Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Octopamine”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,045 records · Page 58Linked to original sources
PubMed1977

Evaluation of the uptake of various amines into storage vesicles of intact human platelets.

1 The uptake of various 3H-labelled amines into a thrombin-releasable compartment of human platelets, thought to represent the platelet vesicular storage pool, has been evaluated. Measurable amounts of 5-hydroxytryptamine (5-HT), dopamine, tyramine, octopamine, and tryptamine accumulate in this pool, and also in a non-thrombin-releasable (cytoplasmic) pool during a 30 min incubation period with 10(-5) M extracellular amine concentrations. 2 No differences in the accumulation of vesicular or cytoplasmic 5-HT, dopamine, and tyramine are found in platelets treated with deprenyl to inhibit platelet monoamine oxidase as compared to controls. 3 Extracellular tyramine or dopamine in concentrations as high as 10(-5) M does not alter the initial rate of 5-HT uptake across the platelet plasma membrane. Similarly, sizable cytoplasmic pools of either amine do not alter the initial rate at which small amounts of 5-HT enter platelet cytoplasm or storage vesicles. 5-HT thus appears to be the preferred substrate for uptake into platelets and for movement from cytoplasm to vesicles.

Biogenic Amines↗
PubMed1979

Content and subcellular localization of catecholamines and 5-hydroxytryptamine in human and animal blood platelets: monoamine distribution between platelets and plasma.

1 The content of adrenaline (Ad), noradrenaline (NA) and dopamine was measured in human, guinea-pig, cat, rabbit and rat blood platelets by a highly sensitive and specific radioenzymatic method.2 In all platelet specimens analyzed, the content of the three catecholamines (CA) was several thousand times lower than that of 5-hydroxytryptamine (5-HT).3 In basal conditions, the NA concentration in platelets and plasma always exceeded that of Ad and dopamine.4 In rat and rabbit platelets, Ad, NA and dopamine were present only in the free (unconjugated) form.5 Platelets of rats with storage pool deficiency (Fawn-hooded) contained much less 5-HT and CA than normal rat platelets.6 Following restraint stress, platelets of Fawn-hooded rats, in contrast to normal rat platelets, did not accumulate CA in spite of a dramatic rise in plasma CA.7 Reserpine, a monoamine depletor, released CA as well as 5-HT from rabbit platelets in vivo.8 Subcellular fractionation experiments with rabbit platelets indicate that both CA and 5-HT are most concentrated in the fraction consisting of pure 5-HT organelles.9 Both in humans and rabbits the concentration gradient between platelets and plasma was much lower for CA than for 5-HT, indicating that a high affinity transport mechanism operates in vivo for 5-HT but not for CA.10 In conclusion, the present data show that both human and animal platelets contain Ad, NA and dopamine. The bulk of the CA seems to be stored as unconjugated amines together with 5-HT, histamine and p-octopamine in a multitransmitter storage site, namely the 5-HT organelle.

Adult↗
PubMed1981

A study on the acute effect of amphetamine on the urinary excretion of biogenic amines and metabolites in monkeys.

1 The effects of an acute dose (3 mg/kg) of amphetamine on the urinary excretion of phenylethylamine (PEA), p-tyramine, their metabolites, catecholamine metabolites and p-hydroxymandelic acid, a major metabolite of p-octopamine were evaluated in the monkey. Amphetamine excretion was also measured. 2 Amphetamine was slowly eliminated from the body, being found in the urine at least six days after administration. 3 Amphetamine increased the excretion of PEA and decreased that of its major metabolite, phenylacetic acid (PAA). This pattern of changes is similar to that previously found in the urine of chronic schizophrenics. 4 The excretion of the dopamine metabolite, 3,4-dihydroxyphenylacetic acid (DOPAC) was markedly reduced, that of vanilmandelic acid (VMA) remained unchanged while 3-methoxy-4-hydroxyphenylglycol (MHPG) was increased on the day of drug administration and persisted for at least a further six days. A similar extended effect on the excretion of p-hydroxymandelic acid (it was reduced) was also observed. 5 The excretion of p-tyramine but not its metabolite, p-hydroxyphenylacetic acid, was decreased by amphetamine during treatment and returned to normal levels six days later. 6 From the results obtained, it was concluded that amphetamine effects on behaviour cannot exclusively be attributed to its influence on catecholamines and that other biogenic amines may be involved. 7 Since PEA elicits many behavioural changes similar to those seen with amphetamine, and since amphetamine increases PEA excretion, we suggest that amphetamine may exert some of its behavioural responses through the release of PEA.

