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Biomedical subjects

C Beyer

Publications and source records attributed to C Beyer.

At least 145 records · Page 8Linked to original sources
PubMed1988

An enzyme-linked immunosorbent assay using monoclonal antibodies for the detection of respiratory syncytial virus in clinical specimens.

An enzyme-linked immunosorbent assay (ELISA) has been developed for the detection of respiratory syncytial virus in nasopharyngeal secretions. This assay employed as immunoreagents two monoclonal antibodies directed against two distinct epitopes of the viral nucleocapsid. One of them (RSV 4) was used for antigen capture and the other (NC 4) was labelled with N-hydroxy-succinimide-epsilon-caproil biotin and used for antigen detection. Streptavidin biotin-peroxidase complexes were employed as amplification mode. The immunoassay was performed in 6 hours and was able to detect as little as 1 ng/ml of purified nucleocapsid. When 87 nasopharyngeal secretions were analyzed by an indirect immunofluorescence assay using commercial reagents and by the newly developed ELISA, the sensitivity and the specificity of the two assays were found to be very similar.

Animals↗
PubMed1988

Possible role of inhibitory glycinergic neurons in the regulation of lordosis behavior in the rat.

Strychnine sulfate (3.9 or 27 micrograms in 0.5 microliter saline) was bilaterally infused into the ventromedial hypothalamic nucleus (VMH) of ovariectomized sexually inexperienced rats primed 40 hr earlier with 4 micrograms of estradiol benzoate (EB). This dose of EB induced only weak lordosis behavior in 25% of the subjects (Ss). Strychnine at the 3 and 9 micrograms dosages, but not at 27 micrograms, induced intense lordosis behavior, but no proceptivity, in most estrogen-primed Ss (69% in 3 micrograms, 94% in 9 micrograms). Ovariectomized adrenalectomized EB-primed Ss also displayed significant lordosis behavior (59%) following infusion of 9 micrograms of strychnine into the VMH. Strychnine (9 micrograms) failed to stimulate lordosis in ovariectomized Ss that were not estrogen-primed. Administration of 5 micrograms EB followed 40 hr later by 2 mg of progesterone (P) elicited intense lordosis behavior in most Ss. Bilateral injections into the VMH of glycine (100 micrograms), beta-alanine (100 micrograms) or taurine (50 micrograms) to rats that were already displaying estrous behavior (greater than 80 LQ) in response to the sequential administration of EB and P failed to depress lordosis when tested between 5 min and 60 min postinjection. Similarly, glycine (20 or 100 micrograms) injected into the VMH of estrogen-primed, ovariectomized rats within 15 minutes of a 2 mg SC injection of P failed to interfere with the subsequent response to this steroid when tested 2 and 4 hr after P. The results suggest that strychnine injected into the VMH facilitates lordosis behavior in estrogen-primed rats by removing a tonic inhibitor effect exerted by glycinergic neurons on VMH neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Blockade of LHRH-induced lordosis by alpha- and beta-adrenergic antagonists in ovariectomized, estrogen primed rats.

The participation of a noradrenergic mechanism in the facilitation of lordosis by luteinizing hormone-releasing hormone (LHRH) was studied in two groups of ovariectomized estrogen primed rats, with or without sexual experience. The administration of 5 micrograms estradiol benzoate (EB) alone to sexually inexperienced subjects (Ss) induced weak lordosis behavior in some of them (mean lordosis quotient, LQ = 12 +/- 19). The SC injection of 5 micrograms LHRH significantly increased this response four hours later (LQ = 38 +/- 41), though great variability was observed (59% of Ss showing LQs below 30). The systemic administration of either prazosin, an alpha-adrenergic antagonist (0.2 or 1 mg/kg), or propranolol, a beta-adrenergic antagonist (20 mg/kg), totally suppressed LHRH-induced lordosis in sexually inexperienced Ss (mean LQs = 8 +/- 11; 5 +/- 10; 18 +/- 31, respectively). In sexually experienced Ss (tested on two previous occasions with EB and LHRH) the administration of EB alone on a third test induced significant levels of lordosis (mean LQ = 51 +/- 41). The administration of 5 micrograms LHRH to sexually experienced, estrogen primed Ss induced near maximal levels of lordosis (LQ = 94 +/- 18). In these Ss, prazosin (0.2 and 1 mg/kg) and, to a lesser extent, propranolol (20 mg/kg) significantly depressed lordosis to values that were not significantly different from those obtained after EB alone (mean LQs = 59 +/- 38; 63 +/- 20; 74 +/- 32, respectively). These results indicate that blockade of noradrenergic transmission by either alpha- or beta-antagonists counteracts the stimulatory effect of LHRH on lordosis in ovariectomized estrogen primed rats with or without sexual experience.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Prevention of the convulsant and hyperalgesic action of strychnine by intrathecal glycine and related amino acids.

