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At least 19 recordsLinked to original sources
PubMed2004

Venom effects on monoaminergic systems.

The monoamines, dopamine, epinephrine, histamine, norepinephrine, octopamine, serotonin and tyramine serve many functions in animals. Many different venoms have evolved to manipulate monoaminergic systems via a variety of cellular mechanisms, for both offensive and defensive purposes. One common function of monoamines present in venoms is to produce pain. Some monoamines in venoms cause immobilizing hyperexcitation which precedes venom-induced paralysis or hypokinesia. A common function of venom components that affect monoaminergic systems is to facilitate distribution of other venom components by causing vasodilation at the site of injection or by increasing heart rate. Venoms of some scorpions, spiders, fish and jellyfish contain adrenergic agonists or cause massive release of catecholamines with serious effects on the cardiovascular system, including increased heart rate. Other venom components act as agonists, antagonists or modulators at monoaminergic receptors, or affect release, reuptake or synthesis of monoamines. Most arthropod venoms have insect targets, yet, little attention has been paid to possible effects of these venoms on monoaminergic systems in insects. Further research into this area may reveal novel effects of venom components on monoaminergic systems at the cellular, systems and behavioral levels.

Animals↗
PubMed1996

Responses in the hypothalamic monoaminergic system activity in ewes to beta-endorphin, CRF and their antagonists.

This article reviews data concerning the action of opioidergic and monoaminergic system on LHRH secretion. Generally, in anestrous ewes beta-endorphin and/or corticoliberin significantly change extracellular concentrations of monoamine metabolites in the MBH-ME, but in estrous ewes both beta-endorphin and CRF alters also dopamine, noradrenaline and serotonin levels. Responses of catecholaminergic and serotoninergic system in the MBH-ME to naloxone or CRF-antagonist depend, to a large degree, on the phase of reproduction. In anestrous ewes subjected to stressful stimuli an opiate receptor blocker, naloxone, and CRF-antagonist attenuate the stress - induced activity of catecholaminergic and serotoninergic system in the MBH-ME; in non-stressed animals they suppress only serotoninergic system activity in this structure. No clear explanation can be offered now for either differences in response of catecholaminergic and serotoninergic system in the MBH to beta-endorphin and CRF in various periods of reproduction or for differences in the responses of these systems to CRF antagonist and naloxone in non-stressed and stressed ewes. It has been suggested that the responses in monoaminergic system activity are highly dependent upon the physiological state of the animal and that beta-endorphin and corticoliberin may indirectly modulate LHRH and other hypothalamic hormone secretion by monoaminergic systems.

Animals↗
PubMed1983

[Role of the somatic monoaminergic systems in the mechanisms of regulation of pain sensitivity during reflex stimulation].

Experiments on rats were performed to study the role of the monoaminergic systems in the mechanisms of analgesia produced by stress (foot shock) and auricular electroacupuncture (AEA). Analgesia was measured by the hot-plate (HP) and the tail-flick (TF) tests. Inhibition of catecholamine synthesis with alpha-methyl-p-tyrosine (alpha-MPT) antagonized the AEA-induced analgesia measured by the TF test. alpha-MPT did not influence the HP test latency after AEA, and HP or TF tests after stress. Inhibition of dopamine receptors by haloperidol produced a decrease in the stress- and AEA-induced analgesia. The similar effects were demonstrated in propranolol treated rats after AEA. P-chlorophenylalanine (an inhibitor of serotonin synthesis) suppressed the stress-induced analgesia measured by the HP test and AEA-induced analgesia measured by the HP or TF tests. The data indicate that the monoaminergic systems are involved in the stress- and AEA-induced analgesia. Apart from the monoaminergic systems, other neurochemical mechanisms are also involved in the stress- and AEA-induced analgesia.

Acupuncture Therapy↗
PubMed1990

Spatial memory deficits in aged rats: contributions of monoaminergic systems.

Age-dependent changes in monoaminergic systems and their relationship to senescent memory decline were investigated in 4- and 25-26-month-old, female, Fischer 344 rats. Spatial memory performance was tested on an 8-arm radial maze, and levels of norepinephrine (NE), dopamine (DA) and metabolites 3,4-dihydroxyphenylacetic acid and homovanillic acid, serotonin (5-HT) and metabolite 5-hydroxyindoleacetic acid were measured in brain areas which contribute to memory function--basal forebrain cholinergic nuclei, subfields of the hippocampus, frontal and entorhinal cortex--and in monoaminergic cell body areas. The performance of aged subjects was significantly impaired as compared to young subjects, and alterations of 20-60% in monoamine and metabolite levels were measured in specific brain areas of aged rats. Decreased NE levels were found in basal forebrain nuclei and cortical areas but not in hippocampal subfields of aged rats. Changes in the 5-HT system were present in hippocampal, cortical and basal forebrain sites. Changes in the DA system were the most pervasive with aged rats showing decreased DA and/or metabolites in several basal forebrain nuclei, cortical areas, and the hippocampus. Aged rats showed 50% decreases of monoamines in locus coeruleus and substantia nigra and 30% decreases in the dorsal raphe nucleus. Some but not all of the changes correlated with memory performance. The present results in rats support evidence that age-dependent changes in monoaminergic function in discrete brain sites contribute to senescent memory decline and suggest that monoaminergic-cholinergic interactions within basal forebrain nuclei may be important in this decline.

