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At least 19 recordsLinked to original sources

PubMed1978

[Quipazine antagonizing baclofen activity. Influence of baclofen and gamma-hydroxybutyric acid on serotonin metabolism in rat brain (author's transl)].

Baclofen increases the concentration of serotonin (5-HT) and 5-hydroxyindolacetic acid (5-HIAA) in the rat c. striatum without causing concomitant increase in 5-HT biosynthesis. The effect of baclofen on 5-HIAA, but not that on 5-HT, was antagonized dose-dependently by quipazine. It is assumed that quipazine acts by stimulating 5-HT autoreceptors.

Aminobutyrates↗

PubMed1992

Comparison of the actions of baclofen at pre- and postsynaptic receptors in the rat hippocampus in vitro.

1. Intracellular microelectrode recordings were used to study the cellular location, pharmacology, and mechanism of action of gamma-aminobutyric acidB (GABAB) receptors on pyramidal cells and presynaptic axonal endings in area CA3 of organotypic hippocampal slice cultures. 2. Baclofen (bath applied at 10 microM) caused a 10-15 mV hyperpolarization of CA3 cells and a 75-100% decrease in the amplitude of excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs). Baclofen reduced the amplitude of monosynaptic IPSPs elicited in the presence of excitatory amino acid receptor antagonists, as well as the amplitude of EPSPs elicited after blocking GABAA receptors and reducing subsequent epileptic bursts with excitatory amino acid receptor antagonists. These data indicate that GABAB receptors are located on both excitatory and inhibitory presynaptic elements. 3. The GABAB receptor antagonist CGP 35 348 blocked the postsynaptic action of baclofen, the late IPSP, and the reduction of EPSPs and monosynaptic IPSPs by baclofen. 3-Aminopropylphosphinic acid (3-APA) mimicked all the pre- and postsynaptic actions of baclofen, and its effects were fully antagonized by CGP 35 348. 4. Incubation of cultures with pertussis toxin (500 ng/ml for 48 h) prevented both the postsynaptic hyperpolarization and the block of monosynaptic IPSPs induced by baclofen. The action of baclofen on isolated EPSPs, however, was not affected by pertussis toxin treatment. Stimulation of protein kinase C with phorbol ester (phorbol 12, 13 dibutyrate, 1 microM for 10 min) reduced all pre- and postsynaptic effects of GABAB receptor activation. 5. Barium (bath applied at 1 mM) prevented both the baclofen-induced hyperpolarization of pyramidal cells and the block of monosynaptic IPSPs by baclofen. In the presence of barium, however, baclofen was fully capable of blocking EPSPs. 6. We conclude that pre- and postsynaptic GABAB receptors are pharmacologically indistinguishable, at present, and that all actions of GABAB receptors are inhibited by stimulation of protein kinase C. Both the postsynaptic action of baclofen and the block of GABA release from interneurons are mediated by pertussis toxin-sensitive G proteins which can be inactivated by stimulation of protein kinase C. Baclofen acts at postsynaptic sites and on the axon terminals of inhibitory interneurons by activating the same barium-sensitive K+ conductance. GABAB receptors on excitatory axons must, however, work through some other mechanism.

Animals↗

PubMed1992

Effect of the GABAB antagonist, phaclofen, on baclofen-induced inhibition of micturition reflex in urethane-anesthetized rats.

The effect of intrathecal or intracerebroventricular administration of the GABAB receptor agonist, baclofen, on rhythmic contractions induced by distension of the urinary bladder (micturition reflex) was evaluated in urethane-anesthetized rats. Baclofen inhibited bladder motility acting at central nervous system sites (spinal and supraspinal) with a comparable potency. The inhibitory effect of i.t. baclofen (0.1-10 nmol) was blocked by i.t. phaclofen (200 nmol) while i.c.v. phaclofen did not affect i.c.v. baclofen (0.1-1 nmol). The inhibition of the micturition reflex induced by bladder distension observed after i.t. administration of baclofen was unaffected by systemic capsaicin pretreatment (50 mg/kg s.c., four days before). On the other hand, i.t. baclofen suppressed, in a phaclofen-sensitive manner, the reflex bladder contraction evoked by chemical stimulation (topical capsaicin) of capsaicin-sensitive bladder afferents. Intrathecal baclofen did not affect the hexamethonium-resistant tonic contraction produced by topical application of capsaicin on to the urinary bladder, which is ascribable to local peptide release from sensory nerves. Bladder motility inhibition by i.t. or i.c.v. baclofen (1 nmol) was unchanged by previous administration of p-chlorophenylalanine, indicating that the serotonergic pathways do not play a role in its action. Baclofen (100 microM) suppressed the release of calcitonin gene-related peptide-like immunoreactivity evoked by electrical field stimulation from the dorsal half of the rat spinal cord. This response was also abolished by in vitro capsaicin desensitization or tetrodotoxin, indicating that baclofen suppresses transmitter release from central endings of capsaicin-sensitive primary afferents. The present findings indicate that baclofen acts at both spinal and supraspinal sites to inhibit, with different mechanisms, the micturition reflex.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

