A GAMMA-AMINOBUTYRIC ACID derivative that is a specific agonist of GABA-B RECEPTORS. It is used in the treatment of MUSCLE SPASTICITY, especially that due to SPINAL CORD INJURIES. Its therapeutic effects result from actions at spinal and supraspinal sites, generally the reduction of excitatory transmission.
Endogenous compounds and drugs that bind to and activate GABA-B RECEPTORS.
Endogenous compounds and drugs that bind to and activate GAMMA-AMINOBUTYRIC ACID receptors (RECEPTORS, GABA).
A heterogeneous group of drugs used to produce muscle relaxation, excepting the neuromuscular blocking agents. They have their primary clinical and therapeutic uses in the treatment of muscle spasm and immobility associated with strains, sprains, and injuries of the back and, to a lesser degree, injuries to the neck. They have been used also for the treatment of a variety of clinical conditions that have in common only the presence of skeletal muscle hyperactivity, for example, the muscle spasms that can occur in MULTIPLE SCLEROSIS. (From Smith and Reynard, Textbook of Pharmacology, 1991, p358)
A subset of GABA RECEPTORS that signal through their interaction with HETEROTRIMERIC G-PROTEINS.
A form of muscle hypertonia associated with upper MOTOR NEURON DISEASE. Resistance to passive stretch of a spastic muscle results in minimal initial resistance (a "free interval") followed by an incremental increase in muscle tone. Tone increases in proportion to the velocity of stretch. Spasticity is usually accompanied by HYPERREFLEXIA and variable degrees of MUSCLE WEAKNESS. (From Adams et al., Principles of Neurology, 6th ed, p54)
Implanted fluid propulsion systems with self-contained power source for providing long-term controlled-rate delivery of drugs such as chemotherapeutic agents or analgesics. Delivery rate may be externally controlled or osmotically or peristatically controlled with the aid of transcutaneous monitoring.
Drugs that bind to but do not activate GABA-B RECEPTORS thereby blocking the actions of endogenous or exogenous GABA-B RECEPTOR AGONISTS.
The sodium salt of 4-hydroxybutyric acid. It is used for both induction and maintenance of ANESTHESIA.
A neurotoxic isoxazole isolated from species of AMANITA. It is obtained by decarboxylation of IBOTENIC ACID. Muscimol is a potent agonist of GABA-A RECEPTORS and is used mainly as an experimental tool in animal and tissue studies.
Introduction of therapeutic agents into the spinal region using a needle and syringe.
Drugs that bind to but do not activate GABA RECEPTORS, thereby blocking the actions of endogenous GAMMA-AMINOBUTYRIC ACID and GABA RECEPTOR AGONISTS.
Inorganic or organic derivatives of phosphinic acid, H2PO(OH). They include phosphinates and phosphinic acid esters.
The most common inhibitory neurotransmitter in the central nervous system.
An isoquinoline alkaloid obtained from Dicentra cucullaria and other plants. It is a competitive antagonist for GABA-A receptors.
Cell surface proteins which bind GAMMA-AMINOBUTYRIC ACID and contain an integral membrane chloride channel. Each receptor is assembled as a pentamer from a pool of at least 19 different possible subunits. The receptors belong to a superfamily that share a common CYSTEINE loop.
Organic compounds that contain phosphorus as an integral part of the molecule. Included under this heading is broad array of synthetic compounds that are used as PESTICIDES and DRUGS.
Substances used for their pharmacological actions on GABAergic systems. GABAergic agents include agonists, antagonists, degradation or uptake inhibitors, depleters, precursors, and modulators of receptor function.
The administration of medication by insertion of a tiny needle or catheter into the spinal sac or epidural cavity.
Cell-surface proteins that bind GAMMA-AMINOBUTYRIC ACID with high affinity and trigger changes that influence the behavior of cells. GABA-A receptors control chloride channels formed by the receptor complex itself. They are blocked by bicuculline and usually have modulatory sites sensitive to benzodiazepines and barbiturates. GABA-B receptors act through G-proteins on several effector systems, are insensitive to bicuculline, and have a high affinity for L-baclofen.
Amino acids with uncharged R groups or side chains.
An involuntary contraction of a muscle or group of muscles. Spasms may involve SKELETAL MUSCLE or SMOOTH MUSCLE.
Stones in the URINARY BLADDER; also known as vesical calculi, bladder stones, or cystoliths.
Endogenous compounds and drugs that bind to and activate GABA-A RECEPTORS.
Habitual moderation in the indulgence of a natural appetite, especially but not exclusively the consumption of alcohol.
Non-consumption of ALCOHOLIC BEVERAGES.
A primary, chronic disease with genetic, psychosocial, and environmental factors influencing its development and manifestations. The disease is often progressive and fatal. It is characterized by impaired control over drinking, preoccupation with the drug alcohol, use of alcohol despite adverse consequences, and distortions in thinking, most notably denial. Each of these symptoms may be continuous or periodic. (Morse & Flavin for the Joint Commission of the National Council on Alcoholism and Drug Dependence and the American Society of Addiction Medicine to Study the Definition and Criteria for the Diagnosis of Alcoholism: in JAMA 1992;268:1012-4)
Substances interfering with the metabolism of ethyl alcohol, causing unpleasant side effects thought to discourage the drinking of alcoholic beverages. Alcohol deterrents are used in the treatment of alcoholism.
Behaviors associated with the ingesting of alcoholic beverages, including social drinking.
An organization of self-proclaimed alcoholics who meet frequently to reinforce their practice of abstinence.
Solid dosage forms, of varying weight, size, and shape, which may be molded or compressed, and which contain a medicinal substance in pure or diluted form. (Dorland, 28th ed)
Drugs whose drug name is not protected by a trademark. They may be manufactured by several companies.
An autoimmune disorder mainly affecting young adults and characterized by destruction of myelin in the central nervous system. Pathologic findings include multiple sharply demarcated areas of demyelination throughout the white matter of the central nervous system. Clinical manifestations include visual loss, extra-ocular movement disorders, paresthesias, loss of sensation, weakness, dysarthria, spasticity, ataxia, and bladder dysfunction. The usual pattern is one of recurrent attacks followed by partial recovery (see MULTIPLE SCLEROSIS, RELAPSING-REMITTING), but acute fulminating and chronic progressive forms (see MULTIPLE SCLEROSIS, CHRONIC PROGRESSIVE) also occur. (Adams et al., Principles of Neurology, 6th ed, p903)
Inflammation of the connective and adipose tissues surrounding the KIDNEY.
Errors in prescribing, dispensing, or administering medication with the result that the patient fails to receive the correct drug or the indicated proper drug dosage.
A medical specialty concerned with maintaining health and providing medical care to children from birth to adolescence.
Institutions specializing in the care of cancer patients.
Voluntary cooperation of the patient in taking drugs or medicine as prescribed. This includes timing, dosage, and frequency.
Studies used to test etiologic hypotheses in which inferences about an exposure to putative causal factors are derived from data relating to characteristics of persons under study or to events or experiences in their past. The essential feature is that some of the persons under study have the disease or outcome of interest and their characteristics are compared with those of unaffected persons.
An epileptic syndrome characterized by the triad of infantile spasms, hypsarrhythmia, and arrest of psychomotor development at seizure onset. The majority present between 3-12 months of age, with spasms consisting of combinations of brief flexor or extensor movements of the head, trunk, and limbs. The condition is divided into two forms: cryptogenic (idiopathic) and symptomatic (secondary to a known disease process such as intrauterine infections; nervous system abnormalities; BRAIN DISEASES, METABOLIC, INBORN; prematurity; perinatal asphyxia; TUBEROUS SCLEROSIS; etc.). (From Menkes, Textbook of Child Neurology, 5th ed, pp744-8)
Recurrent clonic contraction of facial muscles, restricted to one side. It may occur as a manifestation of compressive lesions involving the seventh cranial nerve (FACIAL NERVE DISEASES), during recovery from BELL PALSY, or in association with other disorders. (From Adams et al., Principles of Neurology, 6th ed, p1378)

