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PubMed1970

Effects of amphetamine derivatives on brain dopamine and noradrenaline.

1. Intracisternally administered metaraminol, alpha-methyl-octopamine, alpha-methyl-m-tyramine, and alpha-methyl tyramine were found to lower brain noradrenaline without having an effect on brain dopamine.2. Amphetamine, mephentermine, and norephedrine had no effect on brain catecholamines after intracisternal injection.3. There was no reduction in brain dopamine content after intracisternal injection of alpha-methyl-m-tyramine, yet the resulting brain concentration of alpha-methyl-m-tyramine was several times higher than after intraperitoneal injection of alpha-methyl-m-tyrosine, which decreased brain dopamine.4. The decreased synthesis of labelled catecholamines from (14)C-tyrosine after alpha-methyl-m-tyrosine suggested that this compound inhibits tyrosine hydroxylase in addition to its action of displacing brain amines.

Amphetamine↗
PubMed1974

Modification by drugs of the secretagogue effect of dopamine on the pancrease.

1 The specific stimulating action of dopamine and L-DOPA on exocrine pancreatic secretion was further investigated in the isolated blood-perfused canine pancreas.2 6-Hydroxydopamine (100 mug, i.a.) stimulated the secretion but was far less potent than dopamine. Epinine (0.3-1 mg. i.a.), alpha-methyldopamine (10-300 mug, i.a.) and octopamine (10-300 mug, i.a.) were ineffective.3 alpha-Methyldopa (30 mg, i.a.) inhibited the stimulating effect of L-DOPA (1-3 mg) on pancreatic secretion.4 Apomorphine (1 mg, i.a.) attenuated dopamine-induced (1-30 mug) pancreatic secretion but did not antagonize secretin-induced (0.03-0.3 units) or pancreozymin-induced (0.3-1 units) secretion.5 These observations suggest that L-DOPA is probably converted to dopamine to stimulate the exocrine pancreas, and that dopamine interacts with the specific receptors.6 The noradrenaline and dopamine content of the canine pancreas was estimated in controls and in dogs treated with secretin, reserpine, L-DOPA or alpha-methyldopa. The values for dopamine and noradrenaline in controls were 139 +/- 6 and 375 +/- 40 ng/g tissue (n=13), respectively. Reserpine reduced the noradrenaline content of the pancreatic tissue without affecting the dopamine content. L-DOPA or secretin caused a significant increase in the dopamine, but not in the noradrenaline content. It is suggested that dopamine has a physiological function in the pancreas which is independent of that of the noradrenaline-containing nerve fibres.

Animals↗
PubMed1977

The fate of biogenic monoamines in perfused rabbit lung.

1. Inactivation of beta-phenylethylamine and several of its derivatives was studied in a preparation of rabbit lung perfused with Krebs physiological medium at 37 degrees C. Inactivation or removal of these compounds was calculated as the difference between the concentration of each amine in the perfusion medium and the effluent, collected separately from each lung. The extent of amine metabolic degradation was also measured, by column chromatography, in lung effluent. 2. With this technique the magnitude of amine removal as a function of concentration was determined and an apparent Km and Vmax of removal were calculated for each amine. 3. Percentage removal was highest with phenylethylamine (95%), and decreased, apparently in relation to increasing phenyl- and side chain-hydroxylation (and therefore likely increased hydrophilicity), and 5-hydroxytryptamine (64%), tyramine (53%), octopamine (35%), dopamine (32%) and noradrenaline (23%). 4. Inactivation of each amine could be accounted for by metabolic degradation to deaminated products, which appeared in lung effluent within 90 s of beginning amine perfusion. 5. When intrapulmonary metabolism of phenylethylamine was inhibited by simultaneous perfusion with semicarbazide (10 mM) and pargyline (10 micronM), the removal rate was unaltered, establishing that uptake of the amine from the vascular space is not dependent on metabolism at least for 4 min infusions.