The actions of baclofen on neurones and synaptic transmission in the nucleus tractus solitarii of the rat in vitro.

1. Intracellular and whole-cell patch recordings were made from sixty-seven neurones located in the nucleus tractus solitarii (NTS) in transverse slices of rat brainstem. 2. Baclofen at concentrations of 2-20 microM caused hyperpolarization from normal resting membrane potentials (Vm). This response was associated with a decrease in input resistance (Rm) tested by current pulses in discontinuous current clamp mode when membrane potential was restored to control level by current injection. In single electrode discontinuous voltage clamp mode, baclofen at these concentrations caused a small (< 50 pA) outward current associated with increased membrane conductance measured by voltage steps from holding potentials (Vh) of -50 or -60 mV. Current-voltage relations at these Vhs and the results of varying Vh between -50 and -110 mV during responses to baclofen gave a reversal potential of -73 mV. The amplitudes of baclofen responses were related to K+ concentration tested by comparing responses in media containing 1-24 mM extracellular K+, indicating that postsynaptically baclofen acts via a K+ conductance. 3. These effects were still apparent in the presence of tetrodotoxin (which did not abolish all spontaneous synaptic activity) and also in medium containing a combination of Co2+, the excitatory amino acid antagonist 6-cyano-7-nitro-quinoxaline-2,3-dione (CNQX) and the GABAA antagonist bicuculline which blocked synaptic activity. 4. The amplitude and frequency of spontaneous postsynaptic potentials (spPSPs) and spontaneous postsynaptic currents (spPSCs) were reduced by baclofen at concentrations (1 microM or less) which had no effect on membrane potential or holding current in current or voltage clamp recordings respectively. 5. The amplitude of evoked excitatory (evEPSPs/evEPSCs) and inhibitory (evIPSPs/evIPSCs) synaptic events elicited by electrical stimulation in the vicinity of the tractus solitarius (TS) was reduced by low concentrations of baclofen (250 nM-1 microM) which did not produce discernible postsynaptic responses. 6. In order to examine the effects of baclofen on excitatory synaptic events without contamination with inhibitory events, stimulation of the TS was carried out in the presence of bicuculline. Conversely to investigate actions on purely inhibitory synaptic responses experiments were carried out with CNQX in the bathing solution. Inhibitory synaptic responses could still be evoked, presumably by stimulation of interneurones in the vicinity of the TS. IPSPs/IPSCs were more sensitive to baclofen than EPSPs/EPSCs. 7. The effects of baclofen on membrane potential or holding current and PSP/PSCs were antagonized by 2-hydroxysaclofen (400 microM) confirming that baclofen was acting at gamma-aminobutyric acid (GABA)B receptors.(ABSTRACT TRUNCATED AT 400 WORDS)

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1992

On the inhibitory actions of baclofen and gamma-aminobutyric acid in rat ventral midbrain culture.