Aging↗
PubMed2000

Effects of neonatal rat Borna disease virus (BDV) infection on the postnatal development of the brain monoaminergic systems.

Effects of neonatal Borna disease virus infection (BDV) on the postnatal development of brain monoaminergic systems in rats were studied. Tissue content of norepinephrine (NE), dopamine (DA) and its metabolite, 3,4-dihydroxyphenol acetic acid (DOPAC), and serotonin (5-HT) and its metabolite, 5-hydroxyindole-3-acetic acid (5-HIAA) were assayed by means of HPLC-EC in frontal cortex, cerebellum, hippocampus, hypothalamus and striatum of neonatally BDV-infected and sham-inoculated male Lewis rats of 8, 14, 21, 60 and 90 days of age. Both NE and 5-HT concentrations were significantly affected by neonatal BDV infection. The cortical and cerebellar levels of NE and 5-HT were significantly greater in BDV-infected rats than control animals at postnatal days (PND) 60 and 90. Tissue content of NE in hippocampus was unaffected. In hippocampus, neonatally BDV-infected rats had lower 5-HT levels at PND 8 and significantly elevated levels at PND 21 and onwards. Neither striatal levels of 5-HT nor hypothalamic levels of 5-HT and NE were affected by neonatal BDV infection, suggesting that the monoamine systems in the prenatally maturing brain regions are less sensitive to effects of neonatal viral infection. 5-HIAA/5-HT ratio was not altered in BDV-infected rats indicating no changes in the 5-HT turnover in the brain regions damaged by the virus. Neither DA nor DOPAC/DA ratio was affected by neonatal BDV infection in any of the brain regions examined. The present data demonstrate significant and specific alterations in monoaminergic systems in neonatally BDV-infected rats. This pattern of changes is consistent with the previously reported behavioral abnormalities resulting from neonatal BDV infection.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1988

Aspartame and the rat brain monoaminergic system.

A high dose of aspartame (APM) was administered to rats to study possible effects on brain monoaminergic systems. APM and its metabolite phenylalanine (Phe) were given orally at doses of 1000 and 500 mg/kg, respectively. Significant increases were seen in brain Phe and tyrosine (Tyr) levels. Two different approaches were used to study monoaminergic systems: whole tissue measurements by HPLC-ED and in vivo voltammetry in freely moving rats. Dopamine, serotonin and their metabolites were taken as indexes of neuronal activity. In spite of the high dose used, no modification was found in monoamines or their metabolites in striatum, hippocampus and nucleus accumbens.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1989

Effects of the putative anxiolytic SM-3997 on central monoaminergic systems.

The effects of SM-3997 on central monoaminergic systems were evaluated by ex vivo measurement of monoamines and their metabolite levels in rat brain after intraperitoneal treatment of drugs and by in vitro measurement of monoamine uptake into rat brain slices. The effects of SM-3997 were also compared with those of other new nonbenzodiazepine anxiolytic compounds. SM-3997, buspirone, gepirone and ipsapirone showed no effects on serotonin uptake and dopamine uptake, and a weak inhibition of norepinephrine uptake at the concentration of 100 microM. SM-3997 decreased the serotonin metabolite (5-hydroxyindole-3-acetic acid) level without changing the serotonin level in hippocampus and increased dopamine metabolite (3,4-dihydroxyphenylacetic acid, homovanillic acid) level with no effect on the dopamine level in striatum. SM-3997 also produced an increase in the norepinephrine metabolite (3-methoxy-4-hydroxyphenylglycol) level with a decrease in the norepinephrine levels in hippocampus. Similar effects on serotonin metabolites and norepinephrine metabolites were observed in several other regions. Although the serotonergic effect of SM-3997 was similar to that of buspirone, gepirone and ipsapirone, the dopaminergic effect of SM-3997 was much weaker than that of buspirone.

