m-35 and galantide

m-35 has been researched along with galantide* in 5 studies

Other Studies

5 other study(ies) available for m-35 and galantide

ArticleYear
Suggestive evidence for inhibitory effects of galanin on mesolimbic dopaminergic neurotransmission.
    Brain research, 1999, Mar-20, Volume: 822, Issue:1-2

    The objective was to examine effects of galaninrat on forebrain monoamine synthesis and on spontaneous locomotor activity in the rat. The rate of monoamine synthesis was estimated by measuring the accumulation of l-DOPA and 5-HTP, following inhibition of cerebral aromatic l-amino acid decarboxylase by means of NSD-1015 (100 mg kg-1 i.p.), after i.c.v. or intracerebral administration of galanin in adult male Wistar rats. Spontaneous locomotor activity was observed in an automated open-field arena ( approximately 0.5 m2). The i.c.v. administration of galanin (0.5-5.0 nmol bilaterally) produced a dose-dependent, statistically significant, increase in DOPA accumulation throughout the neostriatum, and in the olfactory bulb, indicating an increase in the rate of DA synthesis. No increase was observed in brain areas where noradrenaline is the predominant catecholamine, such as the neocortex or the ventral hippocampus. In addition, there was a tendency for an increase in 5-HTP accumulation in the dorso-lateral neostriatum and in the accumbens. The same i.c.v. administration of galanin produced a dose-dependent, and statistically significant, decrease in spontaneous locomotor activity. The effect on forebrain DA synthesis could also be produced by local bilateral application of galanin (2x1 nmol) into the ventral tegmental area, but not the nucleus accumbens (2x2 nmol). There were no effects on forebrain DOPA or 5-HTP accumulation by the local application of galanin into the locus coeruleus, or into the dorsal raphe nucleus. It is concluded that the neuropeptide galanin modulates forebrain dopaminergic neurotransmission. The effect appears to be mediated at the somato-dendritic level of the meso-neostriatal pathway, and could perhaps be utilized to normalize perturbations ascribed to dysfunction in this neuronal pathway, such as schizophrenia.

    Topics: 5-Hydroxytryptophan; Animals; Behavior, Animal; Bradykinin; Brain Chemistry; Dopamine; Dose-Response Relationship, Drug; Galanin; Hippocampus; Injections, Intraventricular; Levodopa; Locomotion; Male; Motor Activity; Neocortex; Neostriatum; Neural Inhibition; Nucleus Accumbens; Olfactory Bulb; Peptide Fragments; Rats; Rats, Wistar; Substance P; Synaptic Transmission; Ventral Tegmental Area

1999
Galanin contracts and relaxes guinea pig and canine intestinal smooth muscle cells through distinct receptors.
    Gastroenterology, 1995, Volume: 108, Issue:1

    Galanin induces a contraction or a relaxation of digestive smooth muscle. Receptors mediating these effects have not been pharmacologically characterized. The aim of the study was to evaluate properties of two specific galanin antagonists M15 and M35 on galanin effects on muscle cells.. Isolated muscle cells were obtained separately from circular and longitudinal layers of guinea pig and dog ileums. Contraction was expressed as percentage decrease in cell length from control.. Galanin induced a contraction of cells from guinea pig circular layer (50% effective concentration [EC50], 80 pmol/L) and dog longitudinal layer (EC50, 100 pmol/L). The antagonists inhibited galanin-induced contraction. The most potent was M15 (50% inhibitory concentration [IC50], 80 pmol/L in guinea pig; 90 pmol/L in dog) which was > M35 (IC50, 4 nmol/L in guinea pig; 1 nmol/L in dog). In dog circular layer, galanin inhibited cholecystokinin-induced contraction by relaxing the cells (EC50, 3 pmol/L). The antagonists inhibited this relaxation. The most potent was M35 (IC50, 60 pmol/L) which was > M15 (IC50, 900 pmol/L).. Galanin antagonists M15 and M35 inhibit the contraction and the relaxation induced by galanin with different potency, suggesting the presence of distinct galanin receptors in gastrointestinal tract that each mediates a specific effect.

    Topics: Animals; Bradykinin; Dogs; Galanin; Guinea Pigs; Ileum; Male; Muscle Contraction; Muscle Relaxation; Muscle, Smooth; Neuropeptides; Osmolar Concentration; Peptide Fragments; Peptides; Potassium Chloride; Receptors, Galanin; Receptors, Gastrointestinal Hormone; Sincalide; Substance P

1995
Spinal antinociception by morphine in rats is antagonised by galanin receptor antagonists.
    Naunyn-Schmiedeberg's archives of pharmacology, 1994, Volume: 350, Issue:4