1. Whole-cell voltage-clamp recordings were used to study the effects of (-)-baclofen and of gamma-aminobutyric acid (GABA) on neurones cultured from the ventral midbrain of embryonic rats. 2. Baclofen induced an outward current (IBac) at a holding potential of -60 mV. The maximal current was 80 pA, and half-maximal current was evoked by 5 microM-baclofen. The proportion of cells affected by baclofen was greater in 25-day-old cultures than in 14-day-old cultures. 3. IBac was blocked by barium (1 mM), and it reversed polarity at a potential that changed according to the Nernst equation when the extracellular potassium concentration was changed. The reversal potential was not different when recording electrodes contained caesium instead of potassium. 4. GABA (10-20 microM), in the presence of picrotoxin (50 microM) and bicuculline (50 microM), also evoked a small potassium current at -60 mV. There was no correlation between the amplitude of the potassium current caused by GABA and that caused by baclofen measured in the same neurones. 5. Spontaneous synaptic currents (up to hundreds of picoamps) were observed that were blocked by picrotoxin (20 microM; IPSCs) or by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM; EPSCs); the amplitude and frequency were strongly reduced by baclofen and by GABA. 6. Spontaneous synaptic currents of lower amplitudes (up to 60 pA) remained in the presence of tetrodotoxin. IPSCs (blocked by picrotoxin, reversal at -50 mV) and EPSCs (blocked by CNQX, reversal at 0 mV) were reduced in frequency by baclofen. GABA, in the presence of bicuculline and picrotoxin, had a similar effect on the EPSCs. This action of baclofen persisted in barium (1 mM), and was observed as readily in cells cultured for 14 days as those cultured for 25 days. 7. Some spontaneous synaptic currents remained in the presence of tetrodotoxin and cadmium (100 microM). Their frequency was reduced by baclofen. The effectiveness of baclofen was greater on cells that had been longer in culture. 8. It is concluded that activation of GABAB receptors has two main effects on neurones cultured from rat ventral midbrain. These are potassium conductance increase, and inhibition of the spontaneous release of GABA and excitatory amino acids; both effects can be observed in tetrodotoxin and cadmium.

Animals↗

PubMed1977

Effects of beta-(p-chlorophenyl)-GABA (baclofen) on spinal synaptic activity.

In the isolated perfused spinal cord of the bullfrog, baclofen caused a reduction in the rate of spontaneous discharges in the ventral root at lower concentrations than GABA. The inhibitory effect of baclofen was fully present in a chloride-free medium, whereas that of GABA was markedly reduced. In contrast to GABA, which depolarized the dorsal root, baclofen produced a hyperpolarization in the dorsal root. Moreover, baclofen produced a hyperpolarization in the ventral roots. In the rat, the development of spinal reflex inhibition by baclofen was slow and the effect was long-lasting. Baclofen decreased dorsal root reflexes, suggesting a decreased excitability of presynaptic fibres. Baclofen produced a more pronounced and faster inhibitory effect on monosynaptic reflexes than on polysynaptic reflexes. In the monoamine depleted rat, the effect of baclofen on both types of reflexes was markedly reduced. It appears that catecholamines are involved in the effects produced by baclofen.

Action Potentials↗

PubMed1992

Monoclonal antibodies for ultrastructural visualization of L-baclofen-sensitive GABAB receptor sites.

Monoclonal antibodies were raised against the L-enantiomer of baclofen conjugated by glutaraldehyde to keyhole limpet hemocyanin. Hybridoma clones were selected for their stability and their production of high titers of antibodies directed against the p-chlorophenyl moiety of the L-baclofen molecule. The chosen antibody showed no cross-reactivity with conjugates of GABA and other neurotransmitters to human or bovine serum albumin. Specificity was further confirmed by the ability of L-baclofen-HCl to inhibit the binding of the antibody to L-baclofen-bovine serum albumin conjugate. Immunocytochemical studies were conducted on brain tissue from rats and monkeys injected with baclofen to localize baclofen-sensitive GABAB receptor sites. In these animals, the molecular layer of cerebellar cortex was clearly immunostained and the granular layer showed only some pale immunoreactivity. Ultrastructural observations were conducted in cerebellar cortex, as well as in the substantia nigra and the vestibular nuclei. Discrete labeling of neuronal profiles was observed in these structures, and both immunoperoxidase and colloidal gold methods were employed successfully. Material from saline-injected control animals showed no immunoreactivity at both light and electron microscopic levels. We conclude that the anti-L-baclofen antibody preferentially recognizes the p-chlorophenyl moiety of the baclofen molecule. Antibodies of such specificity are useful tools for the ultrastructural localization of baclofen-sensitive GABAB receptor sites. In general, antibodies directed against accessible moieties of specific neuroactive substances may serve as valuable markers for their sites of action.

Animals↗

PubMed1978

Baclofen (beta-p-chlorophenyl-gamma-aminobutyric acid) enhances [3H]gamma-aminobutyric acid (3H-GABA) release from rat globus pallidus in vitro.

