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PubMedDate not supplied

E-2078, a potent, selective and stable dynorphin analog with preferential activity for the kappa-opioid receptor subtype on the mouse vas deferens neuroeffector junction.

The profile of opioid activity of E-2078, a synthetic stable dynorphin analog, was examined in the mouse vas deferens bioassay and compared to that of methionine enkephalin and nonpeptide kappa agonists in the absence and in the presence of selective antagonists for the mu-, kappa- and delta-opioid receptor subtypes. The inhibitory action of E-2078 and related kappa agonists was specifically and potently antagonized only by norbinaltorphimine, revealing the presence of kappa receptors in this tissue and the predominant kappa activity of E-2078.

Animals↗
PubMed1982

Role of prostaglandins in rat pineal neuroeffector junction. Changes in melatonin and norepinephrine release in vitro.

The effects of prostaglandins (PGs) on melatonin secretion and norepinephrine (NE) and release in rat pineal gland were examined in vitro. To study melatonin secretion, pineal explants were incubated for 6 h in tissue culture 199 medium with 1-1000 nM PGE1, PGE2, or PGF2 alpha. melatonin concentration in pineal glands and media was determined by RIA, PGE2 increased pineal and medium melatonin at all concentrations tested, with a maximum of 1 nM; PGE1 was effective only at concentrations 100-1000 times greater, whereas 100 nM PGF2 alpha gland. Exposure of pineal explants to 10 microM NE brought about a 20-fold increase in melatonin release to the medium. This effect was impaired significantly, but not blocked, by prior exposure to indomethacin, acetylsalicylic acid, or mefenamic acid at supramaximal concentrations to inhibit PG synthesis (100 microM). To examine the effects of PGs on NE release, endogenous NE stores in pineal nerve endings were labeled in vitro by incubating rat pineals with [3H]NE for 30 min. Fifty minutes later, at the time when spontaneous radioactivity efflux had leveled off, transmitter release was elicited by a 1-min exposure to 80 mM K+ (S1), and the stimulus was repeated 35 min later (S2). PGs (10-100 nM) were added to the medium 20 min before S2. Ratios between fractional release of the two consecutive stimulations (S2/S1) varied between 0.84 and 1.16 in control pineals. Only 100 nM PGE2 impaired significantly transmitter release by 40%. These results suggest that PGE2 can play a role in NE-stimulated melatonin synthesis. At greater concentrations PGE2 inhibits NE release from pineal nerve endings.

Alprostadil↗
PubMed1976

Activities of prostaglandins and prostaglandin endoperoxides at adrenergic neuroeffector junctions.

The results presented in this paper indicate that: 1. The prostaglandin synthesis inhibitor, indomethacin, increases noradrenaline turnover in a variety of rat organs. This observation increases the probability that prostaglandins are involved in the control of adrenergic neurotransmission in vivo. 2. Administration of endoperoxides inhibits the release of noradrenaline from adrenergic nerve terminals. The effect can be explained, however, at least in part, by formation of degradation products, presumably mainly prostaglandin E2. 3. Prostaglandin F2 alpha enhances smooth muscle responses to adrenergic nerve stimulation in rabbit heart and guinea pig vas deferens. These actions must be considered prostjunctional, since the release of noradrenaline is unchanged or depressed.

Animals↗
PubMed1976

Prostaglandin action on transmitter release of adrenergic neuroeffector junctions.

The results presented here indicate that 1. The inhibitory action of the endoperoxides on NE release can be at least partly explained in terms of formation of degradation products, presumably mainly PGE2. 2. PGA2 is less active and the PG analogue 16,16-dimethyl-PGE2 more active than PGEs on transmitter release from adrenergic nerves. 3. PGF2alpha seems to enhance vascular responses to renal nerve activity solely by a postjunctional action. 4. PG synthesis inhibition augments NE turnover in a number of rat organs, thereby increasing the probability of PGs being involved in the control of adrenergic neurotransmission in vivo. 5. Prolongation of the duration of the impulse and action potential counteracts the effect of PGE on NE release, thereby strengthening the view that PGs operate on NE release from adrenergic nerve terminals by interfering with Ca2+ influx.