Neurite outgrowth-regulating properties of GABA and the effect of serum on mouse spinal cord neurons in culture. (1/869)

Time-lapse photography was used to examine the effects of gamma-aminobutyric acid (GABA) on the outgrowth and motility of neurites in cultures from mouse spinal cord. GABA at concentrations of 100, 10 and 1 microM caused significant inhibition of neurite outgrowth and the motility of growth cones was significantly reduced by treatment with 100 and 10 microM GABA. This effect was mimicked by the GABA(B) receptor agonist baclofen, whereas the GABA(A) receptor agonist muscimol had no effect. The effect of GABA on outgrowth and motility seems to be dependent on the type of serum employed. The results reported here were obtained only when heat-inactivated serum was used and not when non heat-inactivated serum was added to the culture medium. They suggest that GABA has a role in the regulation of process outgrowth within the embryonic mouse spinal cord.  (+info)

Carbamazepine facilitates effects of GABA on rat hippocampus slices. (2/869)

AIM: To study the influence of carbamazepine (Car) on GABA effect in hippocampus. METHODS: Evoked potentials were recorded on pyramidal cells in CA1 after stimulation (0.5 Hz, 50 microseconds) to Schaffer collaterals in rat hippocampal slices (350 microns). RESULTS: Car 0.1 and 0.2 mmol.L-1 did not affect field potentials, whereas Car 0.2 mmol.L-1 plus GABA (0.1-1 mmol.L-1) gave rise to a stronger inhibition on field potentials than that of GABA alone. Bicuculline did not reverse Car facilitation on GABA inhibition on field potentials. (-)-Baclofen was more effective in inhibiting field potentials than GABA. Car 0.2 mmol.L-1 plus (-)-baclofen (1-5 mumol.L-1) brought an inhibition stronger than that of (-)-baclofen alone. CONCLUSION: Car facilitates the effects of GABA on pyramidal cells in hippocampal CA1 region, probably related to GABAB receptors.  (+info)

Tonic activation of presynaptic GABAB receptors in the opener neuromuscular junction of crayfish. (3/869)

Release of excitatory transmitter from boutons on crayfish nerve terminals was inhibited by (R,S)-baclofen, an agonist at GABAB receptors. Baclofen had no postsynaptic actions as it reduced quantal content without affecting quantal amplitude. The effect of baclofen increased with concentration producing 18% inhibition at 10 microM; EC50, 50% inhibition at 30 microM; maximal inhibition, 85% at 100 microM and higher. There was no desensitization, even with 200 or 320 microM baclofen. Phaclofen, an antagonist at GABAB receptors, competitively antagonized the inhibitory action of baclofen (KD = 50 microM, equivalent to a pA2 = 4.3 +/- 0.1). Phaclofen on its own at concentrations below 200 microM had no effect on release, whereas at 200 microM phaclofen itself increased the control level of release by 60%, as did 2-hydroxy-saclofen (200 microM), another antagonist at GABAB receptors. This increase was evidently due to antagonism of a persistent level of GABA in the synaptic cleft, since the effect was abolished by destruction of the presynaptic inhibitory fiber, using intra-axonal pronase. We conclude that presynaptic GABAB receptors, with a pharmacological profile similar to that of mammalian GABAB receptors, are involved in the control of transmitter release at the crayfish neuromuscular junction.  (+info)

Role of presynaptic L-type Ca2+ channels in GABAergic synaptic transmission in cultured hippocampal neurons. (4/869)

Using dual whole cell patch-clamp recordings of monosynaptic GABAergic inhibitory postsynaptic currents (IPSCs) in cultured rat hippocampal neurons, we have previously demonstrated posttetanic potentiation (PTP) of IPSCs. Tetanic stimulation of the GABAergic neuron leads to accumulation of Ca2+ in the presynaptic terminals. This enhances the probability of GABA-vesicle release for up to 1 min, which underlies PTP. In the present study, we have examined the effect of altering the probability of release on PTP of IPSCs. Baclofen (10 microM), which depresses presynaptic Ca2+ entry through N- and P/Q-type voltage-dependent Ca2+ channels (VDCCs), caused a threefold greater enhancement of PTP than did reducing [Ca2+]o to 1.2 mM, which causes a nonspecific reduction in Ca2+ entry. This finding prompted us to investigate whether presynaptic L-type VDCCs contribute to the Ca2+ accumulation in the boutons during spike activity. The L-type VDCC antagonist, nifedipine (10 microM), had no effect on single IPSCs evoked at 0.2 Hz but reduced the PTP evoked by a train of 40 Hz for 2 s by 60%. Another L-type VDCC antagonist, isradipine (5 microM), similarly inhibited PTP by 65%. Both L-type VDCC blockers also depressed IPSCs during the stimulation (i.e., they increased tetanic depression). The L-type VDCC "agonist" (-)BayK 8644 (4 microM) had no effect on PTP evoked by a train of 40 Hz for 2 s, which probably saturated the PTP process, but enhanced PTP evoked by a train of 1 s by 91%. In conclusion, the results indicate that L-type VDCCs do not participate in low-frequency synchronous transmitter release, but contribute to presynaptic Ca2+ accumulation during high-frequency activity. This helps maintain vesicle release during tetanic stimulation and also enhances the probability of transmitter release during the posttetanic period, which is manifest as PTP. Involvement of L-type channels in these processes represents a novel presynaptic regulatory mechanism at fast CNS synapses.  (+info)