The rat globus pallidus has been investigated as a possible model in which to study pre-synaptic GABA mechanisms in vitro. (+/-)-Baclofen (300 micrometer-1 mM) significantly enhanced the release of radioactivity from superfused slices of rat globus pallidus prelabelled with 3H-GABA in vitro. This releasing action was specific to the (+)-isomer of baclofen: neither the (-)-isomer nor another neuronal depressant dl-alpha-epsilon-diaminopimelic acid had any significant effect. The releasing effect of baclofen appeared unrelated to the phenethylamine moiety of its structure as neither beta-phenethylamine nor dopamine evoked release of 3H-GABA from pallidal slices. Baclofen increased the efflux of radioactivity from pallidal slices prelabelled with either [3H]-beta-alanine or [3H]diaminobutyric acid in vitro. The use of specific glial and neuronal GABA uptake blocking compounds (beta-alanine and (+/-)-cis-1,3-amino-cyclohexanecarboxylic acid) did not permit resolution of the elements from which baclofen was evoking [3H]GABA release. Baclofen also inhibited uptake of [3H]GABA into pallidal slices with an IC50 value of 6 x 10(-4) m. The GABA-like properties of baclofen may be related to the (+)-isomer while non-specific neuronal depressant actions are an effect of the (-)-isomer. The potential of the (+)-isomer as an antipsychotic agent while (-)-baclofen remains the effective antispastic drug free from unwanted side-effects, is discussed.

Alanine↗

PubMed1977

[Effects of beta-(p-chlorophenyl)-GABA (baclofen) on response to noxious stimuli (author's transl)].

Effects of beta-(p-chlorophenyl)-GABA (baclofen), a muscle relaxant, on the response of mice and rats to various noxious stimuli were studied. In mice, 5 approximately 10 mg/kg i.p. of baclofen delayed the response time to tail-pinch and hot-plate stimuli but the relaxation was also apparent with this dose range. Mephenesin also delayed the response time to tail-pinch stimuli with the dose producing muscle relaxation. Baclofen, 3 mg/kg i.p., while producing no muscle relaxation, suppressed the acetic acid-induced writhing. The same effect, suppression of writhing and no muscle relaxation, was achieved with 50 mg/kg i.p. of mephenesin. In rats, baclofen (5 approximately 10 mg/kg i.p.) increased the response threshold in Randall-Selitto method and suppressed the bradykinin-induced symptoms, however, muscle relaxation was also produced with these same doses. Increase in response threshold in Randall-Selitto method was achieved with the dose of mephenesin producing muscle relaxation. The time courses of the depression of response to noxious stimuli and the muscle relaxation induced by baclofen and mephenesin were consistent in mice and rats. A small dose (3 mg/kg i.p. in mice, 2 mg/kg/h s.c. in rats) of baclofen reduced the antinociceptive effect of morphine but a larger dose (5 mg/kg i.p. in mice, 7 mg/kg/h s.c. in rats) of baclofen increased or did not alter the effect of morphine. It seems likely that the antinociceptive effect of baclofen may be nonspecific to analgesia.

Aminobutyrates↗

PubMed1978

The biological activity of d- and l-baclofen (Lioresal).

Racemic d,l-baclofen and l-baclofen depressed the patellar, flexor, linguo-mandibular (0.1--30 mg/kg i.v.) and the H-reflex (1--3 mg/kg i.v.) in a dose-dependent fashion. Racemic and l-baclofen partly antagonized electroshock-induced convulsions in mice (30--60 mg/kg p.o.) and depressed the firing rate of nigral cells when applied iontophoretically. d,l-Baclofen and l-baclofen (0.1--3.0 mg/kg i.v.) moderately reduced the blood pressure in cats. Dextrorotatory baclofen, at identical doses was inactive in all these tests. It is concluded that the biological activity of baclofen resides with the l-enantiomer.

Aminobutyrates↗

PubMed1992

NMDA receptor antagonists block cardiovascular responses to intrathecal administration of D-baclofen in the rat.

In previous studies we found that D and L-baclofen have different effects on sympathetic output when administered intrathecally, yet the actions of both enantiomers are blocked by intrathecal administration of phaclofen. The present experiments were done to determine the mechanism by which D-baclofen expresses its effects. In urethane-anaesthetized Sprague-Dawley rats, when D-baclofen was given intrathecally at the T9 spinal level following pretreatment with 2 nmol of the NMDA receptor antagonist, DL-2-amino-5-phosphonovaleric acid (APV), it increased systolic and diastolic arterial pressures (n = 7), as in the previous studies. However, after intrathecal administration of 10 nmol of APV, administration of D-baclofen had no effect on these parameters (n = 7). Intravenous administration of ketamine (7.5 mg/kg), another NMDA receptor antagonist, also blocked the effect of D-baclofen (n = 6) but it had no effect on the pressor responses produced by intrathecal administration of carbachol (27.4 nmol; n = 6). In additional experiments, L-baclofen (70 nmol) had no effect on the increases in heart rate and arterial pressure produced by N-methyl-D-aspartic acid (NMDA) (2 nmol; n = 8). These results indicate that D-baclofen increases arterial pressure via an NMDA receptor-mediated mechanism, perhaps by provoking the release of an endogenous ligand which activates these receptors.

