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Biomedical subjects

B Beer

Publications and source records attributed to B Beer.

14 recordsLinked to original sources
PubMed1992

Use of two virustatica (AZT, PMEA) in the treatment of FIV and of FeLV seropositive cats with clinical symptoms.

In the present study the therapeutic efficacy and the side effects of two antiretroviral compounds used in human acquired immunodeficiency syndrome (AIDS) research, 3'-azido-2',3'-dideoxythymidine (AZT, zidovudine, Retrovir) and 9-(2-phosphonylmethoxyethyl)adenine (PMEA), were investigated in the treatment of cats naturally infected with feline immunodeficiency virus (FIV) and cats naturally infected with feline leukemia virus (FeLV). AZT was administered subcutaneously at a dose of 5 mg kg-1 body weight every 12 h and PMEA was administered subcutaneously at a dose of 2.5 mg kg-1 body weight every 12 h during a 3 week hospitalization. The therapeutic efficacy of both compounds was investigated. There was a stronger potency of PMEA than of AZT on the regression of stomatitis in FIV and in FeLV infected cats. In addition, in FIV infection PMEA had a stronger effect on the improvement of the general clinical status. Both antiretroviral compounds were potent agents to improve the immunologic status of FIV infected cats by raising the CD4/CD8 ratio. In FeLV infection PMEA and AZT appeared to reduce antigenemia. The hematological side effects caused by PMEA were severe and stronger than those of AZT. Therefore the advantage of PMEA in clinical and immunologic improvement was diminished by the hematologic disorders, which do not allow long term treatment with this drug in the dose used.

Adenine↗
PubMed1992

[Trichomonad infections of the oral cavity in cats in south Germany].

In this investigation trichomonads were isolated from the oral cavity in 21 of 110 examined cats, and only from those which were simultaneously FeLV, FIV or FIP positive. By means of scanning electron microscopy the trichomonads were shown to be round or piriform parasites which were on average 7.9 microns long and 6.2 microns wide at maximum width. They had 4 anterior flagella, which were on average 9.4 microns long, an undulating membrane measuring 6.7 microns with no trailing flagellum as well as an axostyle extending on average 5.0 microns beyond the body, and therefore should be attributed to the genus Trichomonas.

Animals↗
PubMed1979

Resolution of two biochemically and pharmacologically distinct benzodiazepine receptors.

Brain-specific binding sites have been isolated on synaptosomal membrane fragments which recognize pharmacologically active benzodiazepines (BDZ's) and triazolopyridazines (TPZ's). While early evidence indicated the existence of a single homogeneous class of BDZ binding sites, more recent biological and pharmacological studies support the notion of BDZ receptor multiplicity. We now propose that two biochemically distinct BDZ receptors exist in brain which are responsible for the mediation of different pharmacological activities. Type I BDZ receptors display a high affinity for both BDZ's and TPZ's, are not coupled to GABA receptors or to chloride ionophores, and are the sites which mediate anxiolytic actions. Type II BDZ receptors display a high affinity for BDZ's, display a low affinity for TPZ's, are coupled to GABA receptors and/or chloride ionophores, and are the sites which mediate pharmacological effects other than anxiolytic activity.

Animals↗
PubMed1979

A synthetic non-benzodiazepine ligand for benzodiazepine receptors: a probe for investigating neuronal substrates of anxiety.

CL 218,872 is the first non-benzodiazepine to selectively displace brain specific 3H-diazepam binding with a potency comparable to that of the benzodiazepines. Like the benzodiazepines, CL 218,872 increased punished responding in a conflict situation and protected against the convulsions induced by pentylenetetrazole. These three pharmacological properties are highly predictive of anxiolytic activity. Unlike the benzodiazepines, however, CL 218,872 was relatively inactive in tests designed to measure effects on neuronal systems which utilize GABA, glycine and serotonin as transmitters. Furthmore, CL 218,872 was relatively free of the ataxic and depressant side effects commonly associated with the benzodiazepines. Because of this high degree of selectivity, CL 218,872 may represent a new probe for investigating neuronal substrates of anxiety.

Animals↗
PubMed1979

Some properties of brain specific benzodiazepine receptors: new evidence for multiple receptors.

Several new lines of evidence suggest the existence of two or more distinct types of benzodiazepine receptors, in contrast to earlier results suggesting the presence of only one class of receptors. Appropriate thermoinactivation experiments indicate two receptors with different thermostabilities. Several triazolopyridazines, with some of the pharmacological properties of anxiolytics have recently been shown to displace 3H-diazepam and 3H-flunitrazepam with Ki values in the 6 to 100 nanomolar range. These new substances are active in conflict tests in rats and monkeys and prevent metrazol induced seizures in vivo, but strikingly lack the ataxia and sedative properties of the benzodiazepines. Hill analyses of dose-response curves for some of these substances yields Hill coefficients in the range of 0.4--0.6, suggesting that these compounds may be able to discriminate between several types of benzodiazepine receptors.

Amino Acids↗
PubMed1979

Benzodiazepine receptors: cellular and behavioral characteristics.