Interactive effects of the GABABergic modulation of calcium channels and calcium-dependent potassium channels in lamprey. (5/869)

The GABAB-mediated modulation of spinal neurons in the lamprey is investigated in this study. Activation of GABAB receptors reduces calcium currents through both low- (LVA) and high-voltage activated (HVA) calcium channels, which subsequently results in the reduction of the calcium-dependent potassium (KCa) current. This in turn will reduce the peak amplitude of the afterhyperpolarization (AHP). We used the modulatory effects of GABAB receptor activation on N-methyl-D-aspartate (NMDA)-induced, TTX-resistant membrane potential oscillations as an experimental model in which to separate the effects of GABAB receptor activation on LVA calcium channels from that on KCa channels. We show experimentally and by using simulations that a direct effect on LVA calcium channels can account for the effects of GABAB receptor activation on intrinsic membrane potential oscillations to a larger extent than indirect effects mediated via KCa channels. Furthermore, by conducting experiments and simulations on intrinsic membrane potential oscillations, we find that KCa channels may be activated by calcium entering through LVA calcium channels, providing that the decay kinetics of the calcium that enters through LVA calcium channels is not as slow as the calcium entering via NMDA receptors. A combined experimental and computational analysis revealed that the LVA calcium current also contributes to neuronal firing properties.  (+info)

GABA(B) receptor-mediated stimulation of adenylyl cyclase activity in membranes of rat olfactory bulb. (6/869)

Previous studies have shown that GABA(B) receptors facilitate cyclic AMP formation in brain slices likely through an indirect mechanism involving intracellular second messengers. In the present study, we have investigated whether a positive coupling of GABA(B) receptors to adenylyl cyclase could be detected in a cell-free preparation of rat olfactory bulb, a brain region where other Gi/Go-coupled neurotransmitter receptors have been found to stimulate the cyclase activity. The GABA(B) receptor agonist (-)-baclofen significantly increased basal adenylyl cyclase activity in membranes of the granule cell and external plexiform layers, but not in the olfactory nerve-glomerular layer. The adenylyl cyclase stimulation was therefore examined in granule cell layer membranes. The (-)-baclofen stimulation (pD2=4.53) was mimicked by 3-aminopropylphosphinic acid (pD2=4.60) and GABA (pD2=3.56), but not by (+)-baclofen, 3-aminopropylphosphonic acid, muscimol and isoguvacine. The stimulatory effect was counteracted by the GABA(B) receptor antagonists CGP 35348 (pA2=4.31), CGP 55845 A (pA2=7.0) and 2-hydroxysaclofen (pKi=4.22). Phaclofen (1 mM) was inactive. The (-)-baclofen stimulation was not affected by quinacrine, indomethacin, nordihydroguaiaretic acid and staurosporine, but was completely prevented by pertussis toxin and significantly reduced by the alpha subunit of transducin, a betagamma scavenger. The betagamma subunits of transducin stimulated the cyclase activity and this effect was not additive with that produced by (-)-baclofen. In the external plexiform and granule cell layers, but not in the olfactory nerve-glomerular layer, (-)-baclofen enhanced the adenylyl cyclase stimulation elicited by the neuropeptide pituitary adenylate cyclase activating polypeptide (PACAP) 38. Conversely, the adenylyl cyclase activity stimulated by either forskolin or Ca2+/calmodulin-(Ca2+/CaM) was inhibited by (-)-baclofen in all the olfactory bulb layers examined. These data demonstrate that in specific layers of rat olfactory bulb activation of GABA(B) receptors enhances basal and neurotransmitter-stimulated adenylyl cyclase activities by a mechanism involving betagamma subunits of Gi/Go. This positive coupling is associated with a widespread inhibitory effect on forskolin- and Ca2+/CaM-stimulated cyclic AMP formation.  (+info)

Cholinergic and GABAergic regulation of nitric oxide synthesis in the guinea pig ileum. (7/869)

Nitric oxide (NO) synthesis was examined in intact longitudinal muscle-myenteric plexus preparations of the guinea pig ileum by determining the formation of [3H]citrulline during incubation with [3H]arginine. Spontaneous [3H]citrulline production after 30 min was 80-90 dpm/mg, which constituted approximately 1% of the tissue radioactivity. Electrical stimulation (10 Hz) led to a threefold increase in [3H]citrulline formation. Removal of calcium from the medium or addition of NG-nitro-L-arginine strongly inhibited both spontaneous and electrically induced production of [3H]citrulline. TTX reduced the electrically induced but not spontaneous [3H]citrulline formation. The electrically induced formation of [3H]citrulline was diminished by (+)-tubocurarine and mecamylamine and enhanced by scopolamine, which suggests that endogenous ACh inhibits, via muscarinic receptors, and stimulates, via nicotinic receptors, the NO synthesis in the myenteric plexus. The GABAA receptor agonist muscimol and GABA also reduced the electrically evoked formation of [3H]citrulline, whereas baclofen was without effect. Bicuculline antagonized the inhibitory effect of GABA. It is concluded that nitrergic myenteric neurons are equipped with GABAA receptors, which mediate inhibition of NO synthesis.  (+info)

Neuropeptide-mediated facilitation and inhibition of sensory inputs and spinal cord reflexes in the lamprey. (8/869)