Amphetamine↗
PubMed2007

Classical reward conditioning in Drosophila melanogaster.

Negatively reinforced olfactory conditioning has been widely employed to identify learning and memory genes, signal transduction pathways and neural circuitry in Drosophila. To delineate the molecular and cellular processes underlying reward-mediated learning and memory, we developed a novel assay system for positively reinforced olfactory conditioning. In this assay, flies were involuntarily exposed to the appetitive unconditioned stimulus sucrose along with a conditioned stimulus odour during training and their preference for the odour previously associated with sucrose was measured to assess learning and memory capacities. After one training session, wild-type Canton S flies displayed reliable performance, which was enhanced after two training cycles with 1-min or 15-min inter-training intervals. Higher performance scores were also obtained with increasing sucrose concentration. Memory in Canton S flies decayed slowly when measured at 30 min, 1 h and 3 h after training; whereas, it had declined significantly at 6 h and 12 h post-training. When learning mutant t beta h flies, which are deficient in octopamine, were challenged, they exhibited poor performance, validating the utility of this assay. As the Drosophila model offers vast genetic and transgenic resources, the new appetitive conditioning described here provides a useful tool with which to elucidate the molecular and cellular underpinnings of reward learning and memory. Similar to negatively reinforced conditioning, this reward conditioning represents classical olfactory conditioning. Thus, comparative analyses of learning and memory mutants in two assays may help identify the molecular and cellular components that are specific to the unconditioned stimulus information used in conditioning.

Animals↗
PubMed1982

Cholinergic and catecholaminergic receptors in the Xenopus oocyte membrane.

1. Neurotransmitter-receptors in the membrane of Xenopus oocytes have been studied using electrophysiological techniques. Neurotransmitters and related agents were applied while recording either membrane potential or membrane current. The majority of ovarian oocytes used were at stages IV and V.2. Three types of oocytes were examined: inner ovarian epithelium covered (e.c.) oocytes; epithelium manually removed (e.r.) oocytes; and collagenase treated (c.t.) ooctyes.3. Ovarian oocytes are sensitive to some cholinergic and catecholaminergic agents. Responses to serotonin were seldom observed and when present were much weaker than responses to other agents. No responses were observed to the amino acids: aspartate, glutamate, gamma-aminobutyric acid, and glycine; or to octopamine and histamine.4. Acetylcholine (ACh) usually depolarized the membrane, in a dose-dependent manner, with threshold concentrations as low as 10(-9)m. The ACh-potential was due to an increase in Cl permeability and had a reversal potential around - 19 mV. The intracellular Cl ion activity, measured with a Cl-ion sensitive micro-electrode, was about 65 mm and the estimated Cl-ion equilibrium potential, E(Cl), agreed with the reversal potential of the ACh-potential.5. Curare (10(-4)m), tetrodotoxin (10(-6)m), or alpha-bungarotoxin (10(-6) g/ml.) did not block the response to 10(-6)m-ACh; whereas atropine (10(-7)m) blocked it. No response to nicotinic agents (e.g. nicotine, 1,1-dimethyl-4-phenylpiperazinium) was observed. These results suggest that the ACh receptors in the oocyte membrane are muscarinic in nature.6. The apparent latency of the ACh potential, examined by ionophoretic application of ACh to e.r. oocytes and c.t. oocytes, ranged from 0.5 sec to over 20 sec. Intracellular injection of ACh was without effect.7. Responses to catecholamines were observed mostly in e.c. oocytes; while in e.r. and c.t. oocytes they were rare and of very small amplitudes.8. The usual response to both dopamine and (-)-epinephrine was a transient hyperpolarization manifested by an initial increase in K-permeability followed by a decrease. The latency of these responses ranged from 10 sec to over 30 sec and their reversal potential was nearly - 100 mV, which coincided with E(K).9. Oocytes responded to the beta-adrenergic receptor agonist, isoproterenol, as well as (-)-epinephrine. Pre-treatment with the beta-adrenergic receptor blocker, propranolol, abolished the response to both (-)-epinephrine and (-)-isoproterenol. The dopamine potential was also reduced considerably. Both the alpha-adrenergic receptor agonist, phenylephrine, and the alpha-adrenergic receptor blocker, phentolamine, were without effect.10. Maturation of the oocytes, induced in vivo by gonadotropin or in vitro by progesterone, led to loss of responsiveness to both cholinergic and catecholaminergic agents.

