PubMed Health⌕ Search

Biomedical subjects

G Henderson

Publications and source records attributed to G Henderson.

At least 19 recordsLinked to original sources
PubMed1992

Lack of evidence for coupling of the dopamine D2 receptor to an adenosine triphosphate-sensitive potassium (ATP-K+) channel in dopaminergic neurones of the rat substantia nigra.

Whole-cell patch clamp recordings were made from neurones in slices of rat substantia nigra zona compacta. The majority exhibited electrophysiological characteristics seen previously with intracellular recordings and were hyperpolarised by dopamine in a sulpiride-reversible manner. The sulphonylureas, tolbutamide and glibenclamide, did not reverse the response to dopamine and had no effect when applied alone. The potassium channel opener, cromakalim, was also without effect on dopaminergic neurones. Under our recording conditions, the potassium conductance activated by dopamine acting through the D2 receptor does not show the pharmacological characteristics of an ATP-sensitive potassium conductance.

Adenosine Triphosphate↗
PubMed1992

Demonstration of antibodies in archival sera from Canadian seals reactive with a European isolate of phocine distemper virus.

Sera from seals infected during the 1988 European epizootic of phocine distemper virus and sera from Canadian seals collected since 1972 have been tested for the presence of antibodies to morbillivirus. Approximately one third of the Canadian sera have been shown to contain anti-morbillivirus antibodies; the possibility that these populations of seals provided a source of infection for European seals is discussed.

Animals↗
PubMed1992

Antimicrobial susceptibility of anaerobic bacteria in Auckland 1987-90.

The antimicrobial susceptibility of 292 clinical isolates of anaerobic bacteria was determined by a standard agar dilution method. Metronidazole was the most active agent with only one Bacteroides fragilis, two anaerobic cocci, and Propionibacterium acnes being resistant. For B fragilis itself and other members of the B fragilis group: 35/35 (100%) and 43/44 (98%) respectively, were susceptible to amoxycillin-clavulanic acid; 47/47 (100%) and 55/56 (98%) respectively, were susceptible to cefoxitin; and 20/28 (71%) and 7/25 (28%) respectively, were susceptible to ceftriaxone. All four agents and penicillin were almost always active against anaerobic cocci and Fusobacterium species. All agents were active against clostridium isolates except for cefoxitin where only 47/57 (82%) were susceptible. These results allow comparison with isolates from other locations and may be considered when choosing an antimicrobial agent for prophylaxis or therapy of anaerobic infections.

Amoxicillin↗
PubMed1992

Electromyographic monitoring of profound surgical muscle relaxation during cardiac anesthesia.

Quantitative assessment of neuromuscular block produced by large doses of nondepolarizing neuromuscular blocking agents during cardiac surgery is not possible with conventional methods of monitoring. Various "posttetanic responses" can, however, be elicited, even when no twitch response is present. Posttetanic responses measured by electromyography were used in this study. Twenty-four male patients undergoing coronary bypass surgery were anesthetized with sufentanil plus diazepam. Neuromuscular block was provided either with pancuronium 0.1 mg/kg or with vecuronium 0.07 mg/kg initially and supplemented with small increments when indicated. Neuromuscular block was monitored from the hypothenar muscle. The ulnar nerve was stimulated by train-of-four, with superimposed periodic tetanic stimuli to evoke posttetanic responses, once every 7 to 15 minutes. The tetanically potentiated responses were detectable during 96% +/- 3.6 (vecuronium) and during 97% +/- 3.7 (pancuronium) of the entire intraoperative period, while the non-potentiated electromyographic responses were present for less than 50% of the time. The sum (of the amplitudes) of 6 posttetanic responses is significantly (p less than 0.05) greater than the sum of 6 nonpotentiated responses and than the size of a single-peak posttetanic response when compared with the normal, nonpotentiated responses. Higher-frequency tetanic stimuli (100 or 200 Hz) produced greater posttetanic responses (p less than 0.05) than did the 50-Hz tetanic stimulus. There were only slight or no significant differences in the degree of posttetanic potentiation between pancuronium and vecuronium either before, during, or after cardiopulmonary bypass.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗
PubMed1992

Characterisation of the L- and N-type calcium channels in differentiated SH-SY5Y neuroblastoma cells: calcium imaging and single channel recording.