Animals↗
PubMed1976

Tonic inhibitory influence of a supraspinal monoaminergic system on recurrent inhibition of an extensor monosynaptic reflex.

Recurrent inhibition of the extensor (quadriceps) monosynaptic reflex (MSR) was antagonized by a 5-hydroxytryptamine (5-HT) precursor, 5-hydroxytryptophan (5-HTP, 75 mg/kg), and a specific 5-HT neuronal uptake blocker, fluoxetine-HC1 (Lilly 110140, 0.25-6 mg/kg), in unanaesthetized decerebrate cats. This inhibition of the flexor (posterior biceps-semitendinosus) MSR was not altered by fluoxetine. Cyproheptadine-HC1 (5 mg/kg) partially reversed the above blocking actions of 5-HTP and fluoxetine and a thoracic "cold block", which eliminates supraspinal inputs to the caudal spinal cord, also eliminated the blockade by fluoxetine on recurrent inhibition. Cyproheptadine (2.5-5 mg/kg) or phenoxybenzamine-HC1 (2.5-5 mg/kg), administered alone, enhanced recurrent inhibition of the extensor but not of the flexor MSR. Since a "cold block" increased recurrent inhibition of the extensor reflex in control animals but failed to alter the inhibition in animals pretreated with either DL-p-chlorophenylalanine (300 mg/kg i.p. for 2 consecutive days) or DL-a-methyl-p-tyrosine methyl ester-HC1 (125 mg/kg i.p. 16 and 4 h prior to experiment), the monoaminergic system would appear to be tonically active. In addition the neuronal uptake blocker, imipramine-HC1 (0.125-4 mg/kg), was more potent in antagonizing recurrent inhibition when injected intra-arterially to the spinal cord than when administered intra-arterially to the brain stem or intravenously, indicating that this agent acts in the spinal cord to block the inhibition. These results support our previous proposal (ref. 18) that a supraspinal system involving 5-HT and noradrenaline antagonizes recurrent inhibition of the quadriceps MSR. This monoaminergic system is tonically active with the 5-HT nerve terminals located in the spinal cord.

5-Hydroxytryptophan↗
PubMed1982

Changes with age in rat central monoaminergic system responses to cold stress.

Changes with age in responses to stress of certain central monoaminergic systems were investigated. Three groups of rats, 4, 18 and 29 months old, were exposed to cold and the effect of this stress on hypothalamic tyrosine hydroxylase, and on the metabolism of DA and 5HT in different brain regions was evaluated. Senescent rats were unable for several hours to compensate the loss of body heat. Corticosterone secretion however was equally stimulated. Hypothalamic tyrosine hydroxylase activity was enhanced in the young rats but not in the old ones. However, the two groups of senescent rats did not show the increase in HVA levels noted in striata of young rats 2 hours after cold exposure. In contrast, the 18 and 29-month-old rats presented enhanced serotonergic tonus, indicated by the greater increase in 5HIAA determined by stress.

Aging↗
PubMedDate not supplied

[Primary visual cortex response recovery cycles caused by pharmacologic and electrical effects on the monoaminergic systems of the rat brain].

The recovery cycles (RC) of primary responses in the visual cortex were studied in alert rats following the electrical stimulation of raphe nuclei and locus coeruleus as well as following pharmacological and complex (electrical and pharmacological) actions on serotonin- and noradrenergic brain systems. It was found that both electrical and pharmacological actions on the above monoaminergic systems reduce the duration and depth of relative non-reactivity phase of RC. Complex (electrical and pharmacological) action leads to heterodirectional changes in RC. The character of these changes reflects the reciprocity existing in functional interrelations between serotonin- and noradrenergic brain systems. The probable connection of the found effects with memory mechanisms is discussed.

5-Hydroxytryptophan↗
PubMedDate not supplied

Electrophysiological manifestations of the monoaminergic systems' effects on the cerebral cortex.

Consideration is given to a possible mechanism of reinforcement during training mediated through the monoaminergic systems in the brain that modulate the effectiveness of intracortical synapses. Various forms of electroencephalographic manifestations of the effect of these systems on the cerebral cortex are discussed. A comparison of the theoretical and experimental results favors the modulating role of the serotoninergic and noradrenergic systems.

Animals↗
PubMed1990

[Behavioral characteristics associated with acoustic stimulation and the neurochemical alterations of monoaminergic systems in rat brain at the steady state of repeated methamphetamine administration].