The effects of neuromodulators present in the dorsal horn [tachykinins, neuropeptide Y (NPY), bombesin, and GABAB agonists] were studied on reflex responses evoked by cutaneous stimulation in the lamprey. Reflex responses were elicited in an isolated spinal cord preparation by electrical stimulation of the attached tail fin. To be able to separate modulator-induced effects at the sensory level from that at the motor or premotor level, the spinal cord was separated into three pools with Vaseline barriers. The caudal pool contained the tail fin. Neuromodulators were added to this pool to modulate sensory inputs evoked by tail fin stimulation. The middle pool contained high divalent cation or low calcium Ringer to block polysynaptic transmission and thus limit the input to the rostral pool to that from ascending axons that project through the middle pool. Ascending inputs and reflex responses were monitored by making intracellular recordings from motor neurons and extracellular recordings from ventral roots in the rostral pool. The tachykinin neuropeptide substance P, which has previously been shown to potentiate sensory input at the cellular and synaptic levels, facilitated tail fin-evoked synaptic inputs to neurons in the rostral pool and concentration dependently facilitated rostral ventral root activity. Substance P also facilitated the modulatory effects of tail fin stimulation on ongoing locomotor activity in the rostral pool. In contrast, NPY and the GABAB receptor agonist baclofen, both of which have presynaptic inhibitory effects on sensory afferents, reduced the strength of ascending inputs and rostral ventral root responses. We also examined the effects of the neuropeptide bombesin, which is present in sensory axons, at the cellular, synaptic, and reflex levels. As with substance P, bombesin increased tail fin stimulation-evoked inputs and ventral root responses in the rostral pool. These effects were associated with the increased excitability of slowly adapting mechanosensory neurons and the potentiation of glutamatergic synaptic inputs to spinobulbar neurons. These results show the possible behavioral relevance of neuropeptide-mediated modulation of sensory inputs at the cellular and synaptic levels. Given that the types and locations of neuropeptides in the dorsal spinal cord of the lamprey show strong homologies to that of higher vertebrates, these results are presumably relevant to other vertebrate systems.  (+info)