Animals↗
PubMed1982

Ultrastructure of vesicourethral innervation. I. Neuroeffector and cell junctions in the male internal sphincter.

The ultrastructure of neuroeffector and cell junctions in smooth muscle of the internal sphincter was studied in the male cat and rat. Muscle cells of the sphincter have the same features of smooth muscle elsewhere, with frequent adherens-type junctions. Neuroeffector junctions are established with sphincter muscle cells by cholinergic and/or adrenergic axons, which probably are not distributed on a 1:1 nerve:muscle basis. The neuroeffector junctions are classified according to their cleft width, their overall morphology, the functional class of their axonal component, and the number of axonal and muscle cell elements involved. These observations unequivocally confirm the principle of dual cholinergic-adrenergic control of the male internal sphincter, and indicate that its mechanism of neuromuscular transmission is both direct via neuroeffector and indirect via muscle cell junctions.

Animals↗
PubMed1999

Specialised sympathetic neuroeffector associations in immature rat iris arterioles.

Sympathetic nerve-mediated vasoconstriction in iris arterioles of mature rats occurs via the activation of alpha(1B)-adrenoceptors alone, while in immature rat iris arterioles, vasoconstriction occurs via activation of both alpha1- and alpha2-adrenoceptors. In mature rats the vast majority of sympathetic varicosities form close neuroeffector junctions. Serial section electron microscopy of 14 d iris arterioles has been used to determine whether restriction in physiological receptor types with age may result from the establishment of these close neuroeffector junctions. Ninety varicosities which lay within 4 microm of arteriolar smooth muscle were followed for their entire length. Varicosities rarely contained dense cored vesicles even after treatment with 5-hydroxydopamine. 47 % of varicosities formed close associations with muscle cells and 88 % formed close associations with muscle cells or melanocytes. Varicosities in bundles were as likely as single varicosities to form close associations with vascular smooth muscle cells, although the distribution of synaptic vesicles in single varicosities did not show the asymmetric accumulation towards the smooth muscle cells seen in the varicosities in bundles which were frequently clustered together. We conclude that restriction of physiological receptor types during development does not appear to correlate with the establishment of close neuroeffector junctions, although changes in presynaptic structures may contribute to the refinement of postsynaptic responses.

Animals↗
PubMed1993

Sympathetic transmission to the dilator muscle of the rat iris.

The responses of the dilator layer of the rat iris to sympathetic nerve stimulation were examined using intracellular recording techniques. Three different cell types were detected. In two of these, which were assumed to reflect recordings from myoepithelial cells, sympathetic nerve stimulation initiated excitatory junction potentials. These started after a delay of several hundred milliseconds and lasted for several seconds. The excitatory junction potentials were abolished by low concentrations of prazosin and were relatively insensitive to yohimbine, indicating that neurally released noradrenaline activated an alpha 1-adrenoceptor. The adrenoceptor was further characterised as being of the alpha 1b subtype using chlorethylclonidine. The time course of excitatory junction potentials was slowed when the preparation was cooled, suggesting that a second messenger pathway was being activated. The contractions triggered by sympathetic nerve stimulation persisted after excitatory junction potentials had been abolished by reducing the external concentration of chloride ions and after adding the organic calcium antagonist, nifedipine. Thus it seems likely that contractions of the dilator are triggered by the release of calcium ions from internal stores. These observations are discussed in relation to the idea that alpha 1b-adrenoceptors are coupled to a messenger pathway which involves inositol triphosphate and the pulsatile release of calcium ions from internal stores. The second section of the paper deals with the structure of neuro-myoepithelial contacts in the dilator layer. The majority of sympathetic varicosities formed organized neuroeffector junctions with either myoepithelial cells or melanophores. At the junctions the effector cell membrane and varicosity membrane were separated by less than 80 nm, with synaptic vesicles concentrated towards the neuroeffector junction. The synaptic vesicles in varicosities that failed to form junctions did not aggregate towards their regions of exposed membrane. These observations are discussed in relation to the idea that transmission at autonomic varicosities occurs at organised neuroeffector junctions.

