Dopamine is taken up from the circulation by, and released from, local noradrenergic varicose axon terminals in zona glomerulosa of the rat: a neurochemical and immunocytochemical study.

The effect of supramaximal electric field stimulation on [3H]dopamine (DA) release by rat adrenal capsule-glomerulosa preparations was studied using a micro-volume perfusion system. When the tissues were preloaded with [3H]DA, a considerable amount of [3H]DA and [3H]noradrenaline (NA) were released in response to field stimuli. Reserpinization, calcium removal or tetrodotoxin blocking of Na+ influx all completely inhibited the stimulation-evoked release of DA/NA, indicating that the radioactivity released is of neuronal and vesicular origin.

Effect of nicotine on levels of extracellular amino acids in regions of the rat brain in vivo.

The local effect of nicotine on the extracellular levels of amino acids was examined in the striatum and frontal cortex of rats using microdialysis in vivo. The perfusion of 1 mM nicotine in Ringer's solution increased the extracellular levels of aspartic and glutamic acids by 40-50% in the striatum and had no effect on the levels of serine, glycine, glutamine, taurine or threonine. This effect of nicotine was dose- and Ca-dependent.

Effect of neurotensin and immunneutralization with anti-neurotensin-serum on dopaminergic-cholinergic interaction in the striatum.

The effect of neurotensin (NT) on the release of acetylcholine (ACh) and dopamine (DA) from striatal slices of the rat brain was studied. Neurotensin, 1-150 nM, was able to release ACh from cholinergic interneurons of the striatum. Like the response to electrical stimulation, the ACh-releasing effect of NT was completely inhibited by tetrodotoxin indicating that neuronal firing is involved in its effect.

Catecholamines released from local adrenergic axon terminals are possibly involved in fine tuning of steroid secretion from zona glomerulosa cells: functional and morphological evidence.

The effect of supramaximal electric field stimulation on [3H]noradrenaline (NA) release and hormone production by rat adrenal capsule-glomerulosa preparations was studied using a microvolume perfusion system. A substantial proportion (about 20%) of nerve endings (varicosities) were observed close to zona glomerulosa cells, and about half of them appeared to be catecholaminergic, as judged by the chromaffin reaction of the synaptic vesicles studied at electron microscopic level. In tissue, preloaded with [3H]NA, the release of NA in response to electrical stimulation was frequency-dependent.

Presynaptic inhibitory effect of TNF-alpha on the release of noradrenaline in isolated median eminence.

The effect of tumor necrosis factor-alpha (TNF-alpha) on the stimulation-evoked release of noradrenaline (NA) from isolated rat median eminence (ME) was investigated, using a low-volume perfusion system. Median eminence, loaded with [3H]noradrenaline, was superfused with Krebs solution and stimulated electrically (2 Hz, 120 shocks). The effect of TNF-alpha was studied on the S2/S1 ratio.

Is the neuronal ATP release from guinea-pig vas deferens subject to alpha 2-adrenoceptor-mediated modulation?

The effects of a variety of alpha 2-adrenoceptor agonists and antagonists were studied on stimulation-evoked release of endogenous ATP, measured by the luciferin-luciferase assay, and on the release of [3H]noradrenaline from the guinea-pig vas deferens. The biphasic mechanical contraction of the guinea-pig smooth muscle was recorded concomitantly. The alpha 2-adrenoceptor agonist, xylazine (1 microM) inhibited the field stimulation-evoked (8 Hz, 0.

Regulatory interactions among axon terminals affecting the release of different transmitters from rat striatal slices under hypoxic and hypoglycemic conditions.

An in vitro model of ischemia was utilized to study the effects of both oxygen and glucose depletion on transmitter release from rat striatal slices. The spontaneous and stimulation-evoked releases of tritiated dopamine, gamma-aminobutyric acid, glutamate, and acetylcholine were measured. Hypoxia increased the evoked release of glutamate and dopamine without effect on the resting release.

Evidence that ATP released from the postsynaptic site by noradrenaline, is involved in mechanical responses of guinea-pig vas deferens: cascade transmission.

The release of endogenous ATP and [3H]noradrenaline, and the mechanical response of the guinea-pig vas deferens to field stimulation of its motor nerves were examined using a perfusion system. The release of ATP at rest was 0.83 +/- 0.

