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  • 1
    ISSN: 1432-1912
    Keywords: Motor nerve ; Nicotine autoreceptors ; Positive feed-back mechanism ; Desensitization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of 1,1-dimethyl-4-phenylpiperazinium (DMPP) and of nicotine receptor antagonists on [3H]acetylcholine release from the rat phrenic nerve preincubated with [3H]choline were investigated in the absence and presence of cholinesterase inhibitors (presynaptic effects). Additionally, the effects of hexamethonium and tubocurarine on the muscle contraction of the indirectly stimulated diaphragm were examined (postsynaptic effects). DMPP (1–30 μM) increased (76–92%), whereas hexamethonium (0.001–1 mM) and tubocurarine (1–10 μM) decreased (52–60%) the release of [3H]acetylcholine following a train of 100 pulses at 5 Hz. The release caused by a longer train (750 pulses at 5 Hz) was only slightly affected by DMPP and tubocurarine. In the presence of neostigmine (10 μM) neither tubocurarine nor DMPP significantly modulated the evoked [3H]acetylcholine release. High DMPP concentrations (10 and 30 μM) enhanced the evoked release only when the pretreatment interval was reduced from 15 min to 20 s. Tubocurarine and hexamethonium concentration-dependently inhibited the end-organ response. Hexamethonium was 250-fold more potent on presynaptic than on postsynaptic nicotine receptors. It is concluded that the motor nerve terminals are endowed with presynaptic nicotine receptors. These autoreceptors mediate a positive feed-back mechanism that can be triggered by previously released endogenous acetylcholine. Receptor desensitization can be produced by high agonist concentrations (endogenous or exogenous agonists) and is probably one mechanism to limit the autofacilitatory process. The presynaptic receptors appear to differ in their pharmacological properties from the post-synaptic receptors.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1912
    Keywords: Motor nerve ; [3H]Acetylcholine release ; Nicotinic autofacilitation ; Fading
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of (+)-tubocurarine (TC) on the release of [3H]acetylcholine from the rat phrenic nerve-hemidiaphragm preincubated with [3H]choline was investigated at different stimulation frequencies and train lengths. At 0.5 Hz (100 pulses) TC failed to modulate the evoked acetylcholine release. A slight (30%) inhibition was observed at 1 Hz (100 pulses). Release of acetylcholine evoked at 5, 25 and 50 Hz (100 pulses) or 100 Hz (200 pulses) was markedly reduced by TC. The degree of inhibition (60%) was similar between 5 Hz and 100 Hz. A concentration of 1 μmol/l TC was a maximal effective concentration at 5 Hz whilst at all higher stimulation frequencies a 10-fold higher concentration was necessary for the maximal effect. When 300 pulses were continuously applied at 5 Hz or 50 Hz TC caused only a slight inhibition (20%). Additionally, the phrenic nerve was stimulated intermittently. Trains of 15 pulses were repeated 10 times with an interval of 3 s between each train. Under this latter stimulation condition TC failed to reduce acetylcholine release. It is concluded that nicotinic autofacilitation of acetylcholine release from the motor nerve operates at frequencies and stimulation conditions similar to the pattern of nerve activity under in vivo conditions. At least more than 15 pulses are required before the nicotinic autofacilitation becomes apparent. It appears unlikely that the TC induced fading of end-organ responses can only be attributed to a blockade of the presynaptic nicotine receptors.
    Type of Medium: Electronic Resource
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