Adrenergic alpha-Antagonists↗
PubMed1990

On the factors which determine the time-courses of junction potentials in the guinea-pig vas deferens.

The time-courses of junction potentials and junction currents at the sympathetic neuroeffector junction of guinea-pig vas deferens were investigated using simultaneous intracellular and focal extracellular recording. Excitatory junction potentials produced in the smooth muscle cells following electrical stimulation of the sympathetic nerves had duration of 600-1000 ms and were prolonged in time-course compared with the underlying excitatory junction currents which had durations of 40-150 ms. The time-course of the excitatory junction potential could be predicted accurately from the time-course of the underlying excitatory junction current by assuming that the smooth muscle cells were isopotential during the excitatory junction potential. In contrast, the time-course of the spontaneous excitatory junction potential, produced by the action of a single quantum of transmitter, was identical to the time-course of the underlying spontaneous excitatory junction current, both events having durations of 40-150 ms. Local application of 10(-4) M adenosine 5'-triphosphate in the vicinity of an intracellular microelectrode produced depolarizations ("adenosine 5'-triphosphate potentials") of durations ranging between 400 and 2500 ms. When adenosine 5'-triphosphate was applied close to the rim of an extracellular electrode, negative-going signals ("adenosine 5'-triphosphate currents") were produced which reflected the time-course of postjunctional membrane currents evoked by adenosine 5'-triphosphate. Adenosine 5'-triphosphate currents were abolished by alpha, beta-methylene adenosine 5'-triphosphate (10(-6) M) but were unaffected by tetrodotoxin (3 x 10(-7) M or 10(-6) M) and the alpha-adrenoceptor blockers prazosin (10(-6) M) and phentolamine (10(-6) M). The time-courses of adenosine 5'-triphosphate currents were similar to the time-courses of excitatory junction currents recorded in the same preparation. Adenosine 5'-triphosphate currents were generally brief compared with simultaneously recorded adenosine 5'-triphosphate potentials which had durations or greater than or equal to 1000 ms. The time-courses of relatively brief adenosine 5'-triphosphate potentials (duration less than or equal to 800 ms) followed the time-courses of the underlying adenosine 5'-triphosphate currents. These results indicate that the time-course of decay of the excitatory junction potential in the guinea-pig vas deferens is determined mainly by the passive membrane properties of the smooth muscle cells, the duration of underlying transmitter action being brief. However, the factors determining the time-course of adenosine 5'-triphosphate potentials are less clear, and may include passive membrane properties and diffusion of locally applied adenosine 5'-triphosphate.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Triphosphate↗
PubMed1986

Neurovascular function in the rat during pregnancy.

Activity of the vascular neuroeffector junction was examined in pregnant (PG) and nonpregnant (NPG) rats to determine whether changes could account for the reported alterations in sympathetic control of the maternal circulation. Caudal and mesenteric arteries were removed from NPG and 19-21 day PG rats and prepared for isometric tension recording. Frequency-response measurements were obtained, followed by norepinephrine (NE) and tyramine concentration-response measurements. The caudal artery developed more tension in response to NE, tyramine, and electrical stimulation than did the mesenteric artery; however, there were no differences between vessels from NPG and PG rats. NE content, [3H]NE accumulation, and effects of plasma on [3H]NE accumulation of NPG and PG caudal arteries were also compared and found to be similar. Therefore, vascular neuroeffector functions of NE release, receptor sensitivity, and NE accumulation are not modified in the rat during pregnancy. Changes in sympathetic control of the maternal circulation are likely to be dependent on alterations at sites other than the neuroeffector junction.

Animals↗
PubMedDate not supplied

Autonomic neuroeffector mechanisms: recent developments.