Brain specific benzodiazepine receptors appear to mediate the pharmacological properties of benzodiazepines. A neuronal localization for these receptors is suggested by the parallel decrease in the number of benzodiazepine receptors and cerebellar Purkinje cells in "nervous" mutant mice. Electrophysiological results are compatible with an action of benzodiazepines on neuronally localized, physiological receptors. Biochemical, electrophysiological and behavioral experiments highlight the possible importance of frontal cortex in mediating the anxiolytic properties of the benzodiazepines. Triazolenetetrazoles act upon benzodiazepine receptors, increase punished responding and protect against penetylenetetrazole-induced convulsions, but do not produce the side effects associated with benzodiazepines or affect classical neurotransmitter systems. The structural similarities between triazolopyridazines, purines and the indole portion of certain peptides may provide insights into the nature of the endogenous ligand.

Animals↗
PubMed1978

Enhancement of 3H-diazepam binding by SQ 65,396: a novel anti-anxiety agent.

SQ 65,396, a clinically active anti-anxiety agent, enhanced the binding of 3H-diazepam at 1.5 nM. This effect was due to an increase in the affinity for the ligand, without a change in the number of 3H-diazepam binding sites. This action of SQ 65,396 may mediate its anti-anxiety effects by affecting the action of an endogenous modulator of the "benzodiazepine receptor." Several other substances and treatments increase the affinity of 3H-diazepam for its receptors by mechanisms which may be related to the effect produced by SQ 65,396.

Animals↗
PubMed1978

Relationship between benzodiazepine receptors and experimental anxiety in rats.

The in vitro and in vivo ability of benzodiazepines to inhibit specific 3H-diazepam binding correlated with their ability to increase punished responding in a conflict situation. Conflict and foot shock, the punishing stimulus used in most conflict procedures, also altered 3H-diazepam binding. These data implicate 3H-diazepam binding sites in mediating at least some of the anxiolytic properties of benzodiazepines and suggest the existence of some endogenous substance which might be involved in the etiology of anxiety.

Animals↗
PubMedDate not supplied

6-Hydroxydopamine and avoidance: Possible role of response suppression.

The intraventricular administration of 6-HD to rats pretreated with pargyline resulted in severe, long-lasting decreases in avoidance responding with little or no effect on escape responding. Despite the fact that the rats failed to avoid, they appeared to be able to discriminate the CS, as was evident from freezing behavior and other symptoms of an apparent fear reaction during the CS. The increase in freezing, a response that was incompatible with avoidance was seen during the first few test sessions after 6-HD treatment and seemed to be largely responsible for a gradual decline in avoidance responding during this same period. The role of CA depletion in the animal's response to aversive stimuli thus appears to be a significant aspect of the avoidance decrement that follows 6-HD administration.

Animals↗
PubMedDate not supplied

Differential effects of intraventricular administration of 6-hydroxydopamine on behavior of rats in approach and avoidance procedures: Reversal of avoidance decrements by diazepam.

The administration of 6-hydroxdopamine (6-HD) and pargyline to rats produced similar selective decreases in responding during the conditioned stimulus (CS) on a discriminated avoidance test where the unconditioned stimulus (US) was shock and on an analogous conditioned approach test where the US was water. Approach behavior during the CS generally recovered, however, while avoidance decrements in the same rats remained for the duration of testing. This suggested that 6-HD-induced avoidance decrement was a result of two independent but interacting processes: (1) a decrease in conditioned behavior as reflected by the similar decrease in responding on both tests; and (2) a hyper-reaction to aversive stimuli that resulted in a tendency to selectively suppress avoidance behavior after the animal received shock. In support of this hypothesis, it was found that 6-HD-induced avoidance decrements could be reversed (1) by treatment with diazpam, a drug that releases suppressed responses; or (2) by delaying avoidance testing until conditioned responding had recovered, thus minimizing the interaction of the two processes.

Animals↗
PubMedDate not supplied

Modification of avoidance behavior in 6-hydroxydopamine-treated rats by stimulation of central noradrenergic and dopaminergic receptors.

Rats showing reliable decrements in conditioned avoidance behavior after the intraventricular administration of 6-hydroxdopamine (6-HD) with pargyline pretreatment were given various dopaminergic and noradrenergic agonists. Intraventricular injections of DA or L-NE or intraperitoneal injections of apomorphine or L-DOPA reversed the avoidance decrements, often restoring performance to pre-6-HD-treatment levels. Furthermore, these agonists all produced behavior characteristic of activity in dopaminergic neurons. Clonidine, a noradrenergic agonist, also reversed avoidance decrements, but did not produce behavior characteristic of stimulation of dopaminergic neurons in the brain. Pretreatment with spiroperidol, a dopaminergic receptor blocker, prevented the recovery induced by all agonists, although clonidine-induced recovery was affected least. The results are discussed in terms of possible separate roles for dopaminergic and noradrenergic neurons in the brain in avoidance behavior.

Animals↗
PubMedDate not supplied

Relationship of brain levels of norepinephrine and dopamine to avoidance behavior in rats after intraventricular administration of 6-hydoxydopamine.

Rats trained on a discriminated avoidance procedure showed long-term decrements in performance after intraventricular administration of 6-hydroxydopamine. Biochemical assay showed that DA levels were correlated with avoidance performance no matter when behavior was measured, but NE levels were most highly correlated with avoidance behavior at those times when suppression of responding appeared to be the major influence on responding. The data are discussed in terms of possible separate roles for NE and DA in avoidance behavior.

Animals↗