Acetylcholine↗
PubMed1983

The role of 5-hydroxytryptamine as a transmitter between identified leech neurones in culture.

The synthesis, storage, release and synaptic actions of 5-hydroxytryptamine (5-HT or serotonin) were studied in order to characterize the synaptic connexion that develops between pairs of identified neurones dissected from the central nervous system of the leech and maintained in culture. Experiments were made with Retzius cells (which are known to contain 5-HT in vivo) and pressure sensory neurones on which they form chemical synapses in culture. Individual, isolated Retzius cells in culture synthesized [3H]5-HT from either [3H]tryptophan or [3H]5-hydroxytryptophan [( 3H]5-HTP). These cells did not synthesize other putative neurotransmitters, such as acetylcholine, dopamine, octopamine, noradrenaline or gamma-aminobutyric acid from their respective precursors. The monoaminergic character of Retzius cells was also demonstrated by staining with Neutral Red and by histofluorescence. Individual, isolated Retzius cells that had synthesized and accumulated [3H]5-HT released this compound when depolarized. Transmitter release was calcium-dependent and was blocked by magnesium. When incubated with [3H]5-HT and washed, Retzius cells in culture accumulated approximately 100 times more labelled 5-HT than did non-serotonergic cells, and 10 times more than Retzius cell somata acutely isolated from the animal and incubated in vitro. Chlorimipramine, a blocker of 5-HT uptake, decreased the amount of [3H]5-HT accumulated by Retzius cells and also caused a reversible increase in the amplitude of the synaptic response in the pressure sensory cell elicited by stimulation of the Retzius cell. Pressure sensory neurones in culture and in vivo responded to 5-HT focally applied by pressure ejection from a micropipette. Small pulses elicited a small, slow hyperpolarization. This response was due, at least in part, to an increase in chloride conductance and desensitized rapidly. With larger pulses, a larger, faster non-desensitizing depolarization was elicited. Together, these results provide evidence that 5-HT released from Retzius cells could be responsible for the chemical synaptic potentials seen in pressure sensory neurones in culture.

5-Hydroxytryptophan↗
PubMed1986

Are Merkel cell-neurite reciprocal synapses involved in the initiation of tactile responses in salamander skin?