Animals↗
PubMed1986

Stereoselective accumulation of hydroxylated metabolites of amphetamine in rat striatum and hypothalamus.

The stereoselective accumulation of alpha-methyl-p-tyramine (AMPT) and alpha-methyl-p-octopamine (AMPO) in rat striatum and hypothalamus after acute and chronic administration of the (+)- and (-)-isomers of amphetamine (Amphet) and the acute administration of (+)- and (-)-AMPT has been investigated by chemical ionization gas chromatography mass spectrometry (c.i.g.c.m.s.). Two h after the administration of (+)- or (-)-AMPT (5 mg kg-1 i.p.), the concentrations of the isomers in striatal tissue were approximately equal; 18 h later, the concentration of the (+)-isomer was 10 times that of the (-)-isomer. The concentrations of AMPO in the striatum and hypothalamus 20 h after administration of (+)-AMPT were 68 ng g-1 and 484 ng g-1 respectively. After the administration of the (-)-isomer of AMPT, small quantities of AMPO were detected in both brain areas. Twenty h after the last of 7 daily injections of (+)-Amphet (5 mg kg-1, i.p.), the concentration of AMPO in the hypothalamus was 5.4 times the concentration at 20 h after one injection. In the striatum, the corresponding ratio for AMPO was 3.5 and for AMPT was 2.5. These data indicate that, although both isomers of AMPT formed from Amphet administered systemically, cross the blood brain barrier, the (+)-isomers AMPT and AMPO are preferentially stored in striatal and hypothalamic aminergic nerve terminals. The accumulations of AMPT and AMPO in rat striatum and hypothalamus after chronic administration of Amphet demonstrates that these metabolites persist in neuronal storage in these brain areas for days after administration. The half-lives of (+)-AMPT and (+)-AMPO in striatal neuronal storage, calculated from this data, were 1.5 days and 2.5 days, respectively. The corresponding half-life for hypothalamic (+)-AMPO was 7 days. 7. These findings suggest the involvement of accumulated AMPT and AMPO in the development of behavioural augmentation to repeated injections of Amphet (Randrup & Munkvad, 1970).

Amphetamine↗
PubMed1985

Pharmacological studies on the regulation of N-acetyltransferase activity and melatonin content of the pineal gland of the Syrian hamster.

Thus far, all attempts to stimulate melatonin synthesis by beta-adrenergic receptor agonists in the Syrian hamster pineal gland have failed. Neither a wide range of dosages of isoproterenol (0.5 mg/kg to 24 mg/kg), nor prolonged treatment with norepinephrine, the natural neurotransmitter, increased N-acetyltransferase (NAT) activity or melatonin production. In the present study, the administration of isoproterenol at night was likewise ineffective in advancing or enhancing the normal nightly melatonin peak. Also, we did not find a delayed effect 7 or 8 h after the administration of the drug. Furthermore, we tested the idea of coneurotransmitters such as octopamine or dopamine being possibly necessary for stimulation, but could not find any effect of these substances on melatonin synthesis. In addition, a parasympatholytic agent, atropine, did not increase the responsiveness to sympathomimetic agents. Administration of a phosphodiesterase inhibitor was also ineffective in stimulating NAT activity. On the other hand, isoproterenol did retard the drop in NAT and melatonin after lights-on at night, indicating that beta-receptors are involved in maintaining elevated melatonin levels.

Acetyltransferases↗
PubMed1975

Control of the neurotoxicity of 6-hydroxydopamine by intraneuronal noradrenaline in rat iris.