Intrathecal Baclofen Therapy (ITB) is a medical way to treat spasticity, a common symptom of cerebral palsy.Muscle Relaxants - is baclofen controlled substance, baclofen pump spanish, what category of drug is baclofen.Efficacy of intrathecal baclofen therapy in children with intractable spastic cerebral palsy: A randomised controlled trial.Find information and resources for healthcare professionals about Medtronic Intrathecal Baclofen Therapy (ITB Therapy), a treatment option for managing severe.. The purpose of this study is to report the short-term outcome of intrathecal baclofen therapy.Onset time inactive ingredients in baclofen pump training bei spastik.Baclofen acts on the central nervous system to relieve spasms, cramping, and tightness of muscles caused by spasticity in multiple sclerosis.For alcohol dependence spastik baclofen cvz for period pain does help with bladder.. ...
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The present study investigates the effects of centrally or peripherally administered baclofen on gastric acid secretion from pylorus-ligated rats. The influence of baclofen on basal acid secretion from isolated guinea-pig gastric fundus was also evaluated. At all doses employed, intracerebroventricular baclofen significantly decreased acid secretion, this inhibitory action being antagonized by intracerebroventricular phaclofen. Intravenous baclofen induced both gastric inhibitory and excitatory responses at low and high doses, respectively. Intracerebroventricular phaclofen prevented the inhibitory effect, while neither intracerebroventricular nor intravenous phaclofen modified the stimulant action of parenteral baclofen. Both central and parenteral muscimol did not influence gastric acid secretion. Moreover, baclofen or muscimol were without effect on basal acid secretion from isolated guinea-pig gastric fundus, whereas bethanechol caused a marked and concentration-dependent stimulant action. ...
A review of the scientific literature about baclofen overdoses shows that they are uncommon and rarely cause death. This in spite of baclofen being used already for decades to treat millions of people with incurable and often progressive neurological problems such as multiple sclerosis and spinal cord injuries.. The best reviews of baclofen overdoses are those based on review of comprehensive toxicology service databases. These give the truest picture of the spectrum of baclofen overdoses. The other data comes from case reports or reports of small series but will tend to represent more severe or unusual cases.. A 2006 Australian review of baclofen overdoses1 reported on a toxicology database of an unidentified region of Australia with a population of 500,000. A search of their database of presentations from 1992-2003 found 23 baclofen overdoses in these 11 years. Eight overdoses (35%) were ingestions of baclofen alone, three of which required ventilator support. There were no deaths.. The other ...
Baclofen is a muscle relaxer used to treat muscle symptoms caused by multiple sclerosis, including spasm, pain, and stiffness. Includes baclofen side effects, interactions and indications. Also: Baclofen how to order shop, Generic baclofen uk next day, Cost baclofen uk, Purchase now baclofen shop, Online coupon for baclofen, Can you baclofen uk
Background. Severe brain trauma and especially serious brain lesions inducing coma lead to many cases of disability. A large number of these patients (about 30%) present neurovegetative and hypertonic episodes that are associated to a bad vital prognosis and the degree of disability. Several teams including two in France have reported the efficacy of intrathecal baclofen on such neurovegetative episodes that to date have not been able to be treated efficiently.. Objectives. The main objective of this trial is to assess the efficacy of infused intrathecal baclofen on the number of neurovegetative episodes in seriously brain-injured patients. The secondary aims are to evaluate the efficacy of the treatment on hypertonia, to assess changes in waking and treatment safety.. Study design. Double-blind randomized trial on two parallel groups. The second part of the study is open label: both groups receive the experimental treatment.. Intervention. Experimental group: continuous progressive dose of ...
Background. Severe brain trauma and especially serious brain lesions inducing coma lead to many cases of disability. A large number of these patients (about 30%) present neurovegetative and hypertonic episodes that are associated to a bad vital prognosis and the degree of disability. Several teams including two in France have reported the efficacy of intrathecal baclofen on such neurovegetative episodes that to date have not been able to be treated efficiently.. Objectives. The main objective of this trial is to assess the efficacy of infused intrathecal baclofen on the number of neurovegetative episodes in seriously brain-injured patients. The secondary aims are to evaluate the efficacy of the treatment on hypertonia, to assess changes in waking and treatment safety.. Study design. Double-blind randomized trial on two parallel groups. The second part of the study is open label: both groups receive the experimental treatment.. Intervention. Experimental group: continuous progressive dose of ...
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a history of stroke or blood clots.. Using baclofen may increase your risk of developing an ovarian cyst. Talk with your doctor about your specific risk. FDA pregnancy category C. It is not known whether baclofen will harm an unborn baby. Tell your doctor if you are pregnant or plan to become pregnant while using this medication. It is not known whether baclofen passes into breast milk or if it could harm a nursing baby. You should not breast-feed while you are using baclofen. Do not give this medication to a child younger than 12 years old. Older adults may be more sensitive to the effects of this medicine.. Important safety information. This medication may impair your thinking or reactions. Be careful if you drive or do anything that requires you to be alert. Drinking alcohol can increase certain side effects of baclofen. Do not use baclofen at a time when muscle tone is needed to assure safe balance and movement for certain activities. In some situations, it may endanger your physical safety ...
a history of stroke or blood clots.. Using baclofen may increase your risk of developing an ovarian cyst. Talk with your doctor about your specific risk. FDA pregnancy category C. It is not known whether baclofen will harm an unborn baby. Tell your doctor if you are pregnant or plan to become pregnant while using this medication. It is not known whether baclofen passes into breast milk or if it could harm a nursing baby. You should not breast-feed while you are using baclofen. Do not give this medication to a child younger than 12 years old. Older adults may be more sensitive to the effects of this medicine.. Important safety information. This medication may impair your thinking or reactions. Be careful if you drive or do anything that requires you to be alert. Drinking alcohol can increase certain side effects of baclofen. Do not use baclofen at a time when muscle tone is needed to assure safe balance and movement for certain activities. In some situations, it may endanger your physical safety ...
Check this out to Drugs. Stopping baclofen suddenly may cause withdrawal symptoms that include seizures. Once an intrathecal baclofen pump is in place and your dose is stabilised, the aim is to reduce and possibly stop any other anti-spasticity medication you are taking. In some cases, inpatient rehabilitation is needed to adjust the pump and perform functional training before returning home. Unless otherwise indicated cease neurological observations after 24 hours. Postural headaches. Surgical exploration of pump and catheter. Children should be of sufficient body mass to accommodate the implantable pump for chronic infusion. Spasticity is a movement disorder that can occur in conditions which affect the brain or the spinal cord, such as multiple sclerosisstrokebalofen palsyspinal cord injuryor brain injury. Spasticity management: a practical multidisciplinary guide. With oral use Manufacturer advises use with caution-no information available. Rare or very rare With oral use abdominal pain ; ...
