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Spontaneous Motility (spontaneous + motility)
Selected AbstractsQuantification of cockroach allatostatin-like peptide and its myotropic effects in males of the earwig Euborellia annulipesPHYSIOLOGICAL ENTOMOLOGY, Issue 1 2001Roy Phitayakorn Summary A monoclonal antibody to allatostatin I of the cockroach Diploptera punctata was used to establish a competitive enzyme-linked immunosorbent assay for quantification of allatostatin-like peptides in the hindgut of the adult male earwig, Euborellia annulipes. Hindguts of 0-day males contained significantly more allatostatin-positive material than those of 8-day males fed on catfood. However, males starved for the first 8 days of adult life had significantly higher levels of allatostatin-positive material than those of either 0-day or of 8-day fed males. Hindguts from 0-day old males exhibited lower spontaneous motility in vitro than those from 8-day males. Hindguts from males at both ages responded to allostatin with reversible, dosage-dependent decreases in hindgut motility, and responded to proctolin with reversible, dosage-dependent increases in hindgut motility. When both allatostatin and proctolin were applied to hindgut preparations simultaneously and in equal concentrations, the response varied with the stage of the male. Starvation enhanced hindgut motility and abolished the response to allatostatin, but not to proctolin. These results indicate the presence of material similar to cockroach allatostatins in male earwigs, and that the levels change with age and physiological stage. Furthermore, such peptides may indeed be regulatory neuropeptides and could modulate hindgut contraction. There was an increase in sensitivity to exogenous allatostatin in the hindgut during development from day 0 to day 8 in feeding males, but a loss in sensitivity in response to starvation; sensitivity to exogenous proctolin also increased with age, but such responsiveness was not diminished by starvation. [source] Neuropharmacological evaluation of Ginkgo biloba phytosomes in rodentsPHYTOTHERAPY RESEARCH, Issue 10 2006Suresh R. Naik Abstract On oral administration, Ginkgo biloba phytosomes significantly reduced pentobarbitone-induced sleeping time, produced an alteration in the general behaviour pattern, increased spontaneous motility and inhibited the chlorpromazine-induced blockade of conditioned and unconditioned responses in rodents. They exhibited both antiamnestic and antidepressant activities in the scopolamine-induced amnesia test and behavioural despair test, respectively. However, the phytosomes failed to show anticonvulsant activity. The observations suggest that the G. biloba phytosomes possess moderate antiamnestic/nootropic activity. Copyright © 2006 John Wiley & Sons, Ltd. [source] Central nervous system stimulatory action from the root extract of Plumbago zeylanica in ratsPHYTOTHERAPY RESEARCH, Issue 2 2001C. P. Bopaiah Abstract The effects of a 50% ethanol extract of the root of Plumbago zeylanica (P. zeylanica) were investigated on locomotor behaviour and central dopaminergic activity in rats. The effects on the ambulatory behaviour were assessed along with the levels of dopamine (DA) and its metabolite homovanillic acid (HVA) in the striatum after a single oral dose (100, 200 and 300,mg/kg body weight) of the extract. The extract significantly increased the spontaneous motility in animals. The ambulatory and rotatory behaviour in the treated groups were higher than in the control group (p,<,0.05). There were marked differences in the ambulatory behaviour between 100 and 300,mg/kg, indicating that the responses were stimulatory and dose-dependent. The stereotypic behaviour which is characteristic of a dopamine agonist showed biphasic effects. However, there was no significant difference between the groups (p,>,0.05). The results showed that the extract of the root of P. zeylanica specifically enhanced the spontaneous ambulatory activity without inducing stereotypic behaviour. The neurochemical estimations revealed elevated levels of DA and HVA in striatum compared with the control rats (p,<,0.01). The levels were higher for the 100,mg/kg treated group than the other groups. The levels declined by increasing the dosage of the extract to 200,mg/kg and 300,mg/kg, however, these levels remained higher than the control group. The relationship between motor activity and levels of dopamine are not parallel. These behavioural and biochemical results indicated stimulatory properties of the extract of the root of P. zeylanica, which may be mediated by dopaminergic mechanisms in the rat brain. Copyright © 2001 John Wiley & Sons, Ltd. [source] Role of the cholinergic system and of apamin-sensitive Ca2+ -activated K+ channels on rabbit jejunum spontaneous activity and on the inhibitory effects of adrenoceptor agonistsAUTONOMIC & AUTACOID PHARMACOLOGY, Issue 2 2003L. Romanelli Summary 1 One reason why rabbit jejunum is suitable for studying the mechanisms underlying the actions of the various neurotransmitters and their interactions is its spontaneous motility. The main regulator of spontaneous motility is the cholinergic system. How the cholinergic system regulates the spontaneous activity in the rabbit jejunum and how it affects the inhibitory action of , - and , -adrenoceptor agonists remains unclear. 