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Cyclic AMP accumulation in rat superior cervical ganglia during synaptic activity occurs by a noncholinergic, nonadrenergic process. Both preganglionic nerve stimulation and 4-aminopyridine increase ganglion cyclic AMP levels in the presence of atropine or phentolamine. Of the polypeptides tested as putative transmitters, vasoactive intestinal polypeptide(More)
Alterations by ketamine (10-100 microM) and ditran (50-100 microM) of end-plate currents were studied using transected cutaneous pectoris muscles. Both drugs reduced peak current and shortened the time constant for end-plate current decay (tau). Ketamine was more effective at pH 5.3 than at 7.4 or 9.1. Recovery from blockade was asymmetrical in that tau(More)
[3H]Inositol incorporation into phosphatidylinositol was accelerated in rat superior cervical ganglia treated with 4-aminopyridine or Bethanechol. The inositol response to these drugs occurred in intact and denervated ganglia and was prevented by atropine. The possibility that muscarinic receptor subtypes are present in the ganglia is considered because(More)
Complete or partial replacement of Na+ by Li+ resulted in a progressively developing increase in the amplitude and quantal content of end-plate potentials of the frog neuromuscular junction. Analysis of frequency facilitation curves and estimations of the binomial parameters of release indicate that Li+ caused an increase in the probability of transmitter(More)
The effects of lobeline and tubocurarine on the voltage-clamped endplates of frog sartorius and cutaneous pectoris muscles were examined at room temperature (20-23 degrees C). Like tubocurarine, lobeline causes nondepolarizing neuromuscular blockade. The half-time of decay (t((1/2))) of endplate currents (e.p.c.s) recorded at a holding potential (V(m)) of(More)
Preganglionic nerve stimulation or elevated [K+]o increase cAMP levels in isolated guinea-pig superior cervical ganglia, a ganglion lacking adrenergic inhibitory synaptic potentials. The cAMP response to K+ and nerve stimulation is not prevented by atropine or phentolamine. The regulation of cAMP content does not involve cholinergic or adrenergic mechanism.(More)
In rat superior cervical ganglia the regulation of cyclic GMP (cGMP) formation does not involve muscarinic or adrenergic transmitters or receptors. Marked increases in cGMP content during preganglionic axonal stimulation by electric currents, elevated K+, or drugs that cause transmitter release are unaffected by muscarinic and adrenergic receptor blockade.(More)
Preganglionic nerve terminal stimulation in rat superior cervical ganglia causes marked increases in the levels of cyclic nucleotides. Results are similar when preganglionic nerve stimulation is compared with elevated [K+]0 or 4-aminopyridine. Although intact nerve terminals and Ca2+ are required for the response to occur, pharmacological studies indicate(More)
Cutaneous pectoris muscles of Rana pipiens were transected distal to the innervated region. Within 10 min, membrane potentials (Em's) of -33 +/- 2.5 mV and end-plate potentials (3-15 mV) were recorded unaccompanied by muscle action potentials or twitch. The fall in Em was associated with a net loss of [K+]i and a net gain of [Na+]i. Although input(More)