Biomedical subjects
Publications and source records attributed to C S Thompson.
[3H]Naloxone and [3H]dihydromorphine are selective ligands for opiate receptors. Using an in vitro autoradiographic technique, binding of these ligands has been demonstrated to the villi and crypts in rat small intestine. These results indicate the presence of opiate receptor sites in the small intestine which suggests further a role for endogenous opiates in the transport functions of intestinal mucosa.
In view of the marked increase in blood flow into the penis during erection and the association of diabetes mellitus with impotence, we used the diabetic rat model to investigate the possibility that: the penis may produce prostacyclin; and prostacyclin secretion may be decreased in diabetes. Rats given a high dose of streptozotocin (120 mg/kg body weight) developed acute ketotic diabetes and were killed after 48 h. Animals given a low dose of streptozotocin (65 mg/kg body weight) developed non-ketonuric diabetes and were killed after 7 or 62 days. Aortic rings and penile tissue discs were incubated in buffer, which was assayed for 6-oxo-prostaglandin F1 alpha, the stable and spontaneous breakdown product of prostacyclin. Penile tissue from control, ketotic and non-ketonuric (7 days) animals released similar quantities of prostacyclin, whereas that from long-term non-ketonuric animals (62 days) produced significantly less prostacyclin. Production of this prostanoid by the aortic rings paralleled these changes. We conclude that: penile tissue releases prostacyclin in quantities comparable to those of the aorta; long-term diabetes leads to diminished prostacyclin release by penile and aortic tissue: the former may contribute to the pathogenesis of diabetic impotence; and since short-term ketotic diabetes does not inhibit aortic or penile prostacyclin release, duration of diabetes rather than its severity is responsible for diminished prostacyclin release.
Uptake of horseradish peroxidase was studied by examining percentages of labelled synaptic vesicles in nerve endings of the excitatory axon innervating the opener muscle of the walking leg in the crayfish (Procambarus clarkii). Terminals on fibres with large excitatory postsynaptic potentials (EPSP) had higher percentage of labelled vesicles than terminals of fibres with small EJPs. The extent of labelling in the synaptic vesicle pool was greater for terminals with higher transmitter output. Evidence for three possible routes of synaptic vesicle formation was found. Movement of vesicles within the terminal as a whole appeared to be constrained, but rapid movement of vesicles within local populations probably occurs.
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The physiology of the neuromuscular systems in Hymenolepis diminuta and H. microstoma was studied in vitro using intact, adult worm and strips of worm body wall. Intact worms were insensitive to ionic changes in the in vitro buffering system. However, strips of body wall containing longitudinal muscles were extremely sensitive to ionic manipulation. In intact worms tension generated in the strobila had two components; small brief tension peaks up to 500 mg amplitude are superimposed on larger, longer peaks of up to 1200 mg amplitude. Removal of the scolex and neck region either failed to show significant changes in tension, or showed a reduction in amplitude but not of frequency. Muscle contraction of both H. diminuta and H. microstoma were qualitatively similar. In split-worm preparations the concentration of Ca2+ in the bathing solution significantly affected both spontaneous and evoked contractions in H. diminuta and H. microstoma; the addition of CaCl2 greatly reduced the amplitude and frequency of the contractions. The chloride salts of cobalt, barium, cadmium and manganese elicited prolonged contractions of the longitudinal musculature of both H. diminuta and H. microstoma. While CoCl2 was the most effective in stimulating muscle contraction, the magnitude of the response varied with the concentration of Ca2+ in the bath. The results indicate that peripheral inhibition is extremely important in cestode motor control and that extracellular calcium ions may regulate the peripheral inhibitory mechanisms.
The effects of neomycin sulphate on galactose absorption have been studied using in vivo and in vitro preparations of rat small intestine. Neomycin (10(-3)M) produced an increase in the maximum transport capacity (Jmax) for the active component of absorption in vivo. The apparent Kt for absorption was unaffected. The antibiotic caused a dose-dependent increase in the potential difference across the mucosal membrane (Vm) measured in vitro, a maximal effect being seen at a concentration of 10(-4)M. Furthermore, the magnitude of the depolarization induced by the addition of galactose (4 mM) to the mucosal fluid was enhanced by neomycin (10(-4)M). Phlorhizin (10(-4)M) abolished the galactose-induced depolarization in both the absence and presence of the antibiotic. It is concluded that neomycin increases the electrical driving force for Na+ during Na+-coupled galactose entry into the enterocyte.
The effects of starvation on the magnitude of the potential difference across the brush-border membrane of rat small intestine (Vm) have been studied in vitro. The mean values obtained for Vm in jejunal tissue after a fast of either 24 or 72 h duration (-53.5 and -55.0 mV respectively) were significantly greater than the mean value of -45.3 mV recorded using intestine from fed rats. A similar hyperpolarization was observed after a 72 h fast using intestine from a more distal region. The response to fasting seen in the jejunum appears to be caused by a decrease in Na+ permeability of the mucosal membrane. The addition of D-galactose (4 mM) or L-valine (4 mM) to the mucosal fluid caused a depolarization of Vm. Using jejunum from fed animals, Vm in the presence of galactose and valine was found to be -40.3 and -39.2 mV respectively. Following a fast of 72 h duration, the values of Vm for the two substrates were -43.4 and -43.1 mV respectively. Phlorhizin (10(-4) M) abolished the galactose-induced depolarization in both fed and fasted conditions but was without effect on the response to valine. It is concluded that starvation increases the electrical driving force for Na+ during Na+ coupled non-electrolyte transport into the enterocyte. The possible mechanisms involved in this adaptive response are discussed.