Behavioral characteristics associated with acoustic stimulation and the neurochemical alterations of monoaminergic systems in rat brain at the steady state of repeated methamphetamine administration were investigated. We confirmed that reverse tolerance in stereotyped behavior was constructed up to the 28th day after repeated intermittent pretreatment with increasing doses of MAP (2.5, 5, and 7.5 mg/kg x 3 and 10 mg/kg x 2, every other day). During acoustic stimulation, locomotor activity in the saline group was significantly increased, but the activity after the stimulation was completely suppressed. In contrast to the saline group, locomotor activity was not influenced by the acoustic stimulation in the MAP group, suggesting that behavioral hyporesponsiveness to acoustic stimulation was induced by MAP treatment. Two days after the last injection, the contents of 5-hydroxytryptamine (5-HT) and 5-hydroxyphenylacetic acid (5-HIAA) in the cerebral cortex, midbrain + thalamus, hypothalamus and striatum were significantly decreased. These changes were maintained up to the 28th day after the drug withdrawal in the cerebral cortex and the midbrain + thalamus. From these results, the persistence of behavioral hyporesponsiveness to acoustic stimulation might be associated with long-lasting reduction of 5-HT synthesis.

Acoustic Stimulation↗
PubMed2004

Changes in hypothalamic neuropeptide Y and monoaminergic system in tumor-bearing rats: pre- and post-tumor resection and at death.

BACKGROUND: Cancer anorexia is influenced by the neuropeptidergic and monoaminergic systems. We hypothesize that serotonin (5-HT), dopamine (DA) and neuropeptide Y (NPY) concentrations in paraventricular (PVN), ventromedial (VMN), and lateral hypothalamus (LHA) areas are abnormal in tumor-bearing rats. METHODS: Fifty-five Fischer rats (240-280 g) were divided into MCA tumor-bearing (TB), nontumor-bearing (NTB), pair-fed (PF), TB sacrificed at the end of experiment (TB-Terminal), TB resection (TB-Resection), NTB sham-operated (NTB-Sham) and pair-fed sham-operated (PF-Sham) groups. Rats were sacrificed at onset of anorexia (TB, NTB, and PF) and 9 days after tumor resection (TB-Resection, NTB-Sham, PF-Sham, and TB-Terminal). Bilateral PVN, VMN, and LHA were harvested for NPY, 5-HT, and DA analyses. RESULTS: Food intake decreased in TB versus NTB (P < .05). In TB versus NTB, an increase of 5-HT in PVN and VMN occurred with a concomitant decrease in DA. NPY in PVN, VMN, and LHA decreased (P < .05). In TB-Resection versus NTB-Sham, 5-HT, DA, NPY, and FI normalized after tumor resection. CONCLUSIONS: Cancer anorexia is associated with abnormal serotonin, dopamine, and NPY concentrations, expressed by an increase in 5-HT and a decrease in DA and NPY. After tumor resection, these alterations normalized, providing evidence that the levels of these substances change with anorexia in tumor-bearing rats.

Animals↗
PubMed1988

[Changes in behavior and central monoaminergic systems in the rat after repeated methamphetamine pretreatment: presynaptic regulatory mechanism].

We used various methods, including intracerebral dialysis, to investigate behavioral sensitization to methamphetamine (MAP) and neurochemical alterations of monoaminergic systems in rat striatum after repeated intermittent pretreatment with increased doses of MAP (2.5, 5, 7.5, 10 mg/kg sc x 2, every other day for a week) as an experimental model of MAP psychosis. MAP-pretreated rats showed an enhancement in MAP-stimulated striatal dopamine (DA) efflux from the neuron terminals into the synaptic cleft. The MAP-induced behavioral changes correlated significantly with the amount of DA efflux. The number of D2 receptors was not changed after the repeated MAP pretreatment. Therefore, as the possible explanations for the enhanced DA release. mechanism, it was suggested that the repeated exposure to abnormally high concentrations of DA produced by repeated MAP administration changed the presynaptic regulation mechanism as follows. (1) DA autoreceptor became subsensitive because low doses of (+/- ) apomorphine (25-50 micrograms/kg sc), a selective DA agonist, decreased striatal DA efflux below the predrug basal level in controls, but not in MAP-pretreated rats. It is recognized that low doses of apomorphine inhibit DA release via DA autoreceptor. (2) "Releasable DA pool" at the neuron terminals increased as shown by the enhanced DOPA accumulation 30 min after NSD1015 (100 mg/kg ip), an aromatic 1-amino acid decarboxylase inhibitor. (3) DA uptake decreased for the significantly more decreased DOPAC and HVA efflux after MAP challenge in MAP-pretreated rats. Serotonergic alteration was also indicated in MAP-pretreated rats, because of the significant decrease of 5-HIAA efflux after MAP challenge.

Animals↗
PubMed2000

Age-dependent differential responses of monoaminergic systems to high doses of methamphetamine.

