PubMed Health⌕ Search

Biomedical subjects

P Shinnick-Gallagher

Publications and source records attributed to P Shinnick-Gallagher.

81 records · Page 5Linked to original sources
PubMed1980

Possible mechanisms of action of Gymnodinium breve toxin at the mammalian neuromuscular junction.

1 The mechanism of action of a crude fraction of Gymnodinium breve toxin (GBTX) was investigated by intracellular recording techniques in the rat phrenic nerve diaphragm preparation. 2 GBTX (2 micrograms/ml) decreased the input resistance of the muscle membrane concomitantly with a depolarization of the resting membrane potential. 3 A low sodium solution reversed or prevented a GBTX-induced membrane depolarization. 4 Tetrodotoxin (TTX) antagonized a GBTX-induced increase in miniature endplate potential (m.e.p.p.) frequency and repolarized a GBTX-depolarized membrane. Pretreatment with TTX prevented GBTX effects. 5 GBTX reversibly reduced depolarizations produced by bath applied acetylcholine (ACh). The membrane depolarization was not responsible for the depression of ACh responses. 6 These findings suggest that GBTX increases m.e.p.p. frequency and depolarizes the resting membrane potential by increasing sodium permeability. The reduction of ACh-induced depolarizations suggests that GBTX may be acting at some site on the ACh receptor.

Acetylcholine↗
PubMed1980

An intracellular investigation of cat vesical pelvic ganglia.

1. Intracellular recording techniques were used to study individual neurons in the cat parasympathetic vesical pelvic ganglion (VPG). 2. Active and passive electrical properties were determined from 140 ganglion cells (35 preparations). 3. Three types of ganglion cells were distinguished. Type I (A and B) cells were nonaccommodating cells in response to depolarizing current pulses. Type II cells showed accommodation to depolarizing current pulses. Other cells, presumably glia, were also impaled. 4. Type IB cells exhibited two kinds of nonsynaptic spontaneous activity, spontaneous action potentials (60-70 mV) and small spontaneous potentials (up to 5 mV). Characteristics of the spontaneous activity were examined. 5. The duration of the spikes' afterhyperpolarization resulting from either orthodromic or antidromic train stimulation was dependent on the frequency of train stimulation. No long-lasting posttrain hyperpolarization was observed. 6. Chlorisondamine (10(-6) M), d-tubocurarine (10(-5) M), and hexamethonium (10(-5) M) reversibly blocked orthodromic responses. 7. The VPG is a useful model to study parasympathetic ganglionic transmission at the cellular level.

Animals↗
PubMed1977

Cyclic nucleotides injected intracellularly into rat superior cervical ganglion cells.

Intracellular iontophoresis of either adenosine 3',5'-monophosphate or guanosine 3',5'-monophosphate produces a membrane depolarization and an increased membrane conductance in sympathetic ganglion cells of the rat superior cervical ganglion. Since adenosine 3',5'-monophosphate did not cause a membrane hyperpolarization, it is difficult to assign it a second messenger role in the mediation of the slow inhibitory postsynaptic potential. However, these results do not rule out the possibility that the cyclic nucleotides, at the intracellular concentrations attained in these experiments, participate in cellular processes that contribute to conductance changes which result in depolarization of the ganglion cell membrane.

Action Potentials↗
PubMed1976

An analysis of the subsynaptic site of action of theophylline on isolated cat tenuissimus muscle.

The subsynaptic actions of theophylline were studied by employing intracellular recording techniques in the isolated cat tenuissimus muscle. Theophylline produced a dose-dependent increase in miniature end-plate potential (MEPP) amplitude. The maximal increase (30%) in MEPP amplitude occurred at the 1.8 mM concentration of theophylline with a concomitant depolarization of the resting membrane potential. Depolarizations induced by acetylcholine were potentiated by 1.8 mM theophylline. This effect was less evident with a carbachol-induced depolarization, which indicates a possible anticholinesterase action. Input resistance decreased significantly; this effect correlated with the decline in resting membrane potential produced by theophylline. The equilibrium potential of the EPP was shifted to a more positive value in a reversible manner. In addition, the conductance change due to MEPPs, acetylcholine and carbachol was increased by theophylline treatment. These results suggest that the shift in equilibrium potential of the EPP coupled with a slight anticholinesterase action may account for the increase in MEPP amplitude observed with theophylline treatment.

Acetylcholine↗
PubMedDate not supplied

Muscarinic inhibitory transmission in mammalian sympathetic ganglia mediated by increased potassium conductance.

Slow muscarinic inhibition may be a powerful influence on membrane properties in the peripheral and central nervous system. But the location of the muscarinic receptors in sympathetic ganglia, either on interneurones or on the postganglionic membrane, and the underlying mechanism of the inhibitory response, remains controversial. In mammalian sympathetic ganglia synaptic activation of muscarinic receptors located on inhibitory interneurones was thought to release catecholamines leading to a membrane hyperpolarization called the slow inhibitory postsynaptic potential, or s.-i.p.s.p.. However, the s.-i.p.s.p. in parasympathetic ganglia and in amphibian sympathetic ganglia is due to direct monosynaptic activation of muscarinic receptors, accompanied by an increased potassium conductance (but see ref. 11), and is not mediated by catecholamines. The situation is less clear in mammalian sympathetic ganglia and monosynaptic s.-i.p.s.ps observed in other ganglia could be exceptions to the hypothesis. We showed earlier that the s.-i.p.s.p. in rabbit superior cervical ganglia is not affected by catecholamine antagonists. We now show that the s.-i.p.s.p. in a mammalian sympathetic ganglion is due to the monosynaptic activation of muscarinic receptors, probably by an increase in potassium conductance.

Acetylcholine↗
PubMedDate not supplied

Adenosine mediates a slow hyperpolarizing synaptic potential in autonomic neurones.

Considerable evidence has accumulated suggesting that purines, adenosine and ATP function as neurotransmitters in the central and peripheral nervous systems. Burnstock has proposed that purinergic receptors be classified into two types, P1 and P2, having adenosine and ATP, respectively, as agonist prototypes. Recent data suggest that ATP may mediate a synaptic potential in guinea pig vas deferens, but no such evidence exists for adenosine. The presence of a non-cholinergic, non-adrenergic nerve supply to the urinary bladder has been postulated and termed purinergic, as these nerves have been shown to release ATP. Furthermore, atropine-resistant contractions of bladder smooth muscle are thought to be mediated by ATP, while in situ experiments in vesical parasympathetic ganglia have suggested that a purinergic modulatory mechanism may control urinary bladder function. We now report the presence of a slow hyperpolarizing synaptic potential (slow-h.s.p.) in neurones of cat vesical parasympathetic ganglia, produced by stimulating the preganglionic nerves, and provide evidence that the slow-h.s.p. is mediated by adenosine.

Adenosine↗