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Baclofen may impair your thinking or reactions. Be careful if you drive or do anything that requires you to be alert. Drinking alcohol can increase certain side effects of baclofen. Do not use baclofen at a time when muscle tone is needed to assure safe balance and movement for certain activities. In some situations, it may endanger your physical safety to be in a state of reduced muscle tone. You may have withdrawal symptoms such as seizures or hallucinations, when you stop using baclofen after using it over a long period of time. Do not stop using baclofen without first talking to your doctor. You may need to use less and less before you stop the medication completely. Using baclofen may increase your risk of developing an ovarian cyst. Talk with your doctor about your specific risk. You should not use baclofen if you are allergic to it. To make sure you can safely take baclofen, tell your doctor if you have any of these other conditions: kidney disease; epilepsy or other seizure disorder; or ...
Its been 11 years since 19-year-old Taylor Cunningham suffered an AVM rupture, which caused a hemorrhage in her brain and left Taylor unable to walk. Just a young girl at the time, Taylor had to undergo several surgeries. Yet it was the severe spasticity that caused Taylor the most pain, a constant presence in her life for months.. Taylors mother, Dori, recalled doctors initial attempts to treat her daughters spasticity with oral baclofen.. It wasnt helping at all, Dori said. By the time it gets to your system, youve already lost 50 percent of your dosage.. To Dori, 50 percent wasnt good enough. Since the oral baclofen had little effect on Taylors spasticity, Dori and staff at Mary Free Bed Rehabilitation Hospital decided to try the baclofen pump. A device surgically implanted in the lower abdominal area with a catheter running to the spine, the baclofen pump delivers medication directly to the place that needs it most.. Its immediate, Dori said of the pumps effect. It really ...
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Baclofen pump facts The baclofen pump is used to provide medication directly to the spinal cord, typically baclofen, when the oral dose exceeds the recommended maximum dosage. It is produced by Medtronic and is about the size of a hockey puck. A catheter runs from the pump along the abdominal wall where it is anchored to the spine and punctures the spinal cord. It is possible for the catheter to be placed above the point of injury. I have mine placed at C-4. It can provide medication both
Baclofen pump facts The baclofen pump is used to provide medication directly to the spinal cord, typically baclofen, when the oral dose exceeds the recommended maximum dosage. It is produced by Medtronic and is about the size of a hockey puck. A catheter runs from the pump along the abdominal wall where it is anchored to the spine and punctures the spinal cord. It is possible for the catheter to be placed above the point of injury. I have mine placed at C-4. It can provide medication both
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Baclofen, 3-amino-propylphosphonic acid (3-APPA), and beta-phenyl-GABA (BPG), each reduced the frequency of spontaneous paroxysmal discharges in rat neocortical slices maintained in Mg2+-free medium, reversibly antagonised by phaclofen and 4-amino-butylphosphonic acid (4-ABPA). At lower concentrations, not influencing the discharges, both 3-APPA and BPG also reversibly antagonised this action of baclofen. However, des-chloro-phaclofen was inactive. Thus, phaclofen and 4-ABPA are GABAB-receptor antagonists in neocortex, whereas both 3-APPA and BPG have partial agonist/antagonist activity at cortical GABAB-receptors.
We have investigated the regulation of hormone secretion from rat pancreatic islets by the GABAB receptors (GABABRs). Inclusion of the specific GABABR antagonist CGP 55845 in the extracellular medium increased glucose-stimulated insulin secretion 1.6-fold but did not affect the release of glucagon and somatostatin. Conversely, addition of the GABABR agonist baclofen inhibited glucose-stimulated insulin secretion by approximately 60%. Using RT-PCR, transcription of GABABR1a-c,f and GABABR2 subunits was detected in beta-cells. Measurements of membrane currents and cell capacitance were applied to single beta-cells to investigate the mechanisms by which GABABR activation inhibits insulin secretion. In perforated-patch measurements, baclofen inhibited exocytosis elicited by 500-ms voltage-clamp depolarizations to 0 mV by | or = 80% and voltage-gated Ca2+ entry by only approximately 30%. Both effects were concentration-dependent with IC50 values of approximately 2 microm. The inhibitory action of baclofen
a history of stroke or blood clots.. Using baclofen may increase your risk of developing an ovarian cyst. Talk with your doctor about your specific risk. FDA pregnancy category C. It is not known whether baclofen will harm an unborn baby. Tell your doctor if you are pregnant or plan to become pregnant while using this medication. It is not known whether baclofen passes into breast milk or if it could harm a nursing baby. You should not breast-feed while you are using baclofen. Do not give this medication to a child younger than 12 years old. Older adults may be more sensitive to the effects of this medicine.. Important safety information. This medication may impair your thinking or reactions. Be careful if you drive or do anything that requires you to be alert. Drinking alcohol can increase certain side effects of baclofen. Do not use baclofen at a time when muscle tone is needed to assure safe balance and movement for certain activities. In some situations, it may endanger your physical safety ...
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See full prescribing information for complete boxed warning. Abrupt discontinuation of intrathecal baclofen, regardless of the cause, has resulted in sequelae that include high fever, altered mental status, exaggerated rebound spasticity, and muscle rigidity, that in rare cases has advanced to rhabdomyolysis, multiple organ-system failure and death.. Prevention of abrupt discontinuation of intrathecal baclofen requires careful attention to programming and monitoring of the infusion system, refill scheduling and procedures, and pump alarms. Patients and caregivers should be advised of the importance of keeping scheduled refill visits and should be educated on the early symptoms of baclofen withdrawal. Special attention should be given to patients at apparent risk (e.g. spinal cord injuries at T-6 or above, communication difficulties, history of withdrawal symptoms from oral or intrathecal baclofen). Consult the technical manual of the implantable infusion system for additional post-implant ...
See full prescribing information for complete boxed warning. Abrupt discontinuation of intrathecal baclofen, regardless of the cause, has resulted in sequelae that include high fever, altered mental status, exaggerated rebound spasticity, and muscle rigidity, that in rare cases has advanced to rhabdomyolysis, multiple organ-system failure and death.. Prevention of abrupt discontinuation of intrathecal baclofen requires careful attention to programming and monitoring of the infusion system, refill scheduling and procedures, and pump alarms. Patients and caregivers should be advised of the importance of keeping scheduled refill visits and should be educated on the early symptoms of baclofen withdrawal. Special attention should be given to patients at apparent risk (e.g. spinal cord injuries at T-6 or above, communication difficulties, history of withdrawal symptoms from oral or intrathecal baclofen). Consult the technical manual of the implantable infusion system for additional post-implant ...
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Buy Baclofen Online! Baclofen was originally designed in 1960 to treat epilepsy. Baclofen is FDA-approved for the management of reversible spasticity, particularly for the relief of flexor spasms, clonus, and concomitant pain, common sequelae of spinal cord lesions and multiple sclerosis.
Buy Baclofen Online! Baclofen is a muscle relaxer and an antispastic agent. Baclofen is sometimes used to treat muscle spasms and other symptoms in people with injury or disease of the spinal cord.