Effect of selective opiate antagonists on striatal acetylcholine and dopamine release.

We investigated the effect of selective opiate antagonists on striatal acetylcholine (ACh) and dopamine (DA) release. The mu-receptor antagonist beta-funaltrexamine (beta-FNA), the delta-antagonist naltrindole (NTI), and the kappa-antagonist norbinaltorphimine (nor-BNI) were used to selectively block different subtypes of opiate receptors. The experiments were carried out on isolated superfused striatal slices of rats, loaded with [3H]choline or [3H]dopamine.

Presynaptic A1-purinoceptor-mediated inhibitory effects of adenosine and its stable analogues on the mouse hemidiaphragm preparation.

1. The effect of adenosine or its stable analogues (2-chloroadenosine, CADO; 5'-N-ethylcarboxamidoadenosine, NECA; and N6-cyclopentyladenosine, CPA) on the release of [3H]-acetylcholine ([3H]-ACh), and on the development of force of contraction evoked by electrical stimulation of the nerve, were studied in the mouse phrenic nerve-hemidiaphragm preparation. Evidence was obtained that the release of ACh is subject to presynaptic modulation through presynaptic A1(P1)-purinoceptors.

Lipopolysaccharide is able to bypass corticotrophin-releasing factor in affecting plasma ACTH and corticosterone levels: evidence from rats with lesions of the paraventricular nucleus.

Stimulation of the immune system or experimental conditions (bacterial lipopolysaccharide (LPS) treatment) provoke a broad spectrum of physiological responses. It was recently shown that one of them is the activation of the hypothalamic-pituitary-adrenal (HPA) axis. The mechanism and the site or sites through which LPS stimulates the HPA axis are not well understood.

Different sites of action for alpha 2-adrenoceptor antagonists in the modulation of noradrenaline release and contraction response in the vas deferens of the rat.

Rat vas deferens was prepared, loaded with [3H]noradrenaline, and superfused to measure the release of tritium in resting conditions and in response to electrical field stimulation. The alpha 2-adrenoceptor antagonists yohimbine, CH-38083 (7,8-(methylenedioxi)-14 alpha-hydroxyalloberbane HCl), and idazoxan increased the electrically induced release of tritium in a concentration-dependent manner, whereas noradrenaline and the alpha 2-adrenoceptor agonist xylazine exerted opposite effects. The inhibitory effect of noradrenaline on electrically induced tritium release was antagonized by yohimbine, CH-38083, and idazoxan.

Effect of nicotine on extracellular levels of neurotransmitters assessed by microdialysis in various brain regions: role of glutamic acid.

We studied the effect of local administration of nicotine on the release of monoamines in striatum, substantia nigra, cerebellum, hippocampus, cortex (frontal, cingulate), and pontine nucleus and on the release of glutamic acid in striatum of rats in vivo, using microdialysis for nicotine administration and for measuring extracellular amine and glutamic acid levels. Following nicotine administration the extracellular concentration of dopamine increased in all regions except cerebellum; serotonin increased in cingulate and frontal cortex; and norepinephrine increased in substantia nigra, cingulate cortex, and pontine nucleus. Cotinine, the major nicotine metabolite, had no effect at similar concentrations.

Effect of nicotine on dopaminergic-cholinergic interaction in the striatum.

We have investigated the effect of nicotinic receptor stimulation on acetylcholine (ACh) release measured by radioassay in rat striatal slices. Since the release of ACh in the striatum is tonically inhibited by endogenous dopamine and nicotine enhances the release of dopamine, we studied the release of ACh when the dopaminergic input was impaired. We used chemical denervation (6-hydroxydopamine pretreatment) or D2-receptor-blockade by sulpiride to remove the dopaminergic control of the cholinergic neurons.

Functional evidence that acetylcholine release from Auerbach's plexus of guinea-pig ileum is modulated by alpha 2A-adrenoceptor subtype.

The effects of alpha 2-adrenoceptor ligands on electrically stimulated [3H]acetylcholine release from longitudinal muscle strips of guinea-pig ileum were examined. Xylazine or oxymetazoline reduced the release of [3H]acetylcholine in a concentration-dependent manner, both these actions being antagonized by idazoxan, CH 38083, or WB 4101. Prazosin, considered as an alpha 2B-adrenoceptor antagonist, failed to modify the inhibitory effects of xylazine or oxymetazoline.