We have used single cell imaging of [Ca2+]i and single channel cell-attached patch clamp recording to characterise the Ca2+ channels present on the plasma membrane of retinoic acid-differentiated human neuroblastoma (SH-SY5Y) cells. Exposure to raised K+ (45 or 60 mM) for 1 min resulted in a transient rise in [Ca2+]i which was abolished by cadmium (100 microM). The amplitude of the evoked rise varied from cell to cell. Both omega-Conus toxin (500 nM) and nifedipine (10 microM) reduced, but did not abolish, the rise in [Ca2+]i whereas Bay K 8644 (3 microM) potentiated it. In single channel records both L- and N-type Ca2+ channel openings were observed during membrane depolarisations from a holding potential of -90 mV. L-type channel openings (unitary conductance 22.5 pS) were prolonged by S(+)-PN 202-791 (500 nM) and could still be evoked from a depolarised holding potential (-40 mV). N-type channel openings (unitary conductance 12.5 pS) were unaffected by the dihydropyridine agonist but were inactivated at a holding potential of -40 mV. These results indicate that, in contrast to previous observations using whole cell recording, retinoic acid-differentiated SH-SY5Y cells express both L- and N-type Ca2+ channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1992

Chronic exposure to morphine does not induce dependence at the level of the calcium channel current in human SH-SY5Y cells.

mu-Opioid receptors mediate inhibition of the N-type calcium channel current in the human neuroblastoma cell line SH-SY5Y. We have previously shown that chronic exposure to morphine induces homologous tolerance to this effect. Here we show that chronic incubation with morphine (1 microM for three to seven days) does not, however, induce physical dependence at the level of the calcium channel current. Initial experiments were performed using the whole cell voltage-clamp technique. Chronically treated cells were bathed in superfusate which also contained morphine (1 microM). On washout of morphine the current amplitude increased by 12% and this was reversed by re-addition of morphine. Naloxone (1 microM) elicited a similar increase. However, this increase is most likely due to a reversal of the residual inhibitory effect of morphine on the calcium channel current rather than being a novel withdrawal response. Chronic exposure to morphine did not change the voltage-sensitivity of the calcium channel current or induce the appearance of a current sensitive to the L-type calcium channel agonists Bay K 8644 (3 microM) and S(+)-PN 202-791 (1 microM). In a further series of experiments the nystatin-perforated patch technique was employed in order to prevent washout of any L-type current in these cells. Under these conditions a Bay K 8644-sensitive, L-type current was unmasked following treatment with omega Conus Toxin GVIA. The peak current was depressed by omega Conus Toxin GVIA (1 microM) by approximately 90% both in control cells and cells chronically exposed to morphine. Now Bay K 8644 (3 microM) almost doubled the remaining current but the effect was equal in both groups of cells. It is concluded that chronic exposure to morphine does not induce physical dependence and a withdrawal syndrome in the human SH-SY5Y neuroblastoma cell line by changing either N-type or L-type calcium channel activity.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1992

Bilophila wadsworthia isolates from clinical specimens.

Bilophila wadsworthia is an anaerobic, gram-negative, asaccharolytic, bile-resistant, catalase-positive bacillus that is usually urease positive and was originally recognized in specimens of peritoneal fluid and tissue from patients with appendicitis. Additional isolations from clinical specimens, including a scrotal abscess, mandibular osteomyelitis, axillary hidradenitis suppurativa, pleural fluid, joint fluid, and blood, are described here.

Adult↗
PubMed1992

Budesonide in asthma.

Explore the source record for details and available documents.

Administration, Inhalation↗
PubMed1991

Transforming growth factor beta 1 inhibits epidermal growth factor receptor endocytosis and down-regulation in cultured fetal rat hepatocytes.

Incubation of fetal rat hepatocytes (FRH) with transforming growth factor beta 1 (TGF-beta 1) resulted in growth arrest and a biphasic effect on epidermal growth factor (EGF) receptor. After 2 h of exposure, EGF receptor (EGFR) was reduced by 43%. From 6 to 24 h, TGF-beta 1 exposure resulted in progressive increase in EGFR up to 74% over control. The increased binding was due to increase in high affinity EGF binding sites. FRH grown in medium containing EGF exhibited down-regulated EGFR with loss of high affinity EGF binding sites. With TGF-beta 1 exposure, high affinity EGFR was not down-regulated by EGF. Since down-regulation of EGFR involves internalization, the kinetics of EGF receptor-mediated endocytosis were examined. In TGF-beta 1-exposed FRH, EGF endocytosis was inhibited, with a reduction in the first order rate constant for the process from 0.078 to 0.043 min-1. Despite inhibition of growth, receptor down-regulation, and EGF endocytosis after TGF-beta 1 exposure, EGF-induced receptor autophosphorylation was preserved as demonstrated by [32P]phosphate-labeling of immunoprecipitated EGFR. These observations provide direct evidence that TGF-beta 1 regulates growth of fetal cells. Further, they suggest that TGF-beta 1 regulates endocytosis of EGF and possibly of other ligands.

Animals↗
PubMed1991

Mu-opioid-receptor-mediated inhibition of the N-type calcium-channel current.