In salamander skin the Merkel cell-neurite complexes located near the base of the epidermis are the morphological correlates of the rapidly adapting touch receptors (Parducz, Leslie, Cooper, Turner & Diamond, 1977). The present electron microscopic studies revealed that these complexes contain reciprocal synapses polarized in the direction Merkel cell to neurite, and in the opposite direction, neurite to Merkel cell. The possible involvement of chemical transmission in the initiation of the mechanosensory response, was studied in vitro with the aid of a stable skin-nerve preparation in which single mechanoreceptors were activated under controlled conditions. Mechanosensitivity was measured with a calibrated prodder (tip diameter 10-30 micron) applied to random or selected points on the surface of the skin while the afferent impulse was recorded in the attached nerve twig. In some experiments the (tungsten) prodder was also used as a surface electrode, allowing the same mechanosensory axon to be excited mechanically (i.e. physiologically), and/or electrically. When applied at a single 'touch spot', suitably timed subthreshold mechanical and subthreshold electrical stimuli could summate to produce a single action potential. The temperature coefficient (Q10) between 5 and 15 degrees C for the latency of the afferent spike was small, in the range 1.3-2, whether it was evoked by mechanical or electrical stimulation. The latency following the mechanical stimulus, which included the transduction step, was longer than that following the electrical stimulus by 0.5-2.5 ms, and this additional delay was also relatively insensitive to temperature. In several cases removal of the epidermis with its Merkel cells (and presumably the most distal portions of the afferent nerve terminations) did not render the remaining skin totally insensitive to mechanical stimulation; however, the remaining receptive elements, though still rapidly adapting, generally had increased mechanosensory thresholds. The mechanosensitivity of the skin was unaffected by bath application of several aminergic (e.g. noradrenaline, 5-hydroxytryptamine, octopamine) and purinergic (e.g. ATP, quinacrine) compounds at concentrations in the range 0.2-2 mM. Removal of extracellular Ca2+ combined with elevation of extracellular Mg2+ (10-40 mM) had relatively little effect on the mechanosensitivity over periods of up to 1 h. In contrast, application of Co2+ (2-10 mM) produced a decrease or blockade of the mechanosensitivity that was not associated with any obvious alterations in the ultrastructure of the Merkel cell-neurite complex.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1988

Activation of protein kinase C promotes glutamate-mediated transmission at the neuromuscular junction of the mealworm.

1. Actions of protein kinase C activators, 1,2-oleoylacetylglycerol (OAG) and 12-O-tetradecanoylphorbol-13-acetate (TPA), on the glutamate-mediated neuromuscular transmission in the mealworm, Tenebrio molitor, were studied by the microelectrode current-clamp and voltage-clamp techniques. 2. The activators OAG and TPA stimulate the evoked and spontaneous transmitter releases from the presynaptic terminal, as evidenced by an increase in the quantum content estimated by the number of failures of extracellular excitatory postsynaptic potentials (EPSPs), and in the frequency of miniature EPSPs. 3. Both OAG and TPA act on the postsynaptic membrane to enhance responses to the transmitter L-glutamate. Protein kinase C activators increased the apparent maximum of the ionophoretic dose-response curve for glutamate-induced depolarization, without affecting the reversal potential and the voltage-dependent decay rate for the excitatory postsynaptic current (EPSC) under voltage-clamp conditions. 4. The postsynaptic effect of OAG and TPA is distinctly different from that of activators of cyclic nucleotide-dependent protein kinases, such as octopamine, forskolin, CPT-cyclic AMP (8-(4-chlorophenylthio)adenosine 3',5'-cyclic monophosphate), and 8-bromo-cyclic GMP (8-bromoguanosine 3',5'-cyclic monophosphate) which decreased the postsynaptic sensitivity to L-glutamate. 5. I suggest that the responsiveness of the receptor to L-glutamate is under the control of these counteracting enzyme systems in the insect neuromuscular junction.

Action Potentials↗
PubMed1997

Conditional dendritic oscillators in a lobster mechanoreceptor neurone.

