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PubMed1985

Neuromodulation of the cardiac vagus: comparison of neuropeptide Y and related peptides.

Neuropeptide Y (NPY), a putative co-transmitter in noradrenergic sympathetic nerves of the cardiovascular system, inhibits the negative chronotropic action of the cardiac vagus. In the present study, peptides related to NPY were tested for potency in producing this effect. In bilaterally vagotomized, anaesthetised dogs, the increase in pulse interval caused by electrical stimulation of the peripheral stump of the right vagus was measured before and after intravenous administration of peptide. The effects of doses of NPY were compared with those of equimolar doses of peptide YY (PYY), and of avian and human pancreatic polypeptides (APP and HPP). PYY inhibited the vagal action more effectively than did NPY. APP and HPP, however, caused no change in strength of vagal action at the doses used. The response to a second injection of NPY, given soon after the injection of APP or HPP, was not significantly different from the original. Thus no evidence was obtained for a competitive inhibition of the action of NPY by either pancreatic polypeptide. A C-terminal hexapeptide fragment of human pancreatic polypeptide was also tested. Like APP and HPP, it neither inhibited the cardiac vagus nor blocked the action of NPY. The order of potency obtained here (PYY greater than NPY much greater than APP, HPP, CFPP) can be expected to be of use in efforts to distinguish the active site(s) of the NPY molecule, and to characterise the receptors involved in these modulatory effects.

Animals↗
PubMed1985

ACTH neuromodulation of the developing motor system and neonatal learning in the rat.

ACTH peptides influence the developing nervous system during the first three weeks of life in the rat. ACTH 4-10 and Org 2766 (10.0 micrograms/kg) accelerate the expression of motor hyperactivity usually exhibited in 15-day old normal animals, with ACTH 4-10 increasing the force of extensor digitorum longus muscle contraction amplitude. Following cold stress and peptide treatment, rate changes in motor activity from one age to the next are dramatically enhanced, with vertical activity being exhibited at an earlier age than controls. Grasping ability is similarly enhanced in 13-day old ACTH 4-10-treated animals. The retention of a T-maze learning paradigm is significantly enhanced in 16-day old ACTH 4-10 (10.0 micrograms/kg)-treated and Org 2766 (0.01 micrograms/kg)-treated animals, with these animals running the maze significantly faster than controls. Peptide treatment appears to reverse the apparent turning preference in the maze during extinction. It is suggested that ACTH peptides modulate the organization of the nervous system and facilitate neurotransmission, and may act on dopaminergic and cholinergic neurotransmitter systems. Motor behavior seems to reflect underlying neural substrates that are integrated to produce the overt behavior of the organism.

Adrenocorticotropic Hormone↗
PubMed1985

Mammalian bombesin-like peptides: neuromodulators of gastric function and autocrine regulators of lung cancer growth.

Peptides corresponding closely in structure to the biologically active carboxyl terminal region of the amphibian peptide bombesin have now been isolated from several mammalian species, including man. Two principal forms have been found: one contains 27 amino acids and exhibits variations in amino acid sequence in the amino terminal region; the other is the carboxyl terminal decapeptide and probably does not vary among mammals. These peptides exhibit full immunoreactivity with most bombesin antisera and account for "bombesin-like immunoreactivity" that has been described in mammalian brain, sympathetic ganglia, and nerve fibers in the gut as well as in fetal lung endocrine cells and certain lung tumors, especially small cell lung carcinoma. The name gastrin releasing peptide (GRP) was given to the porcine and avian heptacosapeptides by McDonald and Mutt. The larger and smaller mammalian peptides now often are called GRP27 and GRP10. Both forms exhibit the full spectrum of activity shown by bombesin. Evidence has been obtained that neural release of mammalian bombesin-like peptides is physiologically important in regulation of gastrin release from the stomach. Lung tumors that produce bombesin-like peptides also have receptors for bombesin. These receptors appear to be involved in the autocrine regulation of tumor cell proliferation.

Animals↗
PubMed1985

Central neuromodulation of gastric acid secretion by bombesin-like peptides.

The amphibian skin tetrapeptide bombesin shows potent action in reducing gastric acid secretion by intracerebral ventricular (ICV) administration in rats. In order to establish a relationship between this action and the amino acid composition of the bombesin-like peptides, most of the natural bombesin-like peptides and some synthetic analogues were tested on their ability to reduce gastric acid secretion by ICV administration. The amphibian peptides bombesin, its [Tyr4]-bombesin analogue, alytesin, ranatensin and litorin, and the mammalian peptide GRP significantly reduced gastric acid output 2 hr after peptide administration (p less than 0.01). The data support the following prerequisites for the maximal neuromodulatory role of bombesin-like peptides on gastric secretion: Trp is required at position 8; Gln and His are important at positions 7 and 12, respectively; Leu replacement by Phe, which occurs in the litorin subfamily, modifies the response; and unspecified amino acids or sequences are also involved in the N-terminal region of bombesin-like peptides. Synthetic analogues are currently being tested to confirm and extend these conclusions.