The predominant consequences of mu-opioid-receptor activation are depression of both neuronal activity and transmitter release. Mu-Opioid agonists have previously been observed to increase a potassium conductance and to inhibit adenylate cyclase. We now report that activation of mu-opioid receptors directly decreases the N-type calcium-channel current in a differentiated, human neuroblastoma cell line (SH-SY5Y). The coupling between the mu-opioid receptor and the calcium channel involves a pertussis toxin-sensitive G protein and is independent of changes in adenylate cyclase activity. The inhibition of the calcium-channel current is voltage dependent because it is largely overcome by strong membrane depolarization. It is not associated with changes in the kinetics of current inactivation. Therefore, the mu-receptor belongs to the superfamily of G-protein-coupled, inhibitory neurotransmitter receptors which modulate the activity of calcium and potassium channels and adenylate cyclase.

Adenylate Cyclase Toxin↗
PubMed1991

Effects of reducing the remating interval after parturition on the fertility and plasma concentrations of luteinizing hormone, prolactin, oestradiol-17 beta and progesterone in lactating domestic rabbits.

Primiparous crossbred does were remated on Day 1 (n = 15) or 14 (n = 25) post partum and killed on Day 10 post coitum to assess their fertility. Blood samples were taken during the pre- (0-12 h post coitum) and post- (1-10 days post coitum) ovulatory periods and plasma was assayed for luteinizing hormone (LH), prolactin, oestradiol-17 beta and progesterone. Ovulation response was significantly greater (P less than 0.01) and ovulation rate significantly lower (P less than 0.001) in does mated on Day 1 than in those mated on Day 14 post partum. Does failing to ovulate on Day 14 post partum exhibited no preovulatory LH surge and had significantly lower (P less than 0.05) premating concentrations of oestradiol-17 beta and prolactin than those ovulating at this time. No significant differences in hormone concentrations were observed during the preovulatory period between does ovulating on Days 1 and 14 post partum, with the exception of oestradiol-17 beta. Concentrations of this hormone were significantly lower (P less than 0.01) in does mated on Day 1, at 1 h post coitum. We conclude that (i) fertility was affected by the remating interval after parturition, (ii) ovulation failure was associated with an absence of the preovulatory LH surge and a reduction in premating concentrations of oestradiol-17 beta and prolactin and (iii) the lower ovulation rate in early lactation was apparently caused by a reduction in ovarian competence to respond to the gonadotrophic stimulus.

Animals↗
PubMed1991

Mu-opioid receptor inhibition of calcium current: development of homologous tolerance in single SH-SY5Y cells after chronic exposure to morphine in vitro.

The human SH-SY5Y neuroblastoma cell line displays morphological, neurochemical, and electrophysiological characteristics of sympathetic neurons. mu-Opioid receptors mediate inhibition of the N-type calcium current present in these cells. Here we have studied the effects of chronic incubation with morphine (1 microM for 3-7 days) in vitro on the inhibition of this current induced by mu-opioid agonists and noradrenaline. In untreated control cells the mu-opioid agonists and noradrenaline. In untreated control cells the mu-opioid agonists morphine (1 microM) and [D-Ala2,N-MePhe4,Gly-ol] enkephalin (DAMGO) (10 nM to 1 microM), and noradrenaline (10 nM to 10 microM) inhibited the calcium current to a similar extent. The maximal effects of DAMGO and noradrenaline were not additive. Chronic exposure to morphine had no effect on the maximum amplitude of the calcium current evoked or on its voltage sensitivity. However, the concentration-response curve to DAMGO was shifted to the right in a parallel manner, with a 7-fold increase in the IC50 value but no change in the maximum inhibition produced. In contrast, the maximum inhibition in response to morphine appeared to be substantially reduced. Noradrenaline inhibited the calcium current equally in untreated and morphine-tolerant cells. Thus, it is concluded that morphine-induced tolerance to inhibition of the N-type calcium current occurs at the single-cell level and is homologous to the mu-opioid receptor. Also, morphine appears to be an agonist of lower efficacy than DAMGO. The results are consistent with tolerance being due to a functional reduction in the mu-opioid receptor reserve, probably by disruption of the receptor/GTP-binding protein interaction.

Calcium↗
PubMed1990

The sigma [corrected] ligand rimcazole antagonises (+)SKF 10,047, but not (+)3-PPP, in the mouse isolated vas deferens.

We have characterized the actions of several sigma receptor ligands on the electrically evoked, neurogenic contractions of the mouse isolated vas deferens. (-)SKF 10,047 was significantly more potent than (+)SKF 10,047 in potentiating twitch contractions and was equipotent with (+)3-PPP. Rimcazole (1 and 3 microM) antagonised the potentiation induced by 100 microM (+)SKF 10,047 and, to a lesser extent, that induced by 30 microM (-)SKF 10,047 but increased that elicited by (+)3-PPP (30 microM). This apparent contradiction may arise from sigma agonists acting in this tissue at both sigma and non-sigma sites.

Animals↗