1. Intra- and extracellular recordings were made from in vitro preparations of the lobster (Homarus gammarus) stomatogastric nervous system to study the nature and origin of pacemaker-like activity in a primary mechanoreceptor neurone, the anterior gastric receptor (AGR), whose two bilateral stretch-sensitive dendrites ramify in the tendon of powerstroke muscle GM1 of the gastric mill system. 2. Although the AGR is known to be autoactive, we report here that in 20% of our preparations, rather than autogenic tonic discharge, the receptor fired spontaneously in discrete bursts comprising three to ten action potentials and repeating at cycle frequencies of 0.5-2.5 Hz in the absence of mechanical stimulation. Intrasomatic recordings revealed that such rhythmic bursting was driven by slow oscillations in membrane potential, the frequency of which was voltage sensitive and dependent upon the level of stretch applied to the receptor terminals of the AGR. 3. Autoactive bursting of the AGR originated from an endogenous oscillatory mechanism in the sensory dendrites themselves, since (i) during both steady, repetitive firing and bursting, somatic and axonal impulses were always preceded 1:1 by dendritic action potentials, (ii) hyperpolarizing the AGR cell body to block triggering of axonal impulses revealed attenuated somatic spikes that continued to originate from the two peripheral dendrites, (iii) the timing of burst firing could be phase reset by brief electrical stimulation of either dendrite, and (iv) spontaneous bursting continued to be expressed by an AGR dendrite after physical isolation from the GM1 muscle and the stomatogastric nervous system. 4. Although a given AGR in vitro could switch spontaneously from dendritic bursting to tonic firing and vice versa, exogenous application of micromolar (or less) concentrations of the neuropeptide F1 (TNRNFLRFamide) to the dendritic membrane could rapidly and reversibly switch the receptor firing pattern from repetitive firing to the bursting mode. Exposure of the somatic and axonal membrane of the AGR to F1 was without effect, as were applications of other neuroactive substances such as serotonin, octopamine and proctolin. 5. We conclude that, as for many oscillatory neurones of the central nervous system, the intrinsic activity pattern of this peripheral sensory neurone may be dynamically conferred by extrinsic modulatory influences, presumably according to computational demands. Moreover, the ability of the AGR to behave as an endogenous burster imparts considerable integrative complexity since, in this activity mode, sensory coding not only occurs through the frequency modulation of on-going dendritic bursts but also via changes in the duration of individual bursts and their inherent spike frequencies.

Animals↗
PubMed2001

Amphetamine, 3,4-methylenedioxymethamphetamine, lysergic acid diethylamide, and metabolites of the catecholamine neurotransmitters are agonists of a rat trace amine receptor.

The trace amine para-tyramine is structurally and functionally related to the amphetamines and the biogenic amine neurotransmitters. It is currently thought that the biological activities elicited by trace amines such as p-tyramine and the psychostimulant amphetamines are manifestations of their ability to inhibit the clearance of extracellular transmitter and/or stimulate the efflux of transmitter from intracellular stores. Here we report the discovery and pharmacological characterization of a rat G protein-coupled receptor that stimulates the production of cAMP when exposed to the trace amines p-tyramine, beta-phenethylamine, tryptamine, and octopamine. An extensive pharmacological survey revealed that psychostimulant and hallucinogenic amphetamines, numerous ergoline derivatives, adrenergic ligands, and 3-methylated metabolites of the catecholamine neurotransmitters are also good agonists at the rat trace amine receptor 1 (rTAR1). These results suggest that the trace amines and catecholamine metabolites may serve as the endogenous ligands of a novel intercellular signaling system found widely throughout the vertebrate brain and periphery. Furthermore, the discovery that amphetamines, including 3,4-methylenedioxymethamphetamine (MDMA; "ecstasy"), are potent rTAR1 agonists suggests that the effects of these widely used drugs may be mediated in part by this receptor as well as their previously characterized targets, the neurotransmitter transporter proteins.

Amino Acid Sequence↗
PubMed1977

Phenylethanolamine: a new putative neurotransmitter in Aplysia.

Phenylethanolamine is present in the Aplysia nervous system in concentrations similar to that of octopamine. These are receptors that are very specific for phenylethanolamine, which on different neurons mediate sodium, chlorine, or potassium conductance increase responses. These observations indicate that phenylethanolamine may act as a neurotransmitter in Aplysia.

Animals↗
PubMed1979

Distribution of membrane-bound monoamine oxidase in bacteria.

The distribution of membrane-bound monoamine oxidase in 30 strains of various bacteria was studied. Monoamine oxidase was determined by using an ammonia-selective electrode; analyses were sensitive and easy to perform. The enzyme was found in some strains of the family Enterobacteriaceae, such as Klebsiella, Enterobacter, Escherichia, Salmonella, Serratia, and Proteus. Among strains of other families of bacteria tested, only Pseudomonas aeruginosa IFO 3901, Micrococcus luteus IFO 12708, and Brevibacterium ammoniagenes IAM 1641 had monoamine oxidase activity. In all of these bacteria except B. ammoniagenes, monoamine oxidase was induced by tyramine and was highly specific for tyramine, octopamine, dopamine, and norepinephrine. The enzyme in two strains oxidized histamine or benzylamine. Correlations between the distributions of membrane-bound monoamine oxidase and arylsulfatase synthesized in the presence of tyramine were discussed.