2 We studied the influence of the cholinergic system and apamin-sensitive Ca2+ -activated K+ channels on spontaneous contractions in the rabbit jejunum and on the inhibitory effects of,1 - and , -adrenoceptor agonists. 3 In naïve tissues, atropine (ATR, 7.4 × 10,8 m) and tetrodotoxin (8 × 10,8 m) almost completely inhibited , to a similar extent , the amplitude of spontaneous activity. Despite the presence of ATR or TDX, tissue contraction gradually recovered to about 50% of the baseline amplitude within 5,10 min. When ATR or TDX, respectively, were added to the TDX- or ATR-treated tissues, the recovered activity decreased weakly but significantly. After washout and a 45-min rest the contraction amplitude returned to baseline values. A further exposure to ATR or TDX reduced the contraction to a level significantly lower than the one obtained after TDX or ATR added 5 min after ATR or TDX, respectively. In preparations prestimulated for 10 min with acetylcholine (ACh), ATR abolished the TDX-resistant recovered spontaneous activity. 4 Adrenaline (ADR, 0.5,5 × 10,7 m) and phenylephrine (PHE, 1,10 × 10,7 m) inhibited tissue motility in naïve and in ATR- and in TDX-exposed preparations. But whereas in naïve preparations the ,1 -adrenoceptor antagonists completely antagonized inhibition induced by both drugs, in ATR- and TDX-exposed tissues they did so only partially for ADR. Agonist-induced inhibition had a rapid onset but rapidly faded; pendular movements took significantly longer to recover in ATR- and TDX-treated tissues than in naïve tissues. In tissues exposed for 2 min to ADR (0.5,5 × 10,7 m) or PHE (1,10 × 10,7 m), washout or addition of ,1 -adrenoceptor antagonists caused an immediate short-lasting increase in contraction amplitude. 5 Apamin (APAM, 5 × 10,9 m) caused a rapid and persistent increase in the amplitude of contractions. It also blocked the inhibitory responses to ADR and PHE, and removed washout-induced contractions. The APAM-induced increase in the contraction amplitude correlated with the increase obtained by washing out ADR or PHE. 6 Isoprenaline (at concentrations up to 2.8 × 10,7 m) produced no inhibitory response in naïve tissues, but it invariably blocked (at a concentration of 0.7 × 10,7 m) the recovered spontaneous activity (and sometimes depressed muscletone) in tissues exposed to ATR or TDX. Neither propranolol (3.4 × 10,7 m) nor APAM (5 × 10,9 m) counteracted these inhibitory effects. 7 These results indicate that spontaneous motility in the rabbit jejunum is predominantly mediated by neuronal release of ACh and by some other unidentified neuronal activity. Released ACh inhibits myogenic activity and strongly antagonizes , -adrenoceptor-induced APAM-insensitive inhibition but leaves ,1 agonist-induced APAM-sensitive inhibition unchanged. [source] Effects of excitatory and inhibitory neurotransmission on motor patterns of human sigmoid colon in vitroBRITISH JOURNAL OF PHARMACOLOGY, Issue 7 2008M Aulí Background and purpose: To characterize the in vitro motor patterns and the neurotransmitters released by enteric motor neurons (EMNs) in the human sigmoid colon. Experimental approach: Sigmoid circular strips were studied in organ baths. EMNs were stimulated by electrical field stimulation (EFS) and through nicotinic ACh receptors. Key results: Strips developed weak spontaneous rhythmic contractions (3.67±0.49 g, 2.54±0.15 min) unaffected by the neurotoxin tetrodotoxin (TTX; 1 ,M). EFS induced strong contractions during (on, 56%) or after electrical stimulus (off, 44%), both abolished by TTX. Nicotine (1,100 ,M) inhibited spontaneous contractions. Latency of off-contractions and nicotine responses were reduced by NG -nitro- L -arginine (1 mM) and blocked after further addition of apamin (1 ,M) or the P2Y1 receptor antagonist MRS 2179 (10 ,M) and were unaffected by the P2X antagonist NF279 (10 ,M) or ,-chymotrypsin (10 U mL,1). Amplitude of on- and off-contractions was reduced by atropine (1 ,M) and the selective NK2 receptor antagonist Bz-Ala-Ala-D-Trp-Phe-D-Pro-Pro-Nle-NH2 (1 ,M). MRS 2179 reduced the amplitude of EFS on- and off-contractions without altering direct muscular contractions induced by ACh (1 nM,1 mM) or substance P (1 nM,10 ,M). Conclusions and implications: Latency of EFS-induced off-contractions and inhibition of spontaneous motility by nicotine are caused by stimulation of inhibitory EMNs coreleasing NO and a purine acting at muscular P2Y1 receptors through apamin-sensitive K+ channels. EFS-induced on- and off-contractions are caused by stimulation of excitatory EMNs coreleasing ACh and tachykinins acting on muscular muscarinic and NK2 receptors. Prejunctional P2Y1 receptors might modulate the activity of excitatory EMNs. P2Y1 and NK2 receptors might be therapeutic targets for colonic motor disorders. British Journal of Pharmacology (2008) 155, 1043,1055; doi:10.1038/bjp.2008.332; published online 1 September 2008 [source] | ||||||||||