Peripheral autonomic control mechanisms are more sophisticated than formerly recognized. The autonomic neuroeffector junction is defined, with emphasis on 'en passage' release of transmitter from varicosities in extensive terminal branching nerve fibres. In addition to the classical autonomic transmitters acetylcholine and noradrenaline, a multiplicity of other neurotransmitter substances are also present, including peptides, purines, indoleamines and amino acids. There is coexistence of different combinations of these substances which, upon release, act either as cotransmitters or neuromodulators. Examples are described, including cotransmission and neuromodulation at sympathetic, parasympathetic and sensory-motor neuroeffector junctions. The involvement of locally released agents in peripheral control is also described, including substances produced secondarily as a result of release of neurotransmitters, as well as the release of substances from vascular endothelial cells leading to vasodilatation.

Animals↗
PubMed2003

Cannabinoid modulation of peripheral autonomic and sensory neurotransmission.

Cannabinoids are cell membrane-derived signalling molecules that are released from nerves, blood cells and endothelial cells, and have diverse biological effects. They act at two distinct types of G-protein-coupled receptors, cannabinoid CB(1) and CB(2) receptors. Cannabinoid CB(1) receptors are highly localised in the central nervous system and are also found in some peripheral tissues, and cannabinoid CB(2) receptors are found outside the central nervous system, in particular in association with immune tissues. Novel actions of cannabinoids at non-CB(1) non-CB(2) cannabinoid-like receptors and vanilloid VR1 receptors have also recently been described. There is growing evidence that, among other roles, cannabinoids can act at prejunctional sites to modulate peripheral autonomic and sensory neurotransmission, and the present article is aimed at providing an overview of this. Inhibitory cannabinoid CB(1) receptors are expressed on the peripheral terminals of autonomic and sensory nerves. The role of cannabinoid receptor ligands in modulation of sensory neurotransmission is complex, as certain of these (anandamide, an "endocannabinoid", and N-arachidonoyl-dopamine, an "endovanilloid") also activate vanilloid VR1 receptors (coexpressed with cannabinoid CB(1) receptors), which excites sensory nerves and causes a release of sensory neurotransmitter. The fact that the activities of anandamide and N-arachidonoyl-dopamine span two distinct receptor families raises important questions about cannabinoid/vanilloid nomenclature, and as both compounds are structurally related to the archetypal vanilloid capsaicin, all three are arguably members of the same family of signalling molecules. Anandamide is released from nerves, but unlike classical neurotransmitters, it is not stored in and released from nerve vesicles, but is released on demand from the nerve cell membrane. In the central nervous system, cannabinoids function as retrograde signalling molecules, inhibiting via presynaptic cannabinoid CB(1) receptors the release of classical transmitter following release from the postsynaptic cell. At the neuroeffector junction, it is more likely that cannabinoids are released from prejunctional sites, as the neuroeffector junction is wide in some peripheral tissues and cannabinoids are rapidly taken up and inactivated. Understanding the actions of cannabinoids as modulators of peripheral neurotransmission is relevant to a variety of biological systems and possibly their disorders.

Animals↗
PubMed1980

Interaction of the tricyclic antidepressant amitriptyline with prejunctional alpha and muscarinic receptors in the dog saphenous vein.

Amitriptyline can cause tachycardia and arrhythmia associated with an excessive release of cardiac catecholamines. We have investigated its effects on norepinephrine release from adrenergic nerves by using the dog saphenous vein as a model of the sympathetic neuroeffector junction. Isolated strips of vein were mounted for isometric tension recording or incubated with [3H]norepinephrine and mounted for superfusion, tension recording and the superfusate. Amitriptyline (10(-6); 5 x 10(-6) M) increased the overflow of [3H]norepinephrine but decreased that of [3,4-3H]dihydroxyphenylglycol from electrically stimulated strips. The selective decreased in the overflow of this metabolite indicates that amitriptyline inhibits neuronal uptake. However, the increased overflow of [3H]norepinephrine caused by amitriptyline also occurred when neuronal uptake was blocked by cocaine (3 x 10(-5) M) but was abolished when prejunctional alpha receptors were blockade by phentolamine (10(-5) M). Amitriptyline attenuated the prejunctional inhibitory action of exogenous norepinephrine, this indicates that the drug interacts with prejunctional alpha receptors. Amitriptyline also antagonized the prejunctional inhibitory action of acetylcholine, both in the absence and presence of cocaine and phentolamine. These effects were not due to a nonspecific action of the drug as it did not reduce the prejunctional inhibitory effect of histamine. Thus, amitriptyline can increase the concentration of norepinephrine at the neuroeffector junction by blockade of neuronal uptake and by interacting with prejunctional alpha and muscarinic receptors. Since the cardiac adrenergic nerves also possess these receptors, the results could help to explain the cardiotoxic effects of the drug.

