D3.438.473.193 D3.438.513.249. Chlorthalidone D3.438.513.750.500. Cholangiopancreatography, Magnetic Resonance ...
Chlorisondamine / pharmacology Actions. * Search in PubMed * Search in MeSH * Add to Search ...
Chlorisondamine (MeSH Term). *Chlorothiazide (MeSH Term). *Chlorthalidone (MeSH Term). *cicletanine (Supplementary Concept) ...
Chlorisondamine (substance). Code System Preferred Concept Name. Chlorisondamine (substance). Concept Status. Published. ...
Chlorisondamine Chloride Narrower Concept UI. M0004146. Registry Number. 7B58W7756G. Terms. Chlorisondamine Chloride Preferred ... Chlorisondamine Chloride Chlorisondamine Dichloride Ecolid Pharm Action. Antihypertensive Agents. Ganglionic Blockers. ... Chlorisondamine Preferred Term Term UI T007867. Date01/01/1999. LexicalTag NON. ThesaurusID ... Chlorisondamine Preferred Concept UI. M0004145. Registry Number. JD3M24F66I. Related Numbers. 69-27-2. 7701-62-4. 7B58W7756G. ...
Chlorisondamine - Pharmacology [32A], 1954-58, Box: 12, Folder: 24. Edward D. Freis Papers, MS C 550. Archives and Modern ... Chlorisondamine - Pharmacology [32A], 1954-58, Box: 12, Folder: 24. Edward D. Freis Papers, MS C 550. Archives and Modern ...
Chlorisondamine Chloride Narrower Concept UI. M0004146. Registry Number. 7B58W7756G. Terms. Chlorisondamine Chloride Preferred ... Chlorisondamine Chloride Chlorisondamine Dichloride Ecolid Pharm Action. Antihypertensive Agents. Ganglionic Blockers. ... Chlorisondamine Preferred Term Term UI T007867. Date01/01/1999. LexicalTag NON. ThesaurusID ... Chlorisondamine Preferred Concept UI. M0004145. Registry Number. JD3M24F66I. Related Numbers. 69-27-2. 7701-62-4. 7B58W7756G. ...
... chlorisondamine chloride, E0300913,Chlorguanid,chloroguanide, E0300927,Aminazine,chlorpromazine, E0300929,Contomin, ...
of chlorisondamine, or 10 mg. of pentolinium tartrate. For convenience in dispensing, the drugs were manufactured in 1, 5, and ... Chlorisondamine therapy was associated with more frequent disturb- ances of visual accommodation, while mec- amylamine produced ... In the other, severe diarrhea occurred each of three times the patient was given reserpine-chlorisond- amine. There was a ... Thus, 20% of the patients on chlorisondamine required sunglasses while these were needed in only 12% of the patients on the ...
Chlorisondamine D3.438.473.193 D3.438.513.249. Chlorthalidone D3.438.513.750.500. Cholangiopancreatography, Magnetic Resonance ...
Interaction of Chlorisondamine with the Neuronal Nicotinic Acetylcholine Receptor. H.-Y.J. Wang, R.A. Wise and A.S. Woods. ...
Chlorisondamine, Mecamylamine, and Pentolinium Tartrate. Contributor(s):. Veterans Administration Cooperative Study Group on ...
Neurogenic pressor activity assessed by the ganglionic blocker chlorisondamine was greater at 7 days of OVLT activation versus ... vasopressin but eliminated by the ganglionic blocker chlorisondamine. Second, optogenetic activation of OVLT neurons ...
C1741 7902N03BH0 CHLORINDANOL C77037 4R7X1O2820 CHLORINE C68243 JD3M24F66I CHLORISONDAMINE C83619 7B58W7756G CHLORISONDAMINE ...
Pretreatment with the ganglionic blocker chlorisondamine (1 and 3 mg.kg(-1) ) antagonized the increases in BP and HR produced ... Pretreatment with the ganglionic blocker chlorisondamine (1 and 3 mg.kg(-1) ) antagonized the increases in BP and HR produced ... effect of BMPEA was reversed by the α-adrenergic antagonist prazosin but not the ganglionic blocker chlorisondamine. ... effect of BMPEA was reversed by the α-adrenergic antagonist prazosin but not the ganglionic blocker chlorisondamine. ...
A16.331.200 Chlorisondamine D3.438.473.193 D3.438.513.249 Chlorthalidone D3.438.513.750.500 Cholangiopancreatography, Magnetic ...
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