Intrathecal administration of 25 micrograms strychnine induced consistent sensory and motor behavioral events in rats. Sensory events included scratching and biting the lower half of the body, spontaneous vocalizations and skin hyperalgesia, evidenced by vocalization and reflex scratching in response to stimulation with a 5.5 g von Frey fiber. This mild stimulus failed to elicit vocalizations in the preinjection condition. Strychnine induced two types of motor seizures: (1) falling over with tail whipping and (2) convulsions. The effect of equimolar doses of glycine (G) and some related amino acids: beta-alanine (A), taurine (T) and betaine (B) on the strychnine syndrome was tested by administering them (intrathecal route) along with strychnine. T and G but not B significantly decreased most of the sensory events triggered by strychnine. All amino acids significantly decreased the incidence and duration of convulsions; T and B abolished them. A decreased vocalizations and skin hyperalgesia but synergized with strychnine to facilitate scratching and self biting. These results are consistent with findings that G, A and T displace strychnine from its binding sites in the CNS.

Alanine↗
PubMed1988

Lordosis facilitation in estrogen primed rats by intrabrain injection of pregnanes.

Progesterone (P) and nine of its natural metabolites were bilaterally injected (5 micrograms in 0.5 microliter oil) into either the ventromedial hypothalamus (VMH) or the medial preoptic area (MPOA) of estrogen primed rats to assess their relative potencies for stimulating lordosis. P, 5 alpha-pregnanedione and 5 beta, 3 beta-pregnanolone elicited lordosis when injected at either VMH or MPOA. By contrast, 5 alpha, 3 beta-pregnanolone as well as 20 alpha-OH and 20 beta-OH-pregnenone were much more effective in stimulating lordosis when implanted in the MPOA. Finally, 5 beta-pregnanedione and 5 beta,3 alpha-pregnanolone did not stimulate lordosis at neither VMH nor MPOA. The observation that lordosis was induced in estrogen primed rats both by pregnanes that bind to the P receptor (i.e., P; 5 alpha-pregnanedione; 20 alpha- and 20 beta-OH-pregnenone) and by pregnanes that do not (i.e., 5 alpha, 3 beta-; 5 beta,3 beta- and 5 alpha,3 alpha-pregnanolone) indicates that diverse cellular mechanisms are involved in the facilitation of lordosis by pregnanes.

Animals↗
PubMed1987

Pathological supply dependence of O2 uptake during bacteremia in dogs.

When systemic delivery of O2 [QO2 = cardiac output X arterial O2 content (CaO2)] is reduced, the systemic O2 extraction ratio [(CaO2-concentration of O2 in venous blood/CaO2] increases until a critical limit is reached below which O2 uptake (VO2) becomes limited by delivery. Many patients with adult respiratory distress syndrome exhibit supply dependence of VO2 even at high levels of QO2, which suggests that a peripheral O2 extraction defect may be present. Since many of these patients also suffer from serious bacterial infection, we tested the hypothesis that bacteremia might produce a similar defect in the ability of tissues to maintain VO2 independent of QO2, as QO2 reduced. The critical O2 delivery (QO2crit) and critical extraction ratio (ERcrit) were compared in a control group of dogs and a group receiving a continuous infusion of Pseudomonas aeruginosa (5 x 10(7) organisms/min). Dogs were anesthetized, paralyzed, and ventilated with room air. Systemic QO2 was reduced in stages by hemorrhage as hematocrit was maintained. At each stage, systemic VO2 and QO2 were measured, and the critical point was determined from a plot of VO2 vs. QO2. The mean QO2crit and ERcrit of the bacteremic group (11.4 +/- 2.2 ml.min-1.kg-1 and 0.51 +/- 0.09) were significantly different from control (7.4 +/- 1.2 and 0.71 +/- 0.10) (P less than 0.05). These results suggest that bacterial infection can reduce the ability of peripheral tissues to extract O2 from a limited supply, causing VO2 to become limited by O2 delivery at a stage when a smaller fraction of the delivered O2 has been extracted.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Nociceptive responses to altered GABAergic activity at the spinal cord.

GABA agonists and antagonists were injected intrathecally at the spinal cord, to determine their effect on nociceptive thresholds. Tactile stimulation, applied against the flank by a medium diameter von Frey fiber (5.5 g force), elicited distress vocalizations after, but not before injection of the GABA antagonists, bicuculline MI or picrotoxin (0.25 and 1 microgram dosages). Vocalization threshold to tail shock was significantly reduced by bicuculline MI or picrotoxin. Tail flick withdrawal latency from radiant heat was not altered by GABA antagonists. The GABA agonist, muscimol, significantly elevated vocalization threshold to tail shock at a 5 micrograms dose. At a lower dose level (1 microgram), muscimol significantly reduced vocalization threshold to tail shock. Tail flick latency was significantly prolonged by the 5 micrograms dose of muscimol; however, flaccid paralysis of the hind limbs was also evident. Nociceptive thresholds were not altered by GABA or saline injection. These findings indicate that GABAergic activity contributes to the tonic modulation of nociception at the spinal cord.