Bacteria↗
PubMed1981

Regulation of derepressed synthesis of arylsulfatase by tyramine oxidase in Salmonella typhimurium.

The participation of tyramine oxidase in the regulation of arylsulfatase synthesis in Salmonella typhimurium was studied. Arylsulfatase synthesis was repressed by inorganic sulfate, cysteine, methionine, or taurine. This repression was relieved by tyramine, octopamine, or dopamine, which induced tyramine oxidase synthesis, although the level of arylsulfatase activity was very low. The induction of tyramine oxidase and derepression of arylsulfatase by tyramine were strongly inhibited by glucose and ammonium chloride, and the repression of both enzymes was relieved by use of xylose as a carbon source after consumption of glucose or by use of tyramine as the sole source of nitrogen, irrespective of the carbon source used. The initial rates of tyramine uptake by cells grown with glucose and xylose were similar. Results with tyramine oxidase-constitutive mutants showed that constitutive expression of the tyramine oxidase gene resulted in derepression of arylsulfatase synthesis in the absence of tyramine. Thus, catabolite and ammonium repressions of arylsulfatase synthesis and the induction of the enzyme by tyramine seem to reflect the levels of tyramine oxidase synthesis. These results in S. typhimurium support our previous finding that the specific regulation system of arylsulfatase synthesis by tyramine oxidase is conserved in enteric bacteria.

Ammonia↗
PubMed1988

Catabolism of aromatic biogenic amines by Pseudomonas aeruginosa PAO1 via meta cleavage of homoprotocatechuic acid.

Pseudomonas aeruginosa PAO1 catabolized the aromatic amines tyramine and octopamine through 4-hydroxyphenylacetic acid and 3,4-dihydroxyphenylacetic acid (HPA). meta ring cleavage was mediated by 3,4-dihydroxyphenylacetate 2,3-dioxygenase (HPADO), producing 2-hydroxy-5-carboxymethylmuconic semialdehyde (MSA). An NAD-dependent dehydrogenase caused the disappearance of the yellow MSA product, probably forming 2-hydroxy-5-carboxymethylmuconic acid. Induction studies with extracts from mutant cells indicated that the inducer of HPADO was HPA and/or MSA. Strains PAO1.221 (tynC1) and PAO1.303 (tynD1) have chromosomal mutations causing a deficiency in the activity necessary for conversion of 4-hydroxyphenylacetic acid to HPA. Genetic analyses showed that the mutations were in different loci. Strains PAO1.197 (tynE1) and PAO1.185 (tynF1) are deficient in HPADO and the NAD-dependent dehydrogenase, respectively. Plasmid pRO1853 was constructed by cloning approximately 7.3 kilobases of PAO1 chromosomal DNA into the BamHI site of the vector plasmid pRO1614. This recombinant plasmid complemented the tynD1, tynE1, and tynF1 mutations. A putative repressor-binding site involved in the regulation of HPADO synthesis was observed for a subcloned fragment of pRO1853. This recombinant plasmid, pRO1863, failed to complement tynE1 or tynF1 but still complemented tynD1. Another construct, pRO1887, contained 9.2 kilobases of PAO1 chromosomal DNA inserted in the PstI site of the vector pRO1727. Plasmid pRO1887 complemented only the tynC1 mutation. Mapping experiments performed with the chromosome-mobilizing plasmid R68.45 located the mutations described above in a cluster at about 35 to 40 min of the PAO1 chromosome map. The mutations were linked to the proA, thr-48, lys-9015, argF10, and argG markers.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1975

Metabolism distribution, and disappearance of injected beta-phenylethylamine in the rat.

In the absence of a monoamine oxidase inhibitor, the bulk of intravenously injected radioactively labelled beta-phenylethylamine was oxidized to phenylacetic acid. In the presence of pargyline, most of the label in tissues remained as unchanged phenylethylamine; small amounts of labelled phenylethanolamine, tyramine and octopamine were also identified. After intravenous injection of [14-C]phenylalanine, only very small amounts of [14-C] phenylethylamine could be located in urine and faeces. Beta-Phenylethylamine became concentrated in all tissues, including brain, following intravenous introduction both in the presence and absence of pargyline. Its clearance from these tissues and from brain regions was very fast.