In vitro studies with the neurotoxic compounds 6-hydroxydopamine (6-OH-DA) and 6-aminodopamine (6-A-DA) showed that noradrenaline (NA) markedly inhibited the autooxidation of 6-OH-DA, but not of 6-A-DA. In vivo studies of the adrenergic nerves in rat iris showed that the neurotoxic potency of 6-OH-DA, but not 6-A-DA, was increased after NA depletion by alpha-methyl-p-tyrosine methylester (H44/68). Neurotoxicity was evaluated by measuring the associated decrease in 3-H-NA uptake. Intraocular injection of NA counteracted the degenerative action of 6-OH-DA in both untreated and H44/68 pretreated rats. Intraocular NA did not interfere with the neurotoxicity of 6-A-DA. Additionally, octopamine did not affect the rate of autooxidation nor the neurotoxic potency of 6-OH-DA or 6-A-DA. Control experiments with 3-H-6-OH-DA showed that the intraneuronal NA levels did not significantly affect the intraneuronal accumulation of 6-OH-DA. The parallelism between the in vitro results on autooxidation and in vivo data on neurotoxicity makes it appear that the neurotoxic potency of 6-OH-DA and 6-A-DA is closely associated with their rates of autooxidation. The control of the degenerative action of 6-OH-DA by intraneuronal NA may be mediated via reaction of NA with radicals formed from oxygen during autooxidation of 6-OH-DA.

Animals↗
PubMed1975

Microiontophoretic studies of the effects of false transmitter candidates and amphetamine on cerebellar Purkinje cells.

The effects of microiontophoretic applications of equivalent doses (ejection times and currents) of noradrenaline, amphetamine, octopamine and p-hydroxynorephedrine on the spontaneous firing of Purkinje and unidentified cells in the cerebellum of rats were examined. In addition, the effects of amphetamine of Purkinje cells were examined in animals pretreated with the tyrosine hydroxylase inhibitor, alpha-methyltyrosine (alpha-MpT) or with a combination of reserpine plus alpha-MpT. The results indicate that the "false transmitters" are weak agonists when compared to noradrenaline in inhibiting the firing of Purkinje cells. The results of the iontophoretic studies with amphetamine are not consistent with a pre-synaptic releasing effect by amphetamine at noradrenergic synapses in the cns since the efficacy of amphetamine on Purkinje cells was unaltered after pretreatment with alpha-MpT or alpha-MpT plus reserpine.

Action Potentials↗
PubMed2001

The antidepressant-sensitive dopamine transporter in Drosophila melanogaster: a primordial carrier for catecholamines.

Extracellular concentrations of monoamine neurotransmitters are regulated by a family of high-affinity transporters that are the molecular targets for such psychoactive drugs as cocaine, amphetamines, and therapeutic antidepressants. In Drosophila melanogaster, cocaine-induced behaviors show striking similarities to those induced in vertebrate animal models. Although a cocaine-sensitive serotonin carrier exists in flies, there has been no pharmacological or molecular evidence to support the presence of distinct carrier subtypes for other bioactive monoamines. Here we report the cloning and characterization of a cocaine-sensitive fly dopamine transporter (dDAT). In situ hybridization demonstrates that dDAT mRNA expression is restricted to dopaminergic cells in the fly nervous system. The substrate selectivity of dDAT parallels that of the mammalian DATs in that dopamine and tyramine are the preferred substrates, whereas octopamine is transported less efficiently, and serotonin not at all. In contrast, dDAT inhibitors display a rank order of potency most closely resembling that of mammalian norepinephrine transporters. Cocaine has a moderately high affinity to the cloned dDAT (IC50 = 2.6 microM). Voltage-clamp analysis of dDAT expressed in Xenopus laevis oocytes indicates that dDAT-mediated uptake is electrogenic; however, dDAT seems to lack the constitutive leak conductance that is characteristic of the mammalian catecholamine transporters. The combination of a DAT-like substrate selectivity and norepinephrine transporter-like inhibitor pharmacology within a single carrier, and results from phylogenetic analyses, suggest that dDAT represents an ancestral catecholamine transporter gene. The identification of a cocaine-sensitive target linked to dopaminergic neurotransmission in D. melanogaster will serve as a basis for further dissection of the genetic components of psychostimulant-mediated behavior.

Amino Acid Sequence↗
PubMed2001

Nitric oxide and the control of firefly flashing.

