scholarly journals INHIBITORY EFFECT OF ENDOGENOUS MACROMOLECULE ON THE Ca++-STIMULATED ACETYLCHOLINE RELEASE FROM THE CRUDE SYNAPTIC VESICLES

1976 ◽  
Vol 26 (6) ◽  
pp. 762-764
Author(s):  
Fumiaki HATA ◽  
Che-Hui KUO ◽  
Tomohiro MATSUDA ◽  
Hiroshi YOSHIDA
Keyword(s):  
Synaptic Vesicles ◽  
Acetylcholine Release ◽  
Inhibitory Effect

Presynaptic modulation of acetylcholine release from cardiac parasympathetic neurons

1985 ◽  
Vol 248 (1) ◽  
pp. H33-H39 ◽  
Author(s):  
G. T. Wetzel ◽  
J. H. Brown
Keyword(s):  
Receptor Antagonist ◽  
Adrenergic Receptor ◽  
Acetylcholine Release ◽  
Electrical Field Stimulation ◽  
Inhibitory Effect ◽  
Muscarinic Agonist ◽  
Parasympathetic Nerve ◽  
Presynaptic Modulation ◽  
Rat Atria ◽  
Alpha Adrenergic Receptors

Acetylcholine can be released from parasympathetic nerve endings in rat atria by 57 mM K+ depolarization or by electrical field stimulation. We have studied the presynaptic modulation of [3H]acetylcholine release from superfused rat atria prelabeled with [3H]choline. Exogenous acetylcholine and the specific muscarinic agonist oxotremorine inhibit the stimulation-induced overflow of [3H]acetylcholine into the superfusion medium. The half-maximal inhibitory concentration (IC50) of oxotremorine is 0.3 microM. The cholinesterase inhibitor neostigmine also decreases K+-stimulated [3H]acetylcholine overflow, whereas the muscarinic antagonist atropine enhances the overflow of [3H]acetylcholine. These data suggest that acetylcholine release in atria is modulated through negative feedback by the endogenous transmitter. The sympathetic adrenergic neurotransmitter norepinephrine and the neurohormone epinephrine also inhibit the overflow of [3H]acetylcholine by approximately 60%. The IC50 values for the inhibitory effects of these catecholamines are 6.3 and 2.2 microM, respectively. The inhibitory effect of norepinephrine is blocked by the alpha-adrenergic receptor antagonist yohimbine but not by the beta-adrenergic receptor antagonist propranolol. We suggest that presynaptic muscarinic and alpha-adrenergic receptors participate in the physiological and pharmacological control of cardiac parasympathetic activity.

The fine structure of the vertical lobe of Octopus brain

1970 ◽  
Vol 258 (827) ◽  
pp. 379-394 ◽  
Keyword(s):  
Electron Microscopy ◽  
Fine Structure ◽  
Electron Microscope ◽  
Light Microscopy ◽  
Synaptic Vesicles ◽  
Structural Organization ◽  
Amacrine Cells ◽  
Large Cell ◽  
Inhibitory Effect ◽  
Tactile System

Although much is known about the structural organization and connexions of the various lobes of the octopus brain from light microscopy, this is the first attempt at a detailed analysis of one of the lobes— the vertical lobe, with the electron microscope. The vertical lobe consists of five lobules. The median superior frontal (MSF) axons enter each lobule from the MSF lobe. The MSF axons contain both microtubules and neurofilaments. The varicosities of the MSF axons contain both agranular and dense-cored vesicles and synapse with trunks of the amacrine cells. These trunks run together in bundles termed amacrine tracts into the centres of the lobules. The amacrine trunks contain microtubules but no neurofilaments. The trunks contain large and small agranular synaptic vesicles and synapse with what are in all probability branches of the trunks of the large cells. These trunks contain microtubules but no neurofilaments. They run out through the bases of the lobules probably without forming synaptic contacts within the lobule. Fibres signalling ‘pain’ (nocifensor) enter the lobules from below. They can be recognized by their content of neurofilaments. Their terminals contain numerous very small synaptic vesicles and a few larger and dense-cored ones. These ‘pain’ fibres appear to synapse mostly with processes of the large cells. J. Z. Young has shown that the vertical lobe is especially concerned with the integrative action of the visual system, linked with the chemo-tactile system. Electron microscopy supports Young’s suggestion that the superior frontal and interconnected vertical lobe systems constitute a loop which could sustain a positive feed-back mechanism (MSF —> amacrine -> large cell -> lateral superior frontal -> MSF) while the ‘pain’ (nocifensor) input could exert a suppressor (inhibitory) effect on the loop by its action on the large cells.