Animals↗
PubMed1986

Effect of bicuculline on sexual activity in castrated male rats.

The GABA antagonist (+) bicuculline methiodide (30 ng/cannula) was injected in the medial preoptic-anterior hypothalamic area of castrated rats treated with subthreshold dosages of testosterone propionate (150 micrograms/kg/day). The treatment resulted in a facilitation of sexual activity suggesting a role of GABA as a neurotransmitter in neural processes determining sexual arousal.

Animals↗
PubMed1986

Facilitation of lordosis behavior in ovariectomized estrogen-primed rats by medial preoptic implantation of 5 beta, 3 beta, pregnanolone: a ring A reduced progesterone metabolite.

The effect on lordosis behavior of progesterone (P) and some of its ring A reduced metabolites (5 beta pregnane 3 alpha ol 20 one, 5 beta pregnane 3 beta ol 20 one and 5 alpha pregnanes 3 beta ol 20 one) was studied in estrogen primed overiectomized rats by unilaterally implanting them in two brain areas related to the control of lordosis behavior: the ventromedial hypothalamic nucleus (VMH) and the medial preoptic area (mPOA). Of the four pregnanes studied only 5 beta 3 beta pregnanolone consistently induced lordosis behavior when implanted into the mPOA. The present results show that some 5 beta reduced P metabolites can facilitate with a short latency the display of lordosis behavior, probably by depressing the activity of telencephalic neurons inhibitory to sexual behavior.

Animals↗
PubMed1986

Restoration of the copulatory pelvic thrusting pattern in castrated male rats by the intracerebral implantation of androgen.

The characteristics of duration, vigour, frequency and rhythmicity of pelvic thrusting during copulation were studied by an accelerometric technique in 25 male rats before castration and following restoration of sexual behavior by local implants of testosterone propionate (TP) in the medial preoptic area (mPOA). Twenty-one Ss displayed the complete copulatory pattern during the control tests. Implantation of TP in the mPOA restored mounting activity after castration in 14 out of 21 Ss and only six of them "ejaculated." Spinal cord structures involved in pelvic thrusting of castrated Ss implanted with TP were presumably not exposed to circulating androgen since the sexual accessories were atrophic; in spite of this, only modest differences were found in the characteristics of pelvic thrusting, i.e., an increase in the duration of the mounting trains of the TP implanted Ss. Present data suggest that activation of mPOA-anterior hypothalamic neurons would not only affect limbic and cortical areas related to sexual arousal through their ascending connections but would also modulate through descending pathways, the activity of lower spinal structures involved in copulation.

Animals↗
PubMed1986

GABAergic control of masculine sexual behavior.

Drugs affecting the GABAergic transmission were injected into the medial preoptic anterior hypothalamic area (MPOA) and the masculine sexual behavior analyzed. Antagonizing GABAergic neurotransmission by (+) bicuculline methiodide (30 ng/cannula), or 3-mercaptopropionic acid (10 or 20 micrograms/cannula) resulted in a drastic shortening of the postejaculatory intervals and a shortening of the ejaculation latency. Injection of compounds causing an increase in GABAergic activity, muscimol (25 ng/cannula) or ethanolamine-O-sulphate (80 micrograms/cannula) depressed masculine sexual behavior. Systemic treatment or injection into the nucleus caudatus putamen of compounds affecting the GABAergic transmission did not cause any alteration in the mating pattern. It is suggested that the GABAergic neurotransmission is involved in inhibitory processes underlying the masculine sexual behavior.

3-Mercaptopropionic Acid↗
PubMed1986

Lordosis behavior and GABAergic neurotransmission.

gamma-Aminobutyric acid (GABA) (1.0 microgram/cannula) or muscimol (50 ng/cannula) was injected into the ventromedial hypothalamus or the lateral septi nuclei of ovariectomized rats brought to sexual receptivity by combined treatment of estrogen and progesterone. No inhibitory effects of GABA or muscimol were observed on the lordosis behavior. Furthermore, systemic (1.0 mg/kg) or intrahypothalamic (50 ng/cannula) picrotoxin administration was followed by a statistically significant increase in lordosis behavior in ovariectomized, estrogen-primed rats. No such effect was observed in ovariectomized-adrenalectomized animals, indicating its dependence on adrenal secretions. Present results do not support the hypothesis of a GABAergic mechanism in the hormonal control of lordosis behavior.

Adrenalectomy↗