Amino Acid Sequence↗
PubMedDate not supplied

Brain transfer of a new neuromodulating ACTH analog, ebiratide, in rats.

The transfer of ebiratide into the brain was examined in rats. Its brain levels after intravenous administration (2-20 mg/kg), determined by radioimmunoassay, peaked at 5 min and declined almost in parallel with the plasma levels. Brain/plasma ratios (B/P) were constantly about 0.05 ml/g at all doses. Brain distribution study at 5 min after 125I-ebiratide at an effective dose (0.4 microgram/kg) revealed that unchanged ebiratide had larger B/P than the metabolites and region selectivity. The combined use with unlabeled ebiratide resulted in marked decreases in B/P, particularly in the hippocampus, suggesting a specific uptake of this peptide.

Adrenocorticotropic Hormone↗
PubMed1996

Evidence for native NMDA receptor subtype pharmacology as revealed by differential effects on the NMDA-evoked release of striatal neuromodulators: eliprodil, ifenprodil and other native NMDA receptor subtype selective compounds.

NMDA increases the release of [14C]acetylcholine and [3H]spermidine or of [14C]GABA and [3H]dopamine from rat striatal slices. The pharmacology of these responses suggests that release of dopamine and GABA, acetylcholine, and spermidine is mediated, respectively, by three distinct NMDA receptor subtypes. IC50 values of compounds for the inhibition of dopamine and GABA release were closely matched, suggesting mediation by the same subtype. This receptor was generally more sensitive to all NMDA antagonists tested relative to that controlling acetylcholine or spermidine release (channel blockers, glycine antagonists, competitive antagonists and polyamine antagonists). The receptors controlling acetylcholine and spermidine release were characterised by lower antagonist sensitivity in general, and that controlling spermidine release was further defined by a marked insensitivity to ifenprodil, eliprodil, magnesium, dextromethorphan, dextrorphan, memantine, desipramine and polyamine spider toxins. In binding studies in which the displacement of 2 nM [3H]MK801 was studied in membranes prepared from a number of brain regions (in the presence of saturating concentrations of glutamate, glycine and spermidine) small regional differences in IC50 values were observed for a number of channel blockers, but no compound generated biphasic displacement curves that would allow masking of a particular subtype and it was not possible to detect binding components that were insensitive to memantine, dextrorphan dextromethorphan or desipramine. Ifenprodil produced biphasic displacement curves in the 1-day-old rat cortex and midbrain (with IC50 values of approximately 2 and 70 microM) and both ifenprodil and eliprodil displaced a small proportion (18%) of [3H]MK-801 with high affinity in the adult rat spinal cord. Displacement of [3H]MK801 by these compounds in all other adult brain regions (cortex, striatum, hippocampus, thalamus, pons, medulla, cerebellum) was monophasic and of low affinity. In general the subtype selectivity suggested by the release studies was not mirrored in the binding experiments, probably because of excessive heterogeneity of sites in the membrane preparations and to the subtype selectivity of [3H]MK801 itself.

Animals↗
PubMed1984

Neuromodulation of lymphocyte reactivity in aged rats.

Numerous reports indicate that both central nervous system (CNS) and immune system functions decline with age. We have previously shown that the CNS can modulate both mitogen-induced spleen cell proliferation and NK activity in young Fischer 344 rats. In the present study we have determined the effects of AHT lesions on the lymphocyte reactivity of aged Fischer 344 rats. These data show that lesions in the AHT of aged rats cannot modulate splenic mitogen responsiveness, however, NK activity is impaired. This differential effect may be due to multiple factors including enhanced splenic suppressor cell activity, the inability of the brain to send modulatory signals following lesioning, or the failure of the immune system to receive a neural signal and react to it.

Animals↗
PubMed1989

Cholecystokinin receptor subtypes and neuromodulation.

The sulfated octapeptide of cholecystokinin (CCK-8S) and CCK fragments have been administered to mice to determine the subtype and location of the CCK receptor that modulates the release of dopamine (DA) in brain. 1. Centrally (i.c.v.) or peripherally (s.c.) administered CCK-8S lowers DA release, and to a lesser extent, metabolism, in the neostriatum and olfactory tubercle. 2. DA release is decreased when the CCK-B selective compounds, unsulfated CCK-8 (CCK-8U) or the butoxycarbonyl tetrapeptide of CCK (t-boc-CCK-4), are given i.c.v. but not when injected s.c. 3. The increase in DA release following amphetamine administration is attenuated by i.c.v. but not s.c. injections of t-boc-CCK-4 or CCK-8U and by CCK-8S given via either route. 4. None of the s.c. actions of CCK-8S are prevented by the CCK-A receptor antagonist, L 364,718. CCK-B receptors in brain mediate the suppression by CCK of basal and augmented DA release. CCK-B receptor agonists may be useful for the treatment of psychiatric conditions that result from excessive DA release.

Animals↗
PubMed1982

Tryptamine: a neuromodulator or neurotransmitter in mammalian brain?

