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J I Hubbard

Publications and source records attributed to J I Hubbard.

78 records · Page 5Linked to original sources
PubMed1966

An investigation of the post-tetanic potentiation of end-plate potentials at a mammalian neuromuscular junction.

1. End-plate potentials (e.p.p.s) were recorded intracellularly from neuromuscular junctions in curarized or Mg-paralysed rat diaphragm-phrenic nerve preparations in vitro. In Mg-paralysed preparations after 1000 impulses at 100/sec the amplitude of e.p.p.s elicited at 1/sec before and after the tetanus was on average greater than the control amplitude for 120 +/- 30 sec.2. The post-tetanic potentiation (P.T.P.) of e.p.p. amplitudes was not thought to be dependent upon post-tetanic hyperpolarization (P.T.H.) of nerve terminals as it lasted longer than the hyperpolarization generated by an identical tetanus; was unaffected by hyperpolarizing currents which reduced P.T.H. or depolarizing currents which prolonged P.T.H.; and was diminished in solutions containing 30% of the normal NaCl concentration or 1% ethyl alcohol, both of which procedures prolong P.T.H. The magnitude and duration of P.T.P. were influenced by the pH of the bathing solution in the range 7-7.5 although there was no change in P.T.H. under these conditions. The inability of polarizing currents to influence P.T.P. was also thought inconsistent with the hypothesis that P.T.P. is due to an increase in available transmitter.3. P.T.P. was not thought to be due to sodium accumulation in nerve terminals, for P.T.P. was reduced or abolished by procedures which would be expected to increase the intraterminal sodium ion concentration. These procedures were: exhibition of metabolic inhibitors (1.8 x 10(-6)M antimycin A, 3-5 mM sodium azide or 1 mM sodium iodoacetate), exhibition of cardiac glycosides (7.7 x 10(-6)M digoxin or 0.42 mM ouabain), and omission of glucose or potassium ions from the bathing solution. Abolition of P.T.P. by potassium-free solutions was also thought to be inconsistent with the hypothesis that P.T.P. is due to a reduction in the potassium concentration in nerve terminals.4. P.T.P. was not thought to be due to terminal volume changes, for no consistent effect upon the quantal content of e.p.p.s could be detected in hypo- or hyperosmotic solutions.5. It was concluded that the only hypothesis for P.T.P. not excluded by our experiments was that P.T.P. is due to some change in ionized calcium at a membrane site important in transmitter release.

Animals↗
PubMed1966

The effects of hypoxia on neuromuscular transmission in a mammalian preparation.

1. The rat diaphragm-phrenic nerve preparation in vitro failed to contract in response to nerve impulses after 10-20 min exposure to solutions containing 95% N(2) and 5% CO(2) (hypoxic solutions) at temperatures between 33 and 38 degrees C. Intracellular recording revealed that end-plate potential (e.p.p.) amplitudes fell below the firing threshold for muscle fibres and then disappeared probably because of block of intramuscular nerve conduction.2. In curarized and Mg-paralysed preparations the reduction in e.p.p. amplitudes was found to be due to a fall in their quantal content. In about half of the Mg-paralysed preparations, however, and in curarized preparations after repeated exposures, there were increases in quantal content of e.p.p.s during hypoxia.3. Miniature end-plate potential (m.e.p.p. frequency increased in a cyclic fashion during hypoxia and this increase was largely suppressed in the presence of a raised extracellular Mg concentration. M.e.p.p. amplitude increased (range 0-100% of control value) after about 20 min hypoxia.4. Post-tetanic potentiation of e.p.p. amplitudes and m.e.p.p. frequency was reduced after exposure to hypoxic solutions. During hypoxia the e.p.p. amplitude potentiation was reduced but the m.e.p.p. frequency potentiation was augmented.5. There was an increase in the post-synaptic sensitivity to carbamylcholine after 20 min hypoxia which was sufficient to explain the increase in m.e.p.p. amplitude. Other post-synaptic changes were a fall in membrane potential (average 6 mV after 20 min) and a fall in membrane resistance after 30-60 min exposure to hypoxia.6. The effects of hypoxia upon neuromuscular transmission were partially explained by reduction of active transport of sodium and potassium ions and consequent depolarization of nerve and muscle.

Animals↗
PubMedDate not supplied

Subfornical organ lesions in rats abolish hyperdipsic effects of isoproterenol and serotonin.

Isoproterenol (300 micrograms/ml/kg) and serotonin (2 mg/ml/kg) given SC to rats (n = 27) caused significant drinking (Fisher PLSD, Scheffe F test, Dunnett t) in the 1 and 2 hours after injection. Such drinking was completely prevented in rats later shown to have complete lesions of their subfornical organs (n = 7). In contrast a response not significantly different from the prelesion response was found in rats later given cortical lesions (n = 11) or other lesions which did not damage the subfornical organ (n = 7). We conclude that drinking evoked by SC injection of serotonin and isoproterenol is brought about by peripheral production of angiotensin II. Blood borne angiotensin II in turn stimulates neurons in subfornical organ which initiate the neural organization of a drinking response.

Angiotensin II↗