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Biomedical subjects

J Dodd

Publications and source records attributed to J Dodd.

At least 91 records · Page 5Linked to original sources
PubMed1983

A reclassification of B and C neurones in the ninth and tenth paravertebral sympathetic ganglia of the bullfrog.

1. The cellular organization of the ninth and tenth paravertebral sympathetic ganglia in the bullfrog was studied with intracellular and extracellular recording methods. An isolated preparation was used in which anatomical details of individual cells could be resolved while making physiological measurements. This permitted the characterization of neurones in terms of their size, the segmental origin of their cholinergic innervation, and their orthodromic and antidromic conduction velocities. With these criteria, three classes of sympathetic neurones were identified. 2. As in previous studies, C cells were distinguished from B cells by the origin of their innervation. C cells are innervated by slowly conducting axons (0.4 m/sec) from spinal nerves 7 and 8 and B cells are innervated by rapidly conducting axons (2.4 m/sec) from the sympathetic chain above ganglion 7. 3. In earlier work it has been suggested that the conduction velocity of a preganglionic axon generally matches that of its target neurone. In this study we have characterized a large group of B cells for which this is not true. The axons of B cells fall into a rapidly conducting group (2.0 m/sec) and a slowly conducting group (0.6 m/sec). In contrast, C neurones, like their preganglionic inputs, have only slowly conducting axons (0.3 m/sec). Consequently, neurones have been classified as C type, fast B type, and slow B type. Fifty-nine percent of the B cells that we studied were slow B cells. These findings were corroborated by measurements of compound extracellular responses in post-ganglionic nerves. 4. Some neurones can be identified also by the size of their cell bodies. C cells are about 30 microns in diameter while B cells are about 50 microns in diameter. In our sample, 96% of the cells with radius less than 16 microns were C cells and 94% of the cells with radius greater than 21 microns were B cells. However, fast B cells could not be distinguished from slow B cells by size.

Action Potentials↗
PubMed1983

Muscarinic inhibition of sympathetic C neurones in the bullfrog.

1. The muscarinic inhibitory post-synaptic potential (i.p.s.p.) in sympathetic C neurones has been characterized in an isolated preparation of bullfrog paravertebral chain ganglia. Interactions between the i.p.s.p. and two other synaptic potentials have also been examined. 2. A single presynaptic stimulus to a C cell produces a nicotinic excitatory post-synaptic potential (e.p.s.p.) followed by a muscarine i.p.s.p. The latency of the i.p.s.p. is 50 msec or longer and the response lasts for seconds. C cells receive multiple cholinergic innervation but the thresholds for activation of the e.p.s.p. and i.p.s.p. are inseparable. Trains of 50 or more presynaptic stimuli produce a non-cholinergic e.p.s.p. which follows the nicotinic e.p.s.p. and i.p.s.p. and which lasts for tens of seconds. 3. The i.p.s.p. produced by a single presynaptic stimulus can be 30 mV in amplitude. However, in most cells, a short train of stimuli applied at an optimal frequency of 10 Hz is required to produce a large i.p.s.p. 4. The i.p.s.p. is blocked by atropine but is not affected by catecholamine antagonists. 5. Ionophoretically applied acetylcholine (ACh) mimics the i.p.s.p. in its latency, time course and amplitude. In addition, the i.p.s.p. and the muscarinic response to ACh reverse polarity at the same membrane potential: -102 mV in normal Ringer solution. The i.p.s.p. reversal potential shifts by 55 mV/decade change in extracellular K+ concentration and is insensitive to the Cl- gradient. 300 microM-Ba2+ totally blocks the muscarinically activated conductance in a reversible manner. 6. Action potentials, when initiated by a supramaximal nicotinic e.p.s.p. or by an antidromic impulse, are not blocked by the i.p.s.p. 7. Near resting potential (-50 to -60 mV), C cells can fire repetitively. The non-cholinergic slow e.p.s.p. is often accompanied by oscillations in membrane potential and firing of action potentials. This repetitive firing of C cells, which appears to be enhanced by the non-cholinergic e.p.s.p., is strongly inhibited by the i.p.s.p. The inhibition can be mimicked by injection of very small hyperpolarizing currents (e.g. 25 pA). Interactions between the i.p.s.p. and the non-cholinergic e.p.s.p. can generate phasic bursting patterns in C cells. 8. The mechanism underlying the i.p.s.p. and the consequences of these findings for ganglionic integration are discussed.

Acetylcholine↗
PubMed1983

A monoclonal antibody with specificity for Trypanosoma cruzi, central and peripheral neurones and glia.

Of 26 hybridomas secreting anti-Trypanosoma cruzi antibodies, two reacted with murine brain and spinal cord extracts but not other tissues. Both antibodies (5H7 and 3H3) had identical isotypes (IgM) and specificities as judged by western blotting. Antigens of molecular weight 58,000 and 37,000 in mouse brain and spinal cord, and 58,000 and 35,000 in T. cruzi were detected. Different tissue antigens were recognized by a previously reported T. cruzi mammalian neural tissue cross-reacting monoclonal antibody CE5; on immunofluorescence 5H7 stained some glia, and some central and peripheral neurones in rat tissue sections. Pooled sera from mice chronically infected with T. cruzi competed with binding of 5H7 to T. cruzi antigens.