2-Amino-5-phosphonovalerate↗

PubMed1992

Different effects of baclofen on LH and cortisol responses to naloxone in normal men.

The possible involvement of GABAergic B receptors in the control of LH and ACTH/cortisol secretion in response to naloxone was evaluated in seven normal men. Subjects were tested with naloxone (4 mg IV bolus plus 10 mg infused over 2 hr) with or without previous treatment with the gamma-aminobutyric acid (GABA)-ergic B receptor agonist, baclofen (5, 10 or 15 mg PO 30 min before naloxone). In additional experiments, six normal men were tested with 15 mg baclofen or placebo 30 min before a 2-hr infusion of normal saline. Plasma cortisol levels rose 70% in response to naloxone. The naloxone-induced cortisol rise was not modified by pretreatment with baclofen (5, 10 or 15 mg). Plasma LH concentrations rose 66% in response to naloxone. When the lowest dose of baclofen (5 mg) was administered, the LH response to naloxone remained unchanged. In contrast, 10 mg baclofen produced a significant reduction, and 15 mg baclofen completely abolished the naloxone-induced LH rise. The administration of baclofen or placebo alone did not change basal plasma levels of cortisol and LH. These data suggest that, in normal men, GABA B receptors participate in the endogenous opioidergic control of LH secretion, but not of ACTH/cortisol secretion.

Adrenocorticotropic Hormone↗

PubMed1977

Biochemical effects of baclofen (beta-parachlorophenyl-GABA) on the dopamine and the noradrenaline in the rat brain.

Baclofen (beta-parachlorophenyl-GABA) caused an increase in the concentration of dopamine in the rat brain with a maximum of about 170% of the control value after 1 hr and after doses of 50 mg/kg or more intraperitoneally. The alpha-methyltyrosine-induced disappearance of dopamine was inhibited to about the same extent in the corpus striatum and in the limbic system by baclofen. The accumulation of DOPA following decarboxylase inhibition was stimulated more in the corpus striatum than in the limbic system by baclofen, thus accounting for the fact that the concentration of dopamine was elevated about three times as much in the corpus striatum as in the limbic system. Amphetamine almost completely inhibited the rise in dopamine produced by baclofen. Baclofen did not cause any consistent changes in the concentration, the synthesis and the utilization of noradrenaline. These effects of baclofen are similar to those described following gammahydroxybutyric acid or axotomy. Hence, baclofen might also interrupt the nerve impulse flow in central dopamine neurones, perhaps by stimulating a central GABA mechanism.

Aminobutyrates↗

PubMed1979

Baclofen and muscimol: behavioural and neurochemical sequelae of unilateral intranigral administration and effects on 3H-GABA receptor binding.

Log dose-response curves for induction of contralateral rotational behaviour in the rat by unilateral intranigral injections of the GABA agonist muscimol and the GABA analogue baclofen have been compared. Baclofen, 5--1000 ng, produced a maximal rotational response that was only 40% of that produced by 0.25--100 ng muscimol, and log dose-response curves failed to show parallelism. The behavioural effects of both drugs were only weakly antagonised by haloperidol and were not antagonised by 6-hydroxydopamine lesions of ipsilateral dopamine (DA) neurons, indicating that these responses were independent of DAergic mechanisms. The effects of baclofen were weakly antagonised by picrotoxin. Intranigral muscimol and baclofen substantially elevated striatal DA concentrations. While muscimol also substantially elevated striatal dihydroxyphenylacetic acid (DOPAC) but not homovanillic acid (HVA), bactofen did not significantly effect either DOPAC or HVA. Baclofein, GABA and muscimol displaced specific 3H-GABA binding in vitro with IC50's of 40 micron, 400 nM and 40 nM respectively. These results indicate that muscimol and baclofen do not act via a unitary GABAergic mechanism, but suggest that baclofen may be a partial GABA agonist, at least at nigral GABA receptors.