    Galanin, a 29 amino acid peptide, has been reported to possess antinociceptive properties at the spinal site and to potentiate opioid-induced antinociception. Our aim was to investigate whether also endogenous galanin interacts with an exogenously administered opioid, morphine, in the rat spinal cord. This question was investigated by use of the recently developed galanin receptor antagonists galantide [M-15, galanin-(1-13)-substance P-(5-11) amide] and M-35 [galanin-(1-13)-bradykinin-(2-9) amide]. Nociception was assessed in the rat tail-flick test using radiant heat and the rat Randall-Selitto model of inflammatory pain using vocalization as the nociceptive criterion. Intrathecal (i.t.) injections were performed in rats under either anaesthesia. Morphine was administered either i.t. or intraperitoneally (i.p.), and the antagonists were injected i.t. [125I]Galanin binding experiments were performed on crude synaptosomal membranes of the rat spinal cord. In the rat tail-flick test, i.t. injection of 3 micrograms morphine evoked antinociception of about 75% of the maximal possible effect (% MPE). Co-injection of either 2 micrograms galantide or 2 micrograms M-35 with morphine almost completely abolished the antinociceptive effect of morphine. I.p. injection of 2.15 mg/kg morphine elicited about 80% MPE when given 10 min prior to i.t. saline injection. Injection of the antagonists instead of saline antagonised the antinociceptive effect of morphine partially thus showing the spinal proportion of the overall antinociceptive effect. In the rat Randall-Selitto test, 3 micrograms morphine, injected i.t., produced antinociception of almost 100% MPE.(ABSTRACT TRUNCATED AT 250 WORDS)

    Topics: Animals; Binding Sites; Bradykinin; Galanin; Injections, Spinal; Male; Morphine; Pain; Peptide Fragments; Peptides; Rats; Rats, Sprague-Dawley; Receptors, Galanin; Receptors, Gastrointestinal Hormone; Spinal Cord; Substance P; Synaptic Membranes

1994
Chimeric galanin analogs that function as antagonists in the CNS are full agonists in gastrointestinal smooth muscle.
    The Journal of pharmacology and experimental therapeutics, 1993, Volume: 266, Issue:2

    Galanin has numerous effects on gastrointestinal smooth muscle. However, because of the lack of specific inhibitors, it is not known which are physiological and which are pharmacological. This study investigates the ability of two chimeric galanin analogs, [# 1-galantide = (M-15) = [galanin (1-13)-substance P(5-11)] and #2-M-35[galanin(1-13)bradykinin (2-9)], which were recently reported to function as galanin-receptor antagonists in the CNS, to interact with galanin receptors on rat jejunal muscle strips or dispersed smooth muscle cells from guinea pig stomach. In both systems each chimeric analog had agonist activity and was as efficacious as galanin. Cross-desensitization experiments demonstrated that in the jejunal muscle strips, both chimeric analogs were causing muscle contraction by interacting with the galanin receptor. In dispersed smooth muscle cells, galanin, as well as each chimeric analog, caused muscle relaxation, whereas substance P and bradykinin both caused muscle contraction. Each chimeric analog was equipotent to galanin in inhibiting binding of 125I-galanin, and there was close agreement between their abilities to occupy the galanin receptor and cause relaxation. Each chimeric analog also activated adenylate cyclase and increased cAMP characteristic of relaxants. These studies demonstrate these chimeric analogs will not be useful for defining the physiological role of galanin in altering gastrointestinal motility, because they function as full galanin-receptor agonists instead of as galanin-receptor antagonists.

    Topics: Animals; Bradykinin; Cyclic AMP; Digestive System; Digestive System Physiological Phenomena; Galanin; Guinea Pigs; In Vitro Techniques; Male; Muscle Contraction; Muscle, Smooth; Peptide Fragments; Peptides; Rats; Substance P

1993
Differential effects of the putative galanin receptor antagonists M15 and M35 on striatal acetylcholine release.
    European journal of pharmacology, 1993, Sep-21, Volume: 242, Issue:1

    The putative galanin receptor antagonists M15 and M35 were examined for their effects on the basal and the galanin-evoked release of acetylcholine in the striatum. Extracellular concentrations of acetylcholine were measured in male rats using in vivo microdialysis and high pressure liquid chromatography techniques. Galanin (300 microM or 3 nmol/10 microliters), perfused through the microdialysis membrane into the striatum, enhanced (100% increase) basal acetylcholine release. M35 (300 microM or 3 nmol/10 microliters) also stimulated the basal acetylcholine release to some extent (about 50%) while M15 at the same concentration failed to do so. When M15 and M35 were coinfused with galanin, the galanin-evoked acetylcholine release was blocked completely by M15 (300 microM or 3 nmol/10 microliters) but only partially by M35 (300 microM or 3 nmol/10 microliters). The increase in acetylcholine release induced by M35 (300 microM) was blocked by M15 (300 microM). It is concluded that M15 is a full galanin receptor antagonist while M35 behaves as a mixed agonist-antagonist in vivo in the rat striatum. Both M15 and M35 fully displaced 0.2 nM [125I]galanin from its binding sites in the striatal membranes. The Hill coefficient of these [125I]galanin displacement curves with M15 and M35 was 0.4-0.5 compared to unity in the case of galanin. Analysis of the displacement curves suggested that both M15 and M35 recognized two classes of galanin binding sites in striatal membranes of the rat. To explain the difference between M15 and M35 it is suggested that there may exist a putative subtype of galanin receptor in the striatum, which is differentially affected by M15 and M35.

    Topics: Acetylcholine; Animals; Bradykinin; Brain; Chromatography, High Pressure Liquid; Galanin; Male; Microdialysis; Peptide Fragments; Peptides; Rats; Rats, Sprague-Dawley; Receptors, Galanin; Receptors, Gastrointestinal Hormone; Substance P

1993