Bioluminescent flashing is essential for firefly reproduction, yet the specific molecular mechanisms that control light production are not well understood. We report that light production by fireflies can be stimulated by nitric oxide (NO) gas in the presence of oxygen and that NO scavengers block bioluminescence induced by the neurotransmitter octopamine. NO synthase is robustly expressed in the firefly lantern in cells interposed between nerve endings and the light-producing photocytes. These results suggest that NO synthesis is a key determinant of flash control in fireflies.

Animals↗
PubMed1963

Enzymatic formations of adrenaline and other catechols from monophenols.

An enzyme that forms adrenaline from p- and m-sympathol and dopamine from p- and m-tyramine is localized in the microsomes of rabbit liver and requires the reduced form of nicotinamide adenine dinucleotide phosphate. The enzyme is nonspecific and can form catechols from the following normally occurring and foreign phenols: p- and m-octopamine, p-hydroxyephedrine, phenol, stilbestrol, N-acetyl-p-aminophenol, estradiol and N-acetylserotonin.

Animals↗
PubMed1976

Synaptic facilitation and behavioral sensitization in Aplysia: possible role of serotonin and cyclic AMP.

The neural changes accompanying sensitization of the gill-withdrawal reflex in Aplysia are associated with presynaptic facilitation at monosynaptic connections between sensory neurons and motor cells. To analyze the molecular mechanisms underlying the facilitation, the pharmacological actions of serotonin, octopamine, and dopamine were examined. Only serotonin enhanced synaptic transmission between the sensory and the motor neurons. A serotonin antagonist, cinanserin, reversibly blocked the synaptic facilitation. The action of serotonin may be mediated by adenosime 3',5'-monophosphate (cyclic AMP). Exposing the ganglion to dibutyryl cyclic AMP or injecting cyclic AMP into the cell body enhances the synaptic action of a sensory neuron. The mechanism of presynaptic facilitation, therefore, may include activation of one or more serotonergic neurons, which enhance the release of a neurotransmitter by increasing the intracellular concentration of cyclic AMP in the terminals of the sensory neurons.

Action Potentials↗
PubMed1976

Regulation of tyramine oxidase synthesis in Klebsiella aerogenes.

Tyramine oxidase in Klebsiella aerogenes is highly specific for tyramine, dopamine, octopamine, and norepinephrine, and its synthesis is induced specifically by these compounds. The enzyme is present in a membrane-bound form. The Km value for tyramine is 9 X 10(-4) M. Tyramine oxidase synthesis was subjected to catabolite repression by glucose in the presence of ammonium salts. Addition of cyclic adenosine 3',5'-monophosphate (cAMP) overcame the catabolite repression. A mutant strain, K711, which can produce a high level of beta-galactosidase in the presence of glucose and ammonium chloride, can also synthesize tyramine oxidase and histidase in the presence of inducer in glucose ammonium medium. Catabolite repression of tyramine oxidase synthesis was relieved when the cells were grown under conditions of nitrogen limitation, whereas beta-galactosidase was strongly repressed under these conditions. A cAMP-requiring mutant, MK54, synthesized tyramine oxidase rapidly when tyramine was used as the sole source of nitrogen in the absence of cAMP. However, a glutamine synthetase-constitutive mutant, MK94, failed to synthesize tyramine oxidase in the presence of glucose and ammonium chloride, although it synthesized histidase rapidly under these conditions. These results suggest that catabolite repression of tyramine oxidase synthesis in K. aerogenes is regulated by the intracellular level of cAMP and an unknown cytoplasmic factor that acts independently of cAMP and is formed under conditions of nitrogen limitation.

Amino Acid Oxidoreductases↗
PubMed1984

Visual evoked potential: a diagnostic tool for the assessment of hepatic encephalopathy.