Aminobutyrates↗

PubMed1977

Baclofen-induced modification of conditioned discriminative avoidance behaviour and contraversive turning in the rat.

The effects of baclofen, a gamma-aminobutyric acid derivative, on conditioned avoidance behaviour and on the turning produced by unilateral 6-OHDA lesions of the s. nigra were investigated in rats. The small impairment of conditioned avoidance behaviour induced by baclofen (1-4 mg/kg i.p.) was potentiated by combination with benztropine, an anticholinergic agent. Moreover, baclofen reversed the suppression of avoidance responses and the inhibition of turning induced by physostigmine, suggesting an interaction of baclofen with cholinergic transmission processes at the nigrostriatal level. After alpha-methyltyrosine, baclofen like haloperidol, produced a marked increase in avoidance response failures suggesting an additional inhibitory effect of the compound on dopaminergic transmission. The pattern of results indicates that baclofen affects the feedback-loop regulation processes in the nigrostriatal area of the brain.

Aminobutyrates↗

PubMed1975

Developing drug literatures. 1. Bibliometrics of baclofen and dantrolene sodium.

The literatures of two antispastic drugs, baclofen and dantrolene sodium, were studied bibliometrically for their first decade and were found to be generally similar. Baclofen had 93 papers and dantrolene sodium had 70. About a quarter of the baclofen papers were in a foreign language, whereas almost all dantrolene sodium papers were in English. Baclofen literature had a lower nonscholarly content, but the scholarly increase, 5%, was the same for both. Both drugs had an average of 12 references per paper. The literatures of both drugs had a similar degree of internal cohesiveness; almost half of their papers referred to other papers in the same drug collection. The first human paper for baclofen was the second published; for dantrolene sodium, it was the eleventh. The distribution of journals carrying papers on each of these drugs followed Bradford's law. Two authors per paper was the average for each drug. The productivity of authors approximated Lotka's law for both drugs. About two-thirds of the papers of both drugs had a drug-word in their titles. The literature of both drugs contained about 15% legendary papers, typical of clinical pharmacology. The most intense papers, 15 for baclofen and 11 for dantrolene sodium, were identified, using citation, bibliographic coupling, and co-citation frequencies. A generalization predicts what might be expected from the literature of future antispastic drugs.

Aminobutyrates↗

PubMed1976

Baclofen (Lioresal) in the treatment ofneuroleptic-induced tardive dyskinesia.

A double-blind cross-over trial of the effects of baclofen and placebo was carried out in 20 female patients suffering from neuroleptic-induced tardive dyskinesia. After 14 days of treatment 15 patients showed improvement of baclofen, whereas none showed improvement on placebo; baclofen was thus significantly more effective than placebo. Baclofen is a GABA-like drug which passes through the blood-brain barrier and which reduces the neuroleptic-induced increase of dopamine turn-over. In tardive dyskinesia is found dopaminergic hypersensitivity, and baclofen is supposed to exert its action by inhibiting the dopamine activity. Side effects, although temporary, were observed in the form of sedation, muscular hypotonia, dizziness, vomiting, and muscular rigidity. One patient developed a depression. Baclofen or other gabergic drugs used in the treatment of dyskinesias do not increase the dopaminergic hypersensitivity, which is part of the pathogenesis of these conditions; gabergic therapy must therefore be preferred to treatment with dopamine receptor blocking drugs.

Aged↗

PubMed1976

A double-blind trial of baclofen against placebo in the treatment of schizophrenia.

Twenty male chronic schizophrenic patients participated in a double-blond between-patient study of the GABA-like drug baclofen to evaluate the antipsychotic effect of baclofen. No difference was found between the 10 patients who received baclofen and 10 who received placebo with regard to the number of days before a worsening of their psychiatric condition necessitated treatment with chlorpromazine, the total score for psychotic symptoms before and after treatment for 10 weeks, or the total consumption of chlorpromazine. Discontinuation of baclofen did not exacerbate the psychotic symptoms. Baclofen was superior to placebo in the treatment of anxiety, which is of particular interest in view of the recent theories on the mechanism of action of benzodiazepines. The relationship between the gabergic system and the dopaminergic system with regard to the substantia nigra and the corpus striatum is discussed as well as the suggestion based on animal experiments that baclofen has an antipsychotic effect.

Adult↗