Presynaptic modulation of release of noradrenaline from the sympathetic nerve terminals in the rat spleen.

Strips of rat spleen, loaded with [3H]NA, were superfused with Krebs' stimulated electrically at different frequencies (2, 8 and 32 Hz) with the same number of pulses and the effect of different receptor agonists and antagonists was studied on the S2/S1 ratio. Evidence has been obtained that the sympathetic nerve terminals in the spleen of the rat are equipped with presynaptic alpha 2B-adrenoreceptors, M-muscarinic, N-nicotinic and P1-purinoreceptors. Clonidine, an alpha 2-adrenoreceptor agonist, did not change the release of NA at low frequency but increased it at a high frequency of stimulation.

Characterization of somatodendritic neuronal nicotinic receptors located on the myenteric plexus.

The effects of nicotine and dimethylphenylpiperazinium (DMPP) on resting and stimulation-evoked release of [3H]-acetylcholine ([3H]ACh) from cholinergic interneurons and neuro-effector neurons of the ileal longitudinal muscle and the responses of the smooth muscle to nicotinic agonists were studied. (-)-Nicotine was 15 times more effective than (+)-nicotine in releasing ACh. Since tetrodotoxin (1 microM) completely antagonized the effect of nicotinic agonists, the site of action of the nicotinic agonists studied was on the somatodendritic nicotinic receptors.

Presynaptic modulation of the release of noradrenaline from electrically stimulated bicuspid valve leaflet of the rabbit heart.

The bicuspid (mitral) valves were obtained from male albino New Zealand rabbits. The noradrenaline (NA) content (12.93 +/- 1.

Naloxone enhances the release of acetylcholine from cholinergic interneurons of the striatum if the dopaminergic input is impaired.

Naloxone significantly enhanced the release of radioactive acetylcholine ([3H]ACh) from rat striatal slices loaded with [3H]choline either when the nigrostriatal pathway had been destroyed by 6-hydroxydopamine or when the D2 dopamine receptors had been inhibited by sulpiride. This in vitro study supplies the first neurochemical evidence, that, in addition to D2-receptor-mediated dopaminergic tonic control, there is opiate-receptor mediated presynaptic modulation of striatal ACh release, possibly by endogenous enkephalin released from local neurons. Such modulation occurs under conditions in which the dopaminergic input is impaired.

Effect of presynaptic P2 receptor stimulation on transmitter release.

Because ATP is degraded to adenosine, its effect could be mediated by both P1 and P2 receptors. Hence, the actions of an ATP analogue, resistant to enzymatic breakdown (alpha, beta-methylene ATP), were studied on the resting and electrically evoked release of radioactivity from longitudinal muscle strips of guinea pig ileum, preloaded either with [3H]choline or with [3H]noradrenaline. Their effects were compared with the actions of adenosine and ATP.

Comparison of the effects of a bufodienolide and ouabain on neuronal and smooth muscle preparations.

The effect of a bufodienolide (monohydroxy-14,15-epoxy-20,22-dienolide glycoside) purified from toad skin was compared with that of ouabain on 3H-noradrenaline release and on the tension of rabbit pulmonary arterial strips. This compound exerted an ouabain-like activity. The neuronal effects of this bufodienolide derivative on squid axon were also studied and compared with those of ouabain.

Evidence that catecholamines increase acetylcholine release from neuromuscular junction through stimulation of alpha-1 adrenoceptors.

1. The effects of alpha-1 adrenoceptor agonists on 3H-acetylcholine release from mouse phrenic nerve-hemidiaphragm preparation were studied. 2.

Alpha 2-adrenoceptors are not involved in the regulation of striatal glutamate release: comparison to dopaminergic inhibition.

Striatal slices from the rat were loaded with [3H]glutamate ([3H]Glu) and superfused in order to measure release of radioactivity at rest and during potassium-evoked depolarization. Addition of KCl (22-40 mmol/liter) to the perfusion fluid enhanced the release of tritium in a concentration-dependent manner, and this release was abolished by omission of CaCl2. High-performance liquid chromatography (HPLC) separation coupled with radiochemical detection revealed that 23% and 41% of the tritium efflux detected in the perfusion fluid under resting conditions and during potassium stimulation, respectively, was due to [3H]Glu.