Tryptamine synthesized by decarboxylation of L-tryptophan occurs as an endogenous constituent of mammalian brain albeit at very low concentrations (low ng/g range). It is primarily metabolized by oxidative deamination by MAO and possesses an extremely rapid turnover and half-life. Subcellular localization appears to be in nerve terminals and it is releasable by electrical or potassium evoked depolarization. Neuropharmacological and electrophysiological data strongly suggest the existence of post-synaptic receptors for tryptamine independent of those for 5HT. There may exist a rostrally projecting neuronal tryptamine containing system arising from cell bodies in or close to the nucleus raphé medianus. The demonstration of specific receptors for tryptamine in the CNS strongly indicates a transmitter role, although a strong case can be made for a role as a modifier of central 5HT systems. The possibility also exists that 5HT and tryptamine may be mediators of functionally opposite neuronal pathways. Whatever the role of tryptamine in the CNS it is clear that it not simply present as an accident of metabolism or a "biological artefact." The indications are that it possesses important functions in central neurotransmission.

Animals↗
PubMed1994

A vitamin as neuromodulator: ascorbate release into the extracellular fluid of the brain regulates dopaminergic and glutamatergic transmission.

Ascorbate is an antioxidant vitamin that the brain accumulates from the blood supply and maintains at a relatively high concentration under widely varying conditions. Although neurons are known to use this vitamin in many different chemical and enzymatic reactions, only recently has sufficient evidence emerged to suggest a role for ascorbate in interneuronal communication. Ascorbate is released from glutamatergic neurons as part of the glutamate reuptake process, in which the high-affinity glutamate transporter exchanges ascorbate for glutamate. This heteroexchange process, which also may occur in glial cells, ensures a relatively high level of extracellular ascorbate in many forebrain regions. Ascorbate release is regulated, at least in part, by dopaminergic mechanisms, which appear to involve both the D1 and D2 family of dopamine receptors. Thus, amphetamine, GBR-12909, apomorphine, and the combined administration of D1 and D2 agonists all facilitate ascorbate release from glutamatergic terminals in the neostriatum, and this effect is blocked by dopamine receptor antagonists. Even though the neostriatum itself contains a high concentration of dopamine receptors, the critical site for dopamine-mediated ascorbate release in the neostriatum is the substantia nigra. Intranigral dopamine regulates the activity of nigrothalamic efferents, which in turn regulate thalamocortical fibers and eventually the glutamatergic corticoneostriatal pathway. In addition, neostriatonigral fibers project to nigrothalamic efferents, completing a complex multisynaptic loop that plays a major role in neostriatal ascorbate release. Although extracellular ascorbate appears to modulate the synaptic action of dopamine, the mechanisms underlying this effect are unclear. Evidence from receptor binding studies suggests that ascorbate alters dopamine receptors either as an allosteric inhibitor or as an inducer of iron-dependent lipid peroxidation. The applicability of these studies to dopamine receptor function, however, remains to be established in view of reports that ascorbate can protect against lipid peroxidation in vivo. Nevertheless, ample behavioral evidence supports an antidopaminergic action of ascorbate. Systemic, intraventricular, or intraneostriatal ascorbate administration, for example, attenuates the behavioral effects of amphetamine and potentiates the behavioral response to haloperidol. Some of these behavioral effects, however, may be dose-dependent in that treatment with relatively low doses of ascorbate has been reported to enhance dopamine-mediated behaviors. Ascorbate also appears to modulate glutamatergic transmission in the neostriatum. In fact, by facilitating glutamate release, ascorbate may indirectly oppose the action of dopamine, though the nature of the neostriatal dopaminergic-glutamatergic interaction is far from settled. Ascorbate also may alter the redox state of the NMDA glutamate receptor thus block NMDA-gated channel function.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1982

2-Aminoethanol as a possible neuromodulator in the pigeon optic tectum.

A mass fragmentographic method was used for determination of low molecular weight compounds in perfusates collected in vivo in the pigeon optic tectum by a push-pull cannula technique. 2-Aminoethanol (ethanolamine) could be collected under resting conditions (5.6 +/- 0.09 pmol/min). Electrical stimulation of optic nerve induced a 2.3-fold increase of the tectal ethanolamine outflow whereas that of GABA was not affected. Ethanolamine applied iontophoretically to tectal neurons did not influence their spontaneous discharge; however, their glutamate-induced excitation as well as the GABA-induced depression were enhanced if ethanolamine was applied simultaneously. It is suggested that optic nerve stimulation exerts a neuromodulatory effect on tectal neurons.

Animals↗
PubMed1989

Adrenergic neuromodulation by endothelin in guinea pig pulmonary artery.

Endothelin was tested for possible interactions with the noradrenergic neuroeffector transmission in guinea pig pulmonary artery. Endothelin concentration-dependently enhanced nerve-induced contractile responses and concomitantly increased basal tone. Furthermore, endothelin inhibited the stimulation-evoked release of [3H]noradrenaline and enhanced the contractile response to exogenously applied noradrenaline. These results suggest that endothelin, in addition to its direct contractile effect, may function as a modulator of adrenergic neuroeffector transmission in the guinea pig pulmonary artery via both stimulatory post- and inhibitory prejunctional mechanisms.

Adrenergic Fibers↗