The effect of cholinergic drugs on [3H]acetylcholine release from slices of rat hippocampus, striatum and cortex

2. With these stimulation parameters, which yielded about the same fractional secretion of [3H]ACh, and with eserine (10 /LM) present in the medium, atropine (1 /M) enhanced the 'indirectly', electrically evoked secretion 3-65 + 034 (n = 6) fold, and that caused by 40 mm or 80 mM-potassium 1-82+0-06 (n = 6) or 1P55+0-09 (n = 10) fold, respectively. Atropine thus enhanced 'indirectly', electrically evoked secretion 4-fold more than that caused by 'direct' depolarization of varicosities with high potassium (P < 0 001).3. This difference is not likely to be caused by depression of the sensitivity of the presynaptic muscarinic receptors to ACh released by nerve stimulation, caused by the hypertonicity of the medium in the potassium stimulation experiments. The medium made hypertonic by addition of Tris-HEPES (80 mM) did lower the binding affinity of membrane preparations of (pre-and post-synaptic) muscarinic receptors, to carbamylcholine, and also the contractile responsiveness of the longitudinal muscle to this agent, in both cases to about one half. But it did not appear to alter the responsiveness of either pre-or post-synaptic muscarinic receptors to endogenous ACh, released by nerve stimulation.4. The results support a dual-mode model for the muscarinic negative feed-back control of ACh secretion from the nerve terminals of this preparation, mainly operating by restriction of the invasion of terminals, and only secondarily by depression of the efficiency of depolarization-secretion coupling in invaded varicosities.5. Since this model has earlier been proposed to apply for the control of secretion of [3H]noradrenaline from the micro-anatomically similar nerve terminals of P. ALBERTS, T. BARTFAI AND L. STJARNE noradrenergic nerves, the present findings suggest that the model may have a wider biological significance, and possibly apply to the control of the secretary activity of bouton8-en-pa88ant nerve terminals in general.

Section: P Alberts T Bartfai and L Stjarne Discussionmentioning

confidence: 81%

Section: Labellingmentioning

confidence: 99%

The effects of atropine on [³H]acetylcholine secretion from guinea‐pig myenteric plexus evoked electrically or by high potassium

Alberts

Bartfai

Stjärne

1982

“…Increase in the amount of ACh liberated in the presence of atropine was described in vertebrate brain (for a review see Chesselet, 1984). The observed enhancement varied from 25 % (Hadhazy & Szerb, 1977) to 120 % (Jones et al 1973). …”

Section: Presynaptic Action Of Atropinementioning

confidence: 95%

Presynaptic actions of curare and atropine on quantal acetylcholine release at a central synapse of Aplysia.

Baux

Tauc

1987

SUMMARY1. In a cholinergic synaptic couple in the buccal ganglion of Aplysia californica, where the synaptic areas are situated close to the somata (500 ,tm), we were able to control transmitter release by stimulating the cell body of the presynaptic neurone with long depolarizing pulses in the presence of tetrodotoxin (TTX).2. Statistical analysis of noise occurring at the peak of the long-depolarizationinduced post-synaptic current (p.s.c.) responses allowed us to calculate the amplitude and the decay time of the miniature post-synaptic currents (m.p.s.c.s). These data were used to calculate the quantal content of the responses.3. Bath-applied tubocurarine reduced the amplitude of the long-depolarizationinduced p.s.c. more than that of the m.p.s.c.s, indicating that tubocurarine exerts a depressive presynaptic action on the quantal content of the post-synaptic responses.3. Tubocurarine injected into the presynaptic neurone blocked synaptic transmission without decreasing the size of the m.p.s.c.s probably by acting on the mechanism of transmitter release.5. Bath-applied atropine (10-6 and 10-5 M) caused a slight decrease of the m.p.s.c.s but the long-depolarization-induced p.s.c.s increased, as did the quantal content. Higher concentrations of atropine depressed strongly both the m.p.s.c. and the quantal content.6. Injection ofatropine into the presynaptic neurone had the same effect as its bath application, probably due to the leakage of the drug into the synaptic cleft; the effect depended on the concentration reached in the cleft, i.e. on the quantity of injected drug. The synapses of the neighbouring cholinergic neurone were also affected by this leak of atropine.7. The presence of nicotinic presynaptic receptors blocked by tubocurarine, and muscarinic presynaptic receptors blocked by atropine, which regulate synaptic transmission by facilitating and depressing the ACh release respectively, is discussed.

“…Recent experiments on hippocampal slices, which do not possess cholinergic cell bodies (Hadhazy & Szerb, 1977), and on hippocampal synaptosomes (Nordstr6m & Bartfai, 1980) strongly suggest that in the hippocampus at least a part of the effects of atropine and oxotremorine on ACh release involves inhibitory muscarinic autoreceptors on the cholinergic nerve terminals.…”

Section: Introductionmentioning

confidence: 99%

Evidence for a cholinergic inhibitory feed‐back mechanism in the rabbit retina.

Cunningham¹,

Dawson²,

Neal³

1983

SUMMARY1. The effects of muscarine, atropine and nicotinic antagonists on the light-evoked release of radioactivity from rabbit retinas previously exposed to [3H] 7. These results suggest the presence in the retina of a cholinergic inhibitory feed-back mechanism which involves a neuronal loop, rather than presynaptic or post-synaptic inhibitory muscarinic receptors on the cholinergic amacrine cells themselves. Our experiments do not provide evidence on the nature of the proposed inhibitory loop, except that it apparently includes a glycinergic or taurinergic (amacrine) cell.