Visual evoked potential recordings were examined in 45 liver cirrhosis patients with (n = 29) and without (n = 16) encephalopathy, in 15 normal volunteers, and in one patient with an opioid induced stupor state. Visual evoked potential parameters were classified on the basis of EEG recordings. Plasma concentrations of amino acids, octopamine, and ammonia were assayed in order to document the metabolic change of hepatic encephalopathy. Latencies and wave patterns recorded after flash stimulation differentiated the four degrees of the coma one from another according to EEG classification in the 29 patients with encephalopathy. In the group of 16 patients without clinical and EEG evidence of encephalopathy the visual potential recordings discriminated a group of patients (n = 10) in a preclinical stage of encephalopathy. Biochemical parameters and subsequent clinical observation of patients confirmed our judgement of a preclinical stage of encephalopathy. These results suggest that visual evoked potentials are a simple, suitable and objective method for differentiating the degrees of encephalopathy and for identifying the preclinical stage of encephalopathy.

Adult↗
PubMed1979

Neurotransmitter receptors on gill muscle fibers and the gill peripheral nerve plexus in Aplysia.

Isolated pinnules of the gill of Aplysia contract when dopamine (DA) is perfused through the bath. The contraction is not blocked by high-Mg2+ seawater, and reflects excitatory receptors for DA on the smooth muscle cells of the gill. The pinnule often shows irregular, spontaneous contractions which are blocked by high-Mg2+ seawater and 30 mM CoCl2. These contractions reflect spontaneous activity of a peripheral nerve plexus. No other transmitter was found to be directly excitatory on the muscle fibers, although there are inhibitory receptors for serotonin (5-HT). Tactile stimulation of the pinnule evoked a two-component contractile reflex contraction due to activation of the peripheral nerve plexus. Acetylcholine, octopamine, and 5-HT but not several other transmitters depressed these responses, presumably due to inhibitory receptors on the neurons of the peripheral plexus.

Animals↗
PubMed2006

Amine modulation of Ih in a small neural network.

We studied the functional role and modulation of the hyperpolarization-activated inward current (I(h)) in the pyloric network of the lobster stomatogastric ganglion. In isolated neurons, I(h) is a small current with a hyperpolarized voltage of half-activation (V(Act)) and a slow time constant of activation (tau(Act)). Bath application of dopamine (DA), octopamine (OCT), or serotonin (5HT) modified I(h) in selected synaptically isolated pyloric neurons. DA significantly enhanced I(h) in the anterior burster (AB) neuron by depolarizing its V(Act), accelerating its tau(Act), and enhancing its maximal conductance (g(max)). DA more weakly enhanced I(h) in the pyloric constrictor (PY) and ventricular dilator (VD) neurons. OCT weakly depolarized V(Act) and accelerated tau(Act) in the VD and inferior cardiac (IC) neurons. 5HT depolarized V(Act) in the IC neuron. Under control conditions with intact modulatory inputs from other ganglia, the pyloric rhythm cycles strongly at about 1-2 Hz. Bath application of the I(h) blocker cesium (Cs(+)) caused a mean increase in the period of 8%, although this effect was highly variable. When Cs(+) was applied to an isolated ganglion where the pyloric rhythm had been activated only by DA, the cycle period was consistently increased by 13.5%, with no other strong changes in rhythm parameters. These results suggest that I(h) regulates the pyloric rhythm by accelerating AB pacemaker frequency, but that this effect can vary with the modulatory conditions.

Algorithms↗
PubMed2005

Differential receptor activation by cockroach adipokinetic hormones produces differential effects on ion currents, neuronal activity, and locomotion.