Inhibitory effect of hypoxic condition on acetylcholine release is partly due to the effect of adenosine released from the tissue

1990 ◽  
Vol 24 (3) ◽  
pp. 369-373 ◽  
Author(s):  
E. Milusheva ◽  
B. Sperlágh ◽  
B. Kiss ◽  
L. Szporny ◽  
E. Pásztor ◽  
...  
Keyword(s):  
Acetylcholine Release ◽  
Hypoxic Condition ◽  
Inhibitory Effect

Neurotensin inhibition of canine intestinal motility in vivo via α-adrenoceptors

1984 ◽  
Vol 62 (4) ◽  
pp. 403-411 ◽  
Author(s):  
Y. Sakai ◽  
E. E. Daniel ◽  
J. Jury ◽  
J. E. T. Fox
Keyword(s):  
Acetylcholine Release ◽  
Contractile Activity ◽  
Inhibitory Effect ◽  
Inhibitory Effects ◽  
Maximal Inhibition ◽  
Contractile Responses ◽  
Adrenergic Antagonists ◽  
Distal Site ◽  
Stimulation Of

Neurotensin given intra-arterially in bolus doses to the canine small intestine inhibited field-stimulated, atropine-sensitive contractile responses in the duodenum (mean effective dose (ED50) = 3.2 × 10−11 mol) and in the ileum (mean ED50 = 2.1 × 10−11 mol). Norepinephrine (ED50 = 3 × 10−9 mol) also inhibited these contractile responses. Phenylephrine (ED50 = 1.3 × 10−8 mol) was one-fourth as potent as norepinephrine and clonidine (ED50 = 8 × 10−10 mol) was at least as potent as norepinephrine, while isoproterenol (up to 8 × 10−8 mol) failed to show any inhibitory effects. Phentolamine (2 mg/kg) increased significantly the ED50 of neurotensin and norepinephrine. Prazosin (2 mg/kg) increased significantly the ED50 of norepinephrine in the duodenum but had no effect on the ED50 of neurotensin. Yohimbine (2 mg/kg) increased the ED50 values of neurotensin and adrenergic agonists. Both neurotensin and norepinephrine in doses causing maximal inhibition of field-stimulated responses decreased (by 40 to 60%) contractile responses to 9 × 10−10 mol (approximately the intra-arterial ED50 dose) of acetylcholine. Reserpine pretreatment markedly diminished the inhibition of spontaneous or field-stimulated phasic contractions by distention or field stimulation of a distal site. Reserpine also diminished the ED50 for neurotensin from 1 × 10−11 to 2 × 10−11 mol (p < 0.02), but did not abolish neurotensin's inhibitory effect. Tetrodotoxin (10–15 μg, intra-arterially) increased the dose of neurotensin required to inhibit spontaneous activity in the ileum but after this toxin, as after adrenergic antagonists or reserpine, maximal inhibition could still be obtained. These results suggested that neurotensin inhibited contractile activity of canine intestine by acting on neural receptors to release norepinephrine. Norepinephrine activated primarily α2-adrenoceptors and ultimately inhibited acetylcholine release. Neurotensin also inhibited contractions by activating a second, less sensitive receptor on smooth muscle.

Angiotensin II attenuates myocardial interstitial acetylcholine release in response to vagal stimulation

2007 ◽  
Vol 293 (4) ◽  
pp. H2516-H2522 ◽  
Author(s):  
Toru Kawada ◽  
Toji Yamazaki ◽  
Tsuyoshi Akiyama ◽  
Meihua Li ◽  
Can Zheng ◽  
...  
Keyword(s):  
Acetylcholine Release ◽  
Vagal Stimulation ◽  
Sinus Node ◽  
Inhibitory Effect ◽  
Local Administration ◽  
Control Group ◽  
Receptor Subtype ◽  
Ang Ii ◽  
Ach Release ◽  
Parasympathetic Ganglia

Although ANG II exerts a variety of effects on the cardiovascular system, its effects on the peripheral parasympathetic neurotransmission have only been evaluated by changes in heart rate (an effect on the sinus node). To elucidate the effect of ANG II on the parasympathetic neurotransmission in the left ventricle, we measured myocardial interstitial ACh release in response to vagal stimulation (1 ms, 10 V, 20 Hz) using cardiac microdialysis in anesthetized cats. In a control group ( n = 6), vagal stimulation increased the ACh level from 0.85 ± 0.03 to 10.7 ± 1.0 (SE) nM. Intravenous administration of ANG II at 10 μg·kg−1·h−1 suppressed the stimulation-induced ACh release to 7.5 ± 0.6 nM ( P < 0.01). In a group with pretreatment of intravenous ANG II receptor subtype 1 (AT1 receptor) blocker losartan (10 mg/kg, n = 6), ANG II was unable to inhibit the stimulation-induced ACh release (8.6 ± 1.5 vs. 8.4 ± 1.7 nM). In contrast, in a group with local administration of losartan (10 mM, n = 6) through the dialysis probe, ANG II inhibited the stimulation-induced ACh release (8.0 ± 0.8 vs. 5.8 ± 1.0 nM, P < 0.05). In conclusion, intravenous ANG II significantly inhibited the parasympathetic neurotransmission through AT1 receptors. The failure of local losartan administration to nullify the inhibitory effect of ANG II on the stimulation-induced ACh release indicates that the site of this inhibitory action is likely at parasympathetic ganglia rather than at postganglionic vagal nerve terminals.

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