Consistent in vitro behavioral patterns were found in the scolex and strobila of adult Hymenolepis diminuta. These patterns were measured with a force transducer and the behavior analyzed with a slow motion closed circuit T.V. Varying concentrations of serotonin (5-HT), acetylcholine (Ach), histamine and somatostatin, in the range of 10(-3) to 10(-9) M, were tested for their influence on the rhythmic patterns of behavior. High concentrations of 5-HT and of Ach decreased scolex motility. While 5-HT significantly increased motility in the anterior-, mid- and posterior regions of the strobila at 10(-3) M, Ach inhibited motility in all 3 regions of the strobila at the same concentrations. At high concentrations, somatostatin had a smaller stimulatory effect on worm motility in the anterior and mid-regions; histamine only significantly affected worm motility in the posterior region of the strobila. Depending on concentration, the action of 5-HT, Ach and histamine can be reversed, particularly in the anterior and posterior regions of the strobila. The in vivo assay for worm migrational responses suggests that the action of the neuromuscular stimulators and inhibitors on worm migration is indirect.
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A sodium ionophore, monensin, was applied to crustacean neuromuscular preparations to determine whether increased intracellular sodium could lead to enhancement of transmitter release similar to that observed with prolonged stimulation. Following a single application of monensin (3-13 microM), the excitatory postsynaptic potential (e.p.s.p.) increased in amplitude by 50-800%. The increase was entirely due to a presynaptic effect that resulted in higher quantal content of transmission and increased frequency of spontaneous miniature potentials. A second application of monensin was less effective than the first. Application of monensin in calcium-free solutions led to rapid, marked enhancement of the e.p.s.p. upon restoration of the normal physiological solution, indicating that monensin can produce its effects in the absence of external calcium. Spontaneous miniature potentials often occurred more frequently in calcium-free solution after monensin had been applied. The extent of enhancement of e.p.s.p. amplitude depended on the concentration of external sodium, being smaller in solutions of low sodium. Prolonged stimulation of the motor axon usually enhanced the e.p.s.p. to a greater extent than application of monensin alone, but the time course of recovery of e.p.s.p. amplitude was similar in both cases. We conclude that the increase in e.p.s.p. amplitude promoted by monensin can be attributed to increased transmitter output resulting from influx of sodium into the nerve terminal. Increased intracellular sodium may lead to a rise in intracellular calcium ion concentration. Some features of long-term facilitation of transmitter release can be attributed to build-up of intracellular sodium during stimulation.
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Application of the sodium ionophore, Monensin, to crustacean neuromuscular preparations induced a potentiation of the synaptic potential which subsided after removal of Monensin. The rate and extent of potentiation were influenced by the concentration of extracellular sodium, and potentiation occurred when Monensin was applied in calcium-free solutions. Some features of long-lasting facilitation induced by repetitive stimulation of the motor axon were duplicated by Monensin application. The results support the hypothesis that long-lasting facilitation of transmitter release can result from increased intracellular sodium.
Two experiments were undertaken to determine the effects of chlordiazepoxide on intraspecific attack behavior and selected non-aggressive behaviors in male Siamese fighting fish. In Exp. 1, pairs of fish fought while immersed in either 15 mug/ml or 30 mug/ml of chlordiazepoxide, or plain water. The drug groups showed significantly less attack (e.g., biting, jawlocking) than the control group, without noticeable behavioral toxicity. Also, in the drug groups alone, some variants of the copulatory clasp, seen in normal mating, occurred in many pairs. In Exp. 2, individual fish were isolated in one of the same doses or plain water for a period equivalent to that of Exp. 1. These doses produced no changes in measures of arousal, locomotion, and feeding behavior, as compared to the control condition. The drug-related appearance of the intermale mating-like behavior is discussed in terms of a theoretical formulation postulating a mutually inhibitory relationship between sex and aggression in fish.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Avermectins are frequently used to control parasitic infestations in many animal species. Previous studies have shown the long-term persistence of unwanted residues of these drugs in animal tissues and fluids. An immunoassay screening test for the detection and quantification of ivermectin residues in bovine milk has been developed. After an extensive extraction procedure, milk samples were applied to a competitive dissociation-enhanced lanthanide fluoroimmunoassay using a monoclonal antibody against an ivermectin-transferrin conjugate. The monoclonal antibody, raised in Balb C mice, showed cross-reactivity with eprinomectin (92%), abamectin (82%) and doramectin (16%). The limit of detection of the assay (mean + 3 SD), calculated from the analysis of 17 known negative samples, was calculated as 4.6 ng/mL. Intra- and inter-assay RSDs were determined as 11.6% and 15.8%, respectively, using a negative bovine milk sample fortified with 25 ng/mL ivermectin. Six Friesian milking cows were treated with ivermectin, three with a pour-on formulation of the drug and three with an injectable solution at the manufacturer's recommended dose rate. An initial mean peak in ivermectin residue concentration was detected at day 4 (mean level = 47.5 ng/mL) and day 5 post-treatment (mean level = 26.4 ng/mL) with the injectable form and pour-on treatment, respectively. A second peak in residue concentration was observed using the DELFIA procedure 28 days post-treatment in both treatment groups (23.1 ng/mL injectable and 51.9 ng/mL pour-on). These second peaks were not confirmed by HPLC and must at this time be considered to be false-positive results. By day 35 after treatment the mean ivermectin residue concentration of both groups fell below the limit of detection of the assay.