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Baclofen is a GABA agonist specific for GABA-B receptors. Baclofen is a synthetic chlorophenyl-butanoic acid derivative used to treat spasms due to spinal cord damage and multiple sclerosis, muscle-relaxing It acts at spinal and supraspinal sites, reducing excitatory transmission.
Baclofen - The figures are based mostly upon the reports of the native practitioners, who have not had an elaborate medical education, and, therefore, could not be expected to make very reliable diagnoses.
Gamma-aminobutyric acid (GABA) is a major inhibitory neurotransmitter in the central nervous system that affects cellular excitability by opening or closing a variety of ion channels or by modulating...
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The -amino butyric acid (GABA) type B receptors (GABABR) function as chemoattractant receptors in response to GABABR agonists in human neutrophils. pretreatment of cells with type:entrez-protein,attrs:text:CGP52432″,term_id:875421701″,term_text:CGP52432″CGP52432, a GABABR antagonist, blocked such effects. Moreover, baclofen induced Akt phosphorylation was shown to be dependent upon PI-3K and Src kinases. Baclofen failed to stimulate actin polymerization in suspended RBL cells unless exposed to a baclofen gradient. However, baclofen stimulated both actin and tubulin polymerization in adherent RBL-GABABR cells. Blockade of actin and tubulin polymerization by treatment of cells with cytochalasin D or nocodazole respectively, abolished baclofen-mediated chemotaxis. Furthermore, baclofen stimulated Pyk2 and. ...
Your doctor needs to know you medical history, especially about kidney disease, diabetes, seizures, stroke, an unusual or allergic reaction to Baclofen, other medicines, foods, dyes, or preservatives. You should tell you doctor if you are pregnant or trying to get pregnant and if you are breast-feeding. If you suddenly stop taking your medicine, you may develop a severe reaction. The dose will be slowly lowered over time to avoid any side effects and your doctor have to control this process. Follow the advice of your doctor. You may get drowsy or dizzy when you first start taking the medicine or change doses. You should stand or sit up slowly. Do not drive, use machinery, or do anything that may need your attention and can be dangerous. Stop this kind of activity until you know how the medicine affects you ...
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Feeling CARDIO-RESPIRATORY ARREST while using Baclofen? CARDIO-RESPIRATORY ARREST Causes, Patient Concerns and Latest Treatments and Baclofen Reports and Side Effects.
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The time courses of the gamma-aminobutyric acid type B (GABAB) receptor-mediated inhibition of excitatory synaptic transmission and of action potential-evoked calcium currents were studied in hippocampal neurons in vitro with step-like changes of a saturating baclofen concentration. Inhibition media …
New Study Shows Superiority of Intrathecal Baclofen Therapy (ITB Therapy(SM)) Over Oral Medication for the Treatment of Severe Post-Stroke Spasticity
Baclofen is a common drug given to treat spasticity, unfortunately when baclofen is taken in tablet form it may cause side effects. In order to get the baclofen directly to the spinal cord it can be delivered by an implantable pump; this is placed in the abdomen and a catheter delivers the baclofen into the intrathecal space (the space around the spinal cord within the spine). This method uses much smaller amounts of baclofen to treat the spasticity, thus reducing any side effects. If the trials show a beneficial response and the team and patient are in agreement, then a baclofen pump will be fitted. It is important to remember that intrathecal baclofen treatment requires commitment from individuals during the trial and implant phase but also for its ongoing maintenance of regular refills and replacements. Once an individual has a baclofen pump fitted, they will be regularly followed up in the weekly intrathecal baclofen pump clinic. Intrathecal Phenol ...
Spasticity and pain are common features of multiple sclerosis (MS) [6]. Because pain may be relieved by anti-spasticity measures, treatment of spasticity should precede specific pain management. About 20 % of MS patients are either intolerant to oral medications or continue to have significant spasticity despite maximal oral dosage. These patients are optimally managed with continuous intrathecal baclofen infusion (ITB) administered via a surgically implanted programmable pump, a FDA-approved treatment modality [7, 8]. For patients with pain associated
(R)-(-)-Baclofen, Arbaclofen, STX 209, AGI 006 Chemical Names: (R)-Baclofen; Arbaclofen; 69308-37-8; (R)-4-Amino-3-(4-chlorophenyl)butanoic acid; (-)-Baclofen; D-Baclofen Molecular Formula: C10H12ClNO2 Molecular Weight: 213.661 g/mol A GAMMA-AMINOBUTYRIC ACID derivative that is a specific agonist of GABA-B RECEPTORS. It is used in the treatment of MUSCLE SPASTICITY, especially that due to SPINAL CORD INJURIES. Its therapeutic effects result from actions at…
Learn about intrathecal baclofen pump therapy used to treat spasticity symptoms of multiple sclerosis (MS). Surgery, risks, complications, and cost information is provided.
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Baclofen pumps are used as to treat painful back spasms. Receive relief from spinal pain in Colorado with baclofen pump treatment at Colorado Clinic.
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The aim of this study was to determine any possible, baclofen-lactose Maillard reaction products. Granules and tablets of baclofen and lactose were prepared and maintained in heat ovens for a certain time period. The effects of lactose type, addition of magnesium stearate, and water were monitored. Heated lactose and baclofen were analyzed using reverse-phase HPLC. Liquid chromatography tandem mass spectroscopy revealed nominal mass values consistent with baclofen-lactose, early-stage Maillard reaction condensation products (ESMRP). Multiple reaction monitoring confirmed the presence of ESMRP as well. FTIR analysis proved the formation of imine bond. The results indicated that baclofen undergoes a Maillard-type reaction with lactose ...
GABAB receptor-mediated modulation can provide fine control of a cells excitability by multiple mechanisms. Those mechanisms that regulate the voltage-activated conductances in VS-3 neurons can cause decreased excitability and reduction of neurotransmitter release: Reduction of ICa decreases Ca2+ entry during action potentials and increased outwardly rectifying IK may shorten the action potential duration. In addition to modulation of K+ and Ca2+ channels, several other GABAB receptor-mediated mechanisms may be involved, but were not studied here. For example, they can stimulate phospholipase A, inhibit adelylate cyclase, and regulate inositol phosphate hydrolysis (Misgeld et al. 1995). In the mammalian spinal cord and brain, presynaptic GABAB receptor activation has also been shown to modulate glutamate, ACh, and dopamine release (Balon et al. 2002; Li et al. 2002; Towers et al. 2000). We found no evidence of presynaptic GABAB receptors on the efferent neurons surrounding the sensory neurons ...
Inhibitory neurotransmission is mediated primarily by GABA. The metabotropic GABA(B) receptor is a G protein-coupled receptor central to mammalian brain function. Malfunction of GABA(B) receptor has been implicated in several neurological disorders. GABA(B) receptor functions as a heterodimeric asse …
Baclofen is a muscle relaxant and antispastic. Baclofen is useful for the alleviation of signs and symptoms of spasticity resulting from multiple sclerosis, particularly for the relief of flexor spasms and concomitant pain, clonus, and muscular rigidity. Although Baclofen is an analog of the putative inhibitory neurotransmitter gamma-aminobutyric acid (GABA), there is no conclusive evidence that actions on GABA systems are involved in the production of its clinical effects. In studies with animals, Baclofen has been shown to have general CNS depressant properties as indicated by the production of sedation with tolerance, somnolence, ataxia, and respiratory and cardiovascular depression. Baclofen is rapidly and extensively absorbed and eliminated. Absorption may be dose-dependent, being reduced with increasing doses. Baclofen is excreted primarily by the kidney in unchanged form and there is relatively large intersubject variation in absorption and/or elimination ...