Abuse of methamphetamine (METH) by adolescents is a major public health issue in the U.S.A. Because of the neurotoxic potential of METH, we examined the response of CNS monoaminergic systems in young (adolescent) animals [postnatal day (PND) 40] to high-dose treatments (10 mg/kg, four injections, 2-h intervals) of this drug and contrasted these effects to those seen in older (young adult) rats (PND 90). Consistent with previous reports, we observed that PND 40 animals did not manifest the long-term (7-day) deficits in extrapyramidal dopamine (DA) parameters observed in PND 90 rats. In contrast, METH-induced rapid (1-h) reduction in the activity of striatal DA transporters occurred in both age groups. In addition, both persistent (7-day) and rapid (1-h) deficits in serotonergic systems (measured as reductions in tryptophan hydroxylase activity) were observed in PND 40 and 90 rats. Age-related differences in METH-induced hyperthermia did not appear to be a principal cause for our observations; however, age-dependent pharmacokinetics of this drug might have contributed to the differential METH monoaminergic responses by PND 40 and 90 animals.

Age Factors↗
PubMedDate not supplied

[Role of monoaminergic systems in the development of the effect of stimulation of acetylcholinergic brain structures in the cat].

The influence of systemic injection of anticholinesterase substance physostigmine on the behaviour of cats was studied under the conditions of pharmacological stimulation of monoaminergic cerebral systems. Development of the effect of the substance with an increase of its dose was accompanied by a successive alternation of three phases each representing an independent form of behaviour. Each form of behaviour originating in the process of acetylcholinergic stimulation increase was supposed to be caused by an involvement of corresponding monoaminergic system: serotonindopamine-, or noradrenergic one.

Acetylcholine↗
PubMed1992

Long-term alteration in the central monoaminergic systems of the rat by 2,4,5-trihydroxyamphetamine but not by 2-hydroxy-4,5-methylenedioxymethamphetamine or 2-hydroxy-4,5-methylenedioxyamphetamine.

The long-term effects of three metabolites of 3,4-methylenedioxymethamphetamine (MDMA) on the central monoaminergic systems of the rat were examined. Seven days after the intracerebroventricular administration of 0.25 and 0.5 mumol 2,4,5-trihydroxyamphetamine, hippocampal tryptophan hydroxylase (TPH) activity was reduced to 5 and 1% of control, respectively, while norepinephrine (NE) concentration was depressed to 10 and 18% of control. These two respective dosages also decreased striatal tyrosine hydroxylase (TH) activity to 67 and 10% of control, respectively, while nigral TH activity was reduced to 59 and 20% of control. Striatal TPH activity was reduced to 74 and 81% of control, respectively, while the activity in the dorsal and median raphe remained unaltered. The intracerebroventricular administration of 1 mumol 2-hydroxy-4,5-methylenedioxymethamphetamine (6-OH-MDMA) failed to alter TPH activity, TH activity or NE concentration after 14 days. In contrast, 1 mumol of 2-hydroxy-4,5-methylenedioxyamphetamine (6-OH-MDA) induced a 30% increase in striatal TPH activity and a 50% increase in nigral TH activity. The study of the formation of 2,4,5-trihydroxyamphetamine after MDMA treatment may provide insight as to how MDMA destroys serotonergic nerve terminals.

3,4-Methylenedioxyamphetamine↗
PubMed1988

Effects of methamphetamine on central monoaminergic systems in normal and ascorbic acid-deficient guinea pigs.

Repeated injections (s.c.) of methamphetamine (METH) were administered to normal and ascorbic acid-deficient (scorbutic) guinea pigs to assess a potential role for ascorbic acid in the METH-induced effects in central monoaminergic systems. The ascorbic acid-deficient condition differentially influenced the METH-induced responses of dopaminergic and serotonergic variables in the striatum: drug-induced changes in dopaminergic variables were identical in normal and scorbutic animals; METH-induced decreases in serotonergic variables [tryptophan hydroxylase activity, serotonin (5-HT) and 5-hydroxyindoleacetic acid concentrations], however, were prevented in scorbutic animals. The scorbutic condition did not alter significantly the distribution of METH in the brain, nor were striatal concentrations of dopamine (DA) or 5-HT affected. In vitro, ascorbic acid increased significantly DA-mediated [3H]5-HT release from striatal slices, thus suggesting a potential role for ascorbate in DA-mediated actions of METH on serotonergic systems. Although supplemental ascorbate failed to restore the METH-induced serotonergic effects in scorbutic guinea pigs, these data suggest that, in a normal animal, the effects of multiple injections of METH, on serotonergic systems, involve ascorbic acid.

Amphetamine↗