Amitriptyline↗
PubMed1995

Effluxes of 3,4-dihydroxyphenylalanine, 3,4-dihydroxyphenylglycol, and norepinephrine from four blood vessels during basal conditions and during nerve stimulation.

Effluxes of 3,4-dihydroxyphenylalanine, 3,4-dihydroxyphenyglycol, and norepinephrine from four superfused canine blood vessels (saphenous and portal veins and mesenteric and pulmonary arteries) were studied under basal conditions and during nerve stimulation. From quantification of the compounds a series of indices of activities at neuroeffector junctions are proposed. These are (a) basal overflow of 3,4-dihydroxyphenylglycol as an index of vesicular-cytoplasmic translocation of norepinephrine, (b) the increase in 3,4-dihydroxyphenyglycol overflow attributable to nerve stimulation as an index of neuronal reuptake of norepinephrine released by stimulation, (c) the sum of the increases in overflows of norepinephrine and 3,4-dihydroxyphenylglycol attributable to nerve stimulation as an index of evoked release of norepinephrine, and (d) the efflux of 3,4-dihydroxyphenylalanine as an index of the activity of tyrosine hydroxylase, the rate-limiting enzyme in the synthesis of norepinephrine. There were clear differences between these indices in the vessels. Correlation coefficients of the indices among vessels indicated that a high tissue norepinephrine level was associated with high biosynthetic capacity and high vesicular-cytoplasmic exchange but not with high release. There was no evidence suggesting feedback inhibition of synthesis by neuroplasmic norepinephrine--whether arising from vesicular-cytoplasmic translocation or from reuptake from the junctional cleft. The major value of these indices will probably be in determining the integrated effects of pharmacologic agents at neuroeffector junctions in different blood vessels.

Animals↗
PubMed1995

Guinea-pig sympathetic postganglionic neurones contain haem oxygenase-2.

HAEM oxygenase-2 (HO-2) is the neuronal isoform of the only known mammalian enzyme generating the new transmitter candidate, carbon monoxide. Its distribution was investigated in the sympathetic nervous system. A 36 kDa HO-2 immunoreactive protein was identified in the particulate fraction of stellate ganglion and cerebellum in Western blots. Immunohistochemically, all noradrenergic and non-noradrenergic postganglionic neurones were HO-2 immunoreactive in prevertebral ganglia and cervical, thoracic, and lumbar sympathetic chain ganglia. Neither postganglionic nerve branches nor noradrenergic perivascular terminals were HO-2 immunoreactive under control conditions. However, accumulation of HO-2 immunoreactivity was found in noradrenergic axons in explanted sciatic nerves in which axonal transport was interrupted by crushing. We conclude that HO-2 is ubiquitous in perikarya of postganglionic sympathetic neurones, is subjected to axonal transport but does not accumulate at sympathetic neuroeffector junctions. This distribution favours a general role of HO-2 in sympathetic neuronal metabolism rather than a specific association with transmission at autonomic neuroeffector junctions.

Animals↗
PubMed1980

Modulation of adrenergic neuroeffector events in the renal vasculature: role of prostaglandins.