Adipokinetic hormone (AKH) peptides in insects serve the endocrine control of energy supply. They also produce, however, neuronal, vegetative, and motor effects, suggesting that AKHs orchestrate adaptive behavior by multiple actions. We have cloned, for Periplaneta americana, the AKH receptor to determine its localization and, based on current measurements in neurons and heterologous expression systems, the mechanisms of AKH actions. Apart from fat body, various neurons express the AKH receptor, among them abdominal dorsal unpaired median (DUM) neurons, which release the biogenic amine octopamine. They are part of the arousal system and are involved in the control of circulation and respiration. Both the two Periplaneta AKHs activate the Gs pathway, and AKH I also potently activates Gq. AKH I and--with much less efficacy--AKH II accelerate spiking of DUM neurons through an increase of the pacemaking Ca2+ current. Because the AKHs are released from the corpora cardiaca into the hemolymph, they must penetrate the blood-brain barrier for acting on neurons. That this happens was shown electrophysiologically by applying AKH I to an intact ganglion. Systemically injected AKH I stimulates locomotion potently in striking contrast to AKH II. This behavioral difference can be traced back conclusively to the different effectiveness of the AKHs on the level of G proteins. Our findings also show that AKHs act through the same basic mechanisms on neuronal and nonneuronal cells, and they support an integration of metabolic and neuronal effects in homoeostatic mechanisms.

Animals↗
PubMed1977

Synthesis of acetylcholine by excitatory motoneurons in central nervous system of the leech.

1. A study was made of the synthesis of acetylcholine (ACh) and other transmitters by the cell bodies of functionally identified neurons in leech segmental ganglia. 2. Choline acetyltransferase, the synthetic enzyme for ACh, was detected in excitatory motoneurons but not in mechanosensory cells or Retzius cells. The ability of motoneurons to synthesize ACh was also demonstrated by their accumulation of [3H]ACh following incubation of segmental ganglia with [3H]choline. [3H]ACh was not detected in the other cell types. When eserine was included in [3H]choline incubations, the amount of [3H]ACh in motoneurons increased severalfold and small amounts of [3H]ACh (1% that in motor cells) appeared in extracts of sensory and Retzius cells. 3. In addition to [3H]ACh segmental ganglia synthesized [3H]5-HT, [3H]gamma-aminobutyric acid, [3H]dopamine, and [3H]octopamine from exogenous, labeled precursors. None of these labeled transmitters was detected in identified neurons except [3H]5-HT, which was found in Retzius cells. 4. These results provide biochemical evidence that excitatory motoneurons in the leech are cholinergic, but leave open the identity of the sensory transmitter(s).

Acetylcholine↗
PubMed1992

Habituation of an appetitive reflex in the honeybee.

1. The proboscis extension reflex is an appetitive component of the bee's feeding behavior that is elicited by touching one antenna with a droplet of sugar water. Repetitive stimulation leads to a decrement and finally to the disappearance of the response, which can be restored by stimulating the contralateral antenna. This behavioral plasticity conforms to essential parametric characteristics for habituation. 2. The response was quantified by recording extracellularly from a muscle involved in proboscis movement, by measuring the duration of the proboscis extension, or by determining the number of trials necessary to abolish any visible response. 3. Because habituation was restricted to the repetitively stimulated antenna and did not generalize to the contralateral hemisphere, the neural circuits mediating habituation may be confined to one hemisphere. 4. State dependence of habituation could be demonstrated by showing that hungry animals exhibited a smaller response decrement and required more trials until disappearance of the response compared with satiated animals. The initial response and the subsequent response decrement are separate components determined by satiation level and stimulus strength. 5. Depleting the nervous system of monoamines by the use of reserpine abolished the reflex in 30% of the animals and reduced responsiveness in the remainder. Injection of octopamine or its metabolic precursor tyramine restored the reflex in reserpinized unresponsive animals, and tyramine also enhanced the muscle-spike discharge of reserpinized, responsive animals. In undepleted animals, tyramine application also accelerated the rate of habituation of the reflex. We therefore propose that octopaminergic neurons participate in mediating food arousal and the state dependence of habituation and, in a separate process, influence the response decrement during habituation. 6. Application of an acetylcholine esterase (AChE) inhibitor and a cholinergic receptor blocker confirmed histochemical data that implicate cholinergic transmission in the reflex pathways. 7. The combined pharmacological dissection of the reflex and immunocytochemical investigations of its chemical architecture provide evidence that the proboscis extension reflex is mediated by nonaminergic and monoaminergic pathways operating in parallel.

Animals↗