Lingford-Hughes A, Durant C, Paterson L, Turton S, Venkataraman A, Wilson S, Myers J, Muthukumaraswamy S, Mick I, Paterson S, Jones T, Nahar L, Cordero R, Nutt Det al., 2018, Using baclofen to explore GABA-B receptor function in alcohol dependence: insights from pharmacokinetic and pharmacodynamic measures, Frontiers in Psychiatry, Vol: 9, ISSN: 1664-0640 Background: The role of GABA-B neurotransmission in addiction has recently received increased attention, with clinical trials indicating that baclofen, a GABA-B receptor agonist, may reduce alcohol consumption, craving and promote abstinence. However, the optimal dose to treat alcohol dependence is unclear with patients requesting and tolerating much higher doses of baclofen, compared with other clinical uses. We assessed the pharmacokinetics and pharmacodynamics (PK/PD) of baclofen to provide insight into GABA-B sensitivity in this patient group, relative to controls.Methods: Male healthy volunteers (controls, n = 12) and abstinent alcohol ...
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After mixed results in human and animal studies, it is unclear whether baclofen and other pharmacotherapies targeting GABAergic neurotransmission can effectively treat the symptoms of FXS, particularly in the absence of biomarker-based strategies to target treatment to subsets of individuals. In this study, we present evidence that (a) sensory hypersensitivity occurs in Fmr1 KO mice, as indexed by increased evoked EEG gamma power, (b) baclofen normalizes this increased evoked EEG gamma power and improves working memory (T-maze performance), and (c) at an individual level, normalization of evoked gamma oscillations was associated with improvement in working memory. Our study also suggests that some Fmr1 KO-related deficits, such as impaired sociability and episodic memory (radial water maze performance), may be impervious to rescue by baclofen. Overall, these findings indicate that racemic baclofen may have benefit for remediating sensory hypersensitivity and some cognitive deficits in FXS and ...
GABAB receptors are the G protein-coupled receptors (GPCRs) for y-aminobutyric acid (GABA), the main inhibitory neurotransmitter in the central nervous system. They are membrane receptors with a seven membrane-spanning domain and are composed of the principal subunits GABAB1 and GABAB2. Activated GABAB receptors regulate G protein-coupled inwardly rectifying K+ channels (GIRKs), voltage-gated Ca2+ channels (VGCCs) and adenylyl cyclases (ACs). The K+ channel tetramerization domain-containing (KCTD) proteins were shown to be auxiliary subunits of GABAB receptors that constitutively bind to the receptor via GABAB2 and regulate receptor signaling in a KCTD-subtype specific manner (Schwenk et al., 2010). The aim of this thesis was to better understand the KCTD12-mediated modulation of GABAB receptor signaling as well as to explore new mechanisms of receptor fine-tuning ...
Figure 3. A, The fEPSP slope is plotted against the first ISI (see Results). Data shown in A-D are averaged from six experiments using 3 μm baclofen. A smoothed function (gray line) illustrates the analysis described in Results, and this function clearly accounts for some, but not all, of the variance in fEPSP slope. B, A similar analysis to that in A is shown but in the presence of baclofen. C, A summary of the sources of variance in fEPSP slope during the physiologically relevant spike train, in control conditions (black bars) and in baclofen (gray bars). D, The fEPSP slopes during the train in baclofen were normalized to the corresponding slopes in control conditions, and the normalized slope was plotted against the first ISI. Smoothing the normalized data provided a monotonic function (gray line) that accounted for most of the variance in the normalized data. E, Averaged fEPSPs are shown during 1 Hz constant-frequency stimulation (1 Hz) and during a physiologically relevant spike train ...
RefSeq Summary (NM_021903): Gamma-aminobutyric acid (GABA) is the main inhibitory neurotransmitter in the mammalian central nervous system. GABA exerts its effects through ionotropic [GABA(A/C)] receptors, to produce fast synaptic inhibition, and metabotropic [GABA(B)] receptors, to produce slow, prolonged inhibitory signals. The GABA(B) receptor consists of a heterodimer of two related 7-transmembrane receptors, GABA(B) receptor 1 and GABA(B) receptor 2. The GABA(B) receptor 1 gene is mapped to chromosome 6p21.3 within the HLA class I region close to the HLA-F gene. Susceptibility loci for multiple sclerosis, epilepsy, and schizophrenia have also been mapped in this region. Alternative splicing of this gene generates multiple transcript variants. [provided by RefSeq, Jun 2009 ...
Regarding muscle relaxers, I use Baclofen every 2 to 3 hours. I tried Zanaflex but within a short period of time I had severe allergic reaction to it and had to go back to Baclofen. Even with Baclofen I seem to require the use of an over the counter antihistimine to control the urge to itch. Im not sure if it is due to the Baclofen or just the way I am. I had a tendency to scratch my head and neck before I had SM. I havent tried the other two muscle relaxers mentioned but will keep them in mind. I am in big pain trouble without Baclofen ...
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Scheme 1. Total Synthesis of (R)-(−)-Baclofena. a Conditions: (a) MeNO2, NaOMe, MeOH, room temperature, 15 h; (b) MsCl, TEA, THF, room temperature, 1 h; (c) diethyl malonate, 1e, toluene, room temperature, 24 h; (d) NiCl2·6H2O, NaBH4, MeOH, room temperature, 7.5 h; (e) NaOH, EtOH, room temperature, 45 h; (f) toluene, reflux, 6.5 h; (g) 6N HCl, reflux, 24 h.. Total synthesis of (R)-(-)-baclofen. 9: The mixture of 4-chlorobenzaldehyde (1.41 g, 10 mmol), nitromethane (10 equiv, 5.4 ml) and NaOMe (0.10 equiv, 54.0 mg) in MeOH (10 ml) was stirred overnight. Saturated ammonium chloride was added to the mixture and aqueous phase was extracted with AcOEt. The extract was washed with brine, dried over MgSO4, filtrated and concentrated in vacuo. The residue was purified by by column chromatography on silica gel (Hexane/AcOEt = 3/1 as eluent) to afford desired nitroalcohol 8 (1.82 g, 90%). To the stirred solution of the obtained nitroalcohol 8 and MsCl (1.2 equiv, 0.84 ml) in THF (9.0 ml) was added TEA ...
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The goal of our review was to emphasize important aspects that physicians should take into consideration when prescribing topical analgesics as part of chronic neuropathic pain treatment. We discuss the dermatopharmacokinetics and microstructural components of the skin, differences between topical and transdermal drug delivery, and topical medication effects on peripheral neuropathy and central sensitization. Even though the US FDA approved topical analgesics are 8%-capsaicin and 5%-lidocaine patches for treating postherpetic neuralgia, there are many other studies conducted on the efficacy of topical ketamine cream, clonidine gel, topical gabapentin, topical baclofen and topical phenytoin for peripheral neuropathic pain, either alone or in combination with other formulations ...
Purpose of Review Despite its widespread use, oral baclofen requires a critical review of the pharmacology to determine potential precision medicine applications to improve medication administration....
Results of a randomized trial show alcohol-dependent patients with liver cirrhosis were able to attain alcohol abstinence at a higher rate with baclofen than with placebo. The researchers say the drug might play an important role in the management of these patients.
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The IUPHAR/BPS Guide to Pharmacology. baclofen ligand page. Quantitative data and detailed annnotation of the targets of licensed and experimental drugs.
The IUPHAR/BPS Guide to Pharmacology. (-)-baclofen ligand page. Quantitative data and detailed annnotation of the targets of licensed and experimental drugs.
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Question - Having severe lower back pain that extends to hips. Having nerve pain during sitting or bending. On Naprosyn and baclofen. Suggest?. Ask a Doctor about diagnosis, treatment and medication for Nerve pain, Ask an Orthopaedic Surgeon
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