Animals↗
PubMed1978

Hypothalamic catecholaminergic effects on prolactin release in vitro.

Hypothalamic catecholaminergic influences on prolactin release were investigated in vitro. Both dopamine and norepinephrine caused long lasting inhibition of prolactin release from either an isolated hemipituitary or a hemipituitary coincubated with a hypothalamus. Epinephrine also inhibited prolactin release. L-Dihydroxyphenylalanine (L-dopa) inhibited prolactin release from pituitaries in the presence of a hypothalamus but not in isolated pituitaries. DL-Threodihydroxyphenylserine (threodops), serotonin, 5-hydroxy-L-tryptophan (5-HTP), tyramine, octopamine, synephrine, thyrotropin-releasing hormone (TRH), luteinizing hormone releasing hormone (LH-RH), and somatostatin all failed to alter prolactin release. Results confirm that dopamine and norepinephrine directly inhibit prolactin release from pituitary and suggest that the hypothalamic mechanism inhibiting prolactin involves dopamine but not norepinephrine.

Animals↗
PubMed1995

Characterization of the vasorelaxant activity of tyramine and other phenylethylamines in rat aorta.

We recently reported that tyramine caused concentration-dependent relaxation of rat aorta, which was endothelium independent and was not exerted via alpha 1-adrenoceptors (AR), alpha 2AR, beta 1AR, beta 2AR, or receptors for 5-hydroxytryptamine, histamine, and adenosine. The present studies were done on endothelium-denuded strips to determine structure-vasorelaxant activity after blockade of beta AR by propranolol plus irreversible blockade of alpha 1AR with benextramine. Vasorelaxation under these conditions was limited to noncatecholamines, and their vasorelaxant potencies were methoxyphenamine > tyramine > p-hydroxyephedrine > L-amphetamine > L-ephedrine > phenylethylamine > synephrine > methoxamine > octopamine. beta 3AR agonists (BRL 37344 and CGP 12177A) did not produce vasorelaxation, although tyramine could compete for cyanopindolol binding to murine L cells expressing human beta 2AR or beta 3AR. There was no significant specific binding of [3H]tyramine to aortic membrane preparations after the inhibition of monamine oxidase. Yohimbine, which has a high affinity for Drosophila tyramine receptors, also caused dose-dependent vasorelaxation like tyramine. It is concluded that tyramine and several other phenylethylamines produce relaxation of rat aorta, which does not involve any of the known adrenoceptors but may be exerted via novel tyramine receptors.

Animals↗
PubMed1982

Transmitterlike action of serotonin in phase shifting a rhythm from the Aplysia eye.

The presence of serotonin (5-HT) and the characteristics of the phase-response curve for 5-HT indicate that 5-HT acts as a transmitter of circadian information in the Aplysia eye. Additional evidence for such a neurotransmitter role of 5-HT in the eye is presented. The isolated eye has the capacity to synthesize 5-HT from exogenous tryptophan. The receptors mediating the phase-shifting effect of 5-HT have a high affinity for 5-HT (threshold for phase shifting is less than or equal to 10(-7) M). Also these receptors demonstrate a high degree of structural specificity for 5-HT. Some structurally similar indoles to 5-HT do not cause phase shifts (5-hydroxytryptophan, 5-hydroxyindoleacetic acid), whereas others (bufotenine, tryptamine, LSD) do cause phase shifts but are less effective than 5-HT. Furthermore phase shifts in the rhythm are not produced by other monoamine neurotransmitters (dopamine, octopamine) or acetylcholine. Changes in membrane conductance to Na+, Cl-, or Ca2+ do not appear to be involved in phase shifting by 5-HT. Since large reductions in extracellular Ca2+ did not affect phase shifting by 5-HT, 5-HT is acting either directly on the circadian pacemaker cell(s) or on cells electronically coupled to the pacemaker cell(s).

Animals↗