Animals↗
PubMed1981

The excitatory action of acetylcholine on hippocampal neurones of the guinea pig and rat maintained in vitro.

In preliminary experiments on 39 identified pyramidal cells in the in vitro slice preparation of the guinea-pig hippocampus the depolarization evoked by acetylcholine (ACh) applied by microiontophoresis was always associated with an increase in membrane resistance. In 9 slices cut from the rat hippocampus similar results were obtained from 24 cells. In a more detailed analysis on 13 cells from the rat hippocampus, whose mean resting potential was -74 mV and mean resting input resistance 33 M omega, the mean peak depolarization evoked by ACh was 11.6 mV and the mean increase in membrane resistance 12 M omega. The reversal potential for the excitatory action of ACh was 29 mV more hyperpolarizing than the resting membrane potential. The depolarization evoked by ACh was linearly related to the corresponding increase in membrane resistance expressed as a fraction of the resting membrane resistance determined before and after the application of ACh. This was true throughout each of the individual applications of ACh and of the peak response evoked by each of the 13 applications. The constancy of this relationship is compatible with the usual model used to describe synaptic events thought to be mediated by the closure of ionic channels which are open in the absence of the transmitter. The onset of the response to ACh was always approximately 4 times slower than that evoked by a near equipotent microiontophoretic application of glutamate from an adjacent barrel of the same multibarrelled micropipette. Following the application of ACh, recovery was also slow and, on average, was approximately 10 times longer than that following a near equipotent application of glutamate. It is suggested that the slow onset and offset of the responses evoked by ACh are not compatible with models based on diffusion and are best explained by postulating a sequential generation of one or more intermediates.

Acetylcholine↗
PubMed1981

The actions of cholecystokinin and related peptides on pyramidal neurones of the mammalian hippocampus.

The presence of cholecystokinin octapeptide (CCK-8) immunoreactivity in the vicinity of the pyramidal neurones of the mammalian hippocampus has allowed us to investigate the central postsynaptic actions of CCK-8 and a number of related peptides, at a site thought to be innervated by a peptidergic pathway. Intracellular records from pyramidal cells of the CA1 region of the hippocampal slice preparation were used to determine changes in excitability and associated changes in membrane potential and resistance evoked by the pressure application of peptides into the cell body layer, from an independently mounted multibarrelled micropipette. The tetra- and octa-peptide C-terminal fragments of cholecystokinin evoked abrupt and rapidly reversible depolarizations which were accompanied by marked increases in excitability and a decrease in membrane input resistance. A comparison was made of the actions of these peptides with those of glutamate, released by iontophoresis from an adjacent barrel of the same multibarrelled pipette. The rate of onset of the cholecystokinin-evoked response was similar to that of the response evoked by glutamate. C-terminal fragments of gastrin (G-13 and G-14) and bombesin were also found to be excitatory to pyramidal neurones in the CA1 region. However, the nonsulphated form of CCK-8 was inactive, as was substance P, a peptide not present in the hippocampus.

Animals↗
PubMed1979

Analysis of alloantisera against bovine lymphocytes. Joint report of the 1st International Bovine Lymphocyte Antigen (BoLA) workshop.

The results and agreements of the 1 international BoLA workshop, held in Edinburgh, Scotland in August 1978, are reported. Most of these concern the results from a comparison test of 249 alloantisera to bovine lymphocytes, the antisera being contributed by 9 laboratories. These sera were compared directly in Edinburgh on a panel of lymphocytes from 130 cattle of 21 breeds. In the microlymphocytotoxicity test used 75% of the sera reacted. Sixty eight of these sera were grouped into clusters according to their reaction patterns against the lymphocyte panel. Eleven of these clusters were clearly defined and were given workshop BoLA designations. In addition 22 sera were assigned to subgroups of the agreed clusters. There was no evidence that the method of production of the sera had any effect on their specificity. Although genetic data was not available, the phenotypes of the test panel of lymphocytes are consistent with the clusters detecting antigens controlled by multiple alleles at a single autosomal locus. It was agreed to name the genetic region where this putative locus is located BoLA (bovine lymphocyte antigen).

Animals↗
PubMed1976

Thymus-dependent (T) lymphocyte deficiency in progressive systemic sclerosis.

Circulating thymus-dependent (T) lymphocytes were estimated in twenty-seven patients with progressive systemic sclerosis (PSS) and in forty-five normal controls using the property of T lymphocytes to form rosettes with sheep red blood cells. The patients with PSS were found to have a reduction of T lymphocytes which correlated with the extent of visceral involvement by the disease, those with the lowest counts having the most extensive disease. These findings support the suggestion that immunological factors may be involved in the pathogenesis of PSS.

Adult↗