The major products of arachidonic acid metabolism in the kidney (PGE2, PGI2, PGF2 alpha) influence adrenergic neuroeffector events. PGE2 and PGI2 inhibit the vasoconstrictor responses elicited by sympathetic nerve stimulation and by injected norepinephrine in the rabbit and dog kidney. PGE2 also reduces release of the adrenergic transmitter from the rabbit kidney. In contrast, PGF2 alpha enhances adrenergically induced vasoconstriction. In the rabbit kidney, release of the adrenergic transmitter and the vasoconstrictor responses to nerve stimulation and to injected norepinephrine are enhanced by blockade of prostaglandin synthesis, and are reduced during stimulation of prostaglandin synthesis by either arachidonic acid or bradykinin. In contrast, in the rat kidney, adrenergically induced vasoconstriction is enhanced by PGE2, PGI2, and arachidonic acid and is reduced by prostaglandin synthesis inhibitors. This suggests major species differences in the modulatory action of prostaglandins at the adrenergic neuroeffector junction. This difference between rat and other species could be due to difference in prostaglandin receptors or in the events resulting from the interaction of prostaglandins with the receptors at the adrenergic neuroeffector junction.

Animals↗
PubMed2004

Nitric oxide decreases the biological activity of norepinephrine resulting in altered vascular tone in the rat mesenteric arterial bed.

Nitric oxide (NO) reacts with catecholamines resulting in their deactivation. In this study, we demonstrated that coincubation of NO donors with sympathetic neurotransmitters decreased the amount of norepinephrine detected but not ATP or neuropeptide Y (NPY). Furthermore, we found that the ability of norepinephrine to increase perfusion pressure in the isolated perfused mesenteric arterial bed of the rat was attenuated by the incubation of norepinephrine with the NO donor diethylamine NONOate. Conversely, the vasoconstrictive ability of NPY and ATP was unaffected by incubation with NONOate. Periarterial nerve stimulation in the presence of the NO synthase (NOS) inhibitor Nomega-nitro-l-arginine methyl ester (l-NAME) resulted in an increase in both perfusion pressure response and norepinephrine levels. This was prevented by l-arginine, demonstrating that the effects of l-NAME were indeed specific to the inhibition of NOS. To confirm that NO was not altering the release of norepinephrine from the sympathetic nerve via presynaptic activation of guanylate cyclase, we repeated the experiments in the presence of the guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]-quinoxaloine-one (ODQ). Unlike l-NAME, ODQ infusion did not increase norepinephrine overflow, demonstrating that modulation of norepinephrine by NO at the vascular neuroeffector junction of the rat mesenteric vascular bed is not the result of presynaptic guanylate cyclase activation. These results demonstrate that, in addition to being a direct vasodilatator, NO can also alter vascular reactivity at the sympathetic neuroeffector junction in the rat mesenteric bed by deactivating the vasoconstrictor norepinephrine.

Animals↗
PubMed1989

Mathematical model of dependence of heart rate on tissue concentration of acetylcholine.

The change in sinus period elicited by vagal stimulation depends on the rate of acetylcholine (ACh) release from the nerve endings, the rate of ACh degradation in the nodal tissue, and the responsiveness of the sinus node to ACh. Vagal stimulation in anesthetized dogs prolonged sinus period. After cessation of vagal stimulation, the sinus period returned to the prestimulation period. We developed a mathematical model to analyze the dynamics of ACh degradation in the neuroeffector junction and the dependence of sinus period on the concentration of ACh. From the in vitro reaction kinetics of acetylcholinesterase, we derived an analytical expression for the rate of ACh degradation in the intact animal. Our model represents the electrical behavior of the sinus node by the electrical activity of one pacemaker cell with six membrane ionic currents. This model predicts the decline in sinus period of the intact anesthetized dog as acetylcholinesterase degrades ACh in the neuroeffector junction. The half-life of ACh after cessation of vagal stimulation was estimated to be 2.7 s. We conclude that following termination of vagal stimulation, the sinus node of the intact animal responds to ACh as if the sinus node were one oscillator.

Acetylcholine↗