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Biomedical subjects

D J Jones

Publications and source records attributed to D J Jones.

At least 145 records · Page 8Linked to original sources
PubMed1985

Hamster and rat pineal gland beta-adrenoceptor characterization with iodocyanopindolol and the effect of decreased catecholamine synthesis on the receptor.

Rat and hamster pineal glands were used in binding studies to characterize their beta-adrenoceptors with a new specific antagonist ligand, iodocyanopindolol. The receptors were saturable, and the ligand was selective and demonstrated stereospecificity for both species. The rat pineal had a 20-fold greater density of beta-adrenoceptors, while the affinity was one-third that of the hamster pineal. utilizing this radioligand, we examined the effects of decreased sympathetic input to the pineal on beta-adrenergic receptors in both species. Decreased noradrenergic input to the pineal gland of the hamster was accomplished by superior cervical ganglionectomy, or by exposing the animals to continuous light for 36 hours. Parallel studies were conducted with hamster pineal gland in which catecholamine synthesis was measured. The results indicate that a selective decrease in catecholamine synthesis in the hamster pineal does not change the beta-adrenoceptor density or affinity. In contrast, a concomitant increase in beta-adrenoceptor density but not affinity occurs in the rat pineal gland after similar decreased sympathetic input.

Animals↗
PubMed1984

Comparison of capsaicin and substance P induced cyclic AMP accumulation in spinal cord tissue slices.

Capsaicin (CAP) caused a time, concentration and Ca++ dependent increase in cyclic AMP accumulation in tissue slices from rat and guinea pig spinal cord. The CAP-induced increase occurred uniquely in slices from dorsal cord of both rat and guinea pig and the increase was significantly greater in dorsal cord slices from guinea pig vs rat spinal cord. CAP mediated release of substance P does not appear to mediate the CAP-induced increase in cyclic AMP accumulation since the increase in cyclic AMP is significantly less with substance P and the substance P antagonist [D-Pro2, D-Trp7,9]-substance P does not antagonize the CAP-induced increase. The CAP-induced increase in cyclic AMP accumulation appears to be a direct effect. Structural requirements for this effect are both the substituted aromatic and alkyl side chain portion of the CAP molecule. The present results suggest that CAP has the ability to interact with sites in dorsal spinal cord which are linked to the synthesis of cyclic AMP, which could modulate spinal processing of nociceptive information.

Animals↗
PubMed1984

Supersensitivity of the noradrenergic system in the spinal cord following intracisternal injection of 6-hydroxydopamine.

The intracisternal administration of 6-hydroxydopamine (6-OHDA; 100 micrograms on two consecutive days) resulted in a 90-95% depletion of norepinephrine (NE) in the spinal cord 3-60 days following administration of the drug. At 90 days following injection of 6-OHDA, the depletion was only 60% suggesting the regrowth of NE-containing fibers. Consistent with the depletion of NE, 3-60 days after the injection of 6-OHDA a 50-80% decrease in the uptake NE occurred with only a 25% decrease 90 days after administration of 6-OHDA. Associated with decreases in NE and its uptake was a 100-200% increase in the accumulation of NE-stimulated cyclic AMP in slices of spinal cord tissue from 6-OHDA-treated rats. The increased response was evident at 3-60 days after injection of 6-OHDA decreasing on day 90 to 40% above control. No shift in the EC50 for NE was evident and the specificity of agonists for this response was limited to agents with alpha and/or beta-adrenergic receptor activation properties. Radioligand receptor binding techniques, utilizing [3H]prazosin for alpha1 receptors and [3H]dihydroalprenolol for beta receptors demonstrated that increases in the Bmax of response of alpha1 (30-50%) and beta (15-20%) receptors in spinal cord may mediate the enhanced response of NE-stimulated cyclic AMP following the administration of 6-OHDA. This is indicated by similar time-dependent patterns of onset and termination of increased receptor binding and the accumulation of NE-stimulated cyclic AMP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed1984

Synergistic effect of acidosis and succinylcholine-induced hyperkalemia in spinal cord transected rats.

The effects of spinal cord transection and acidosis on succinylcholine (SCC)-induced hyperkalemia were studied in Sprague-Dawley rats. The effectiveness of pretreatment with subparalyzing doses ("self-taming") of SCC or with the cholinesterase inhibitor hexafluorenium bromide in preventing hyperkalemia was also studied. The increase in plasma potassium after administration of SCC (1 mg/kg) was found to be significantly increased 10 days after spinal cord transection. This potassium increase could not be prevented by pretreatment with either hexafluorenium (0.3 mg/kg) or subparalyzing doses (0.15 mg/kg) of SCC. Respiratory acidosis caused an increase in plasma K+ in both normal and in spinal cord transected rats. Acidosis had a synergistic effect on succinylcholine-induced hyperkalemia. These findings support the clinical practice of not using succinylcholine in patients at risk of having a pathological sensitivity to SCC. Furthermore, SCC may be especially dangerous when administered to patients who are acidotic.

Acidosis, Respiratory↗
PubMed1982

Depolarizing agent-induced cyclic AMP accumulation in isolated rat spinal cord.

The stimulation of cyclic adenosine 3',5'-monophosphate (cyclic AMP) accumulation by the depolarizing agents K+, ouabain and veratridine, was studied in rat and guinea pig spinal cord tissue slices. Significantly increased accumulation of cyclic AMP was produced by each of the agents in a concentration-dependent manner. Veratridine and ouabain were equipotent (EC50 = 5 x 10(-5)M) and approximately 500 fold more potent than K+ (EC50 = 10(-2)M). Depolarizing agent-induced cyclic AMP accumulation in slices from guinea pig spinal cord was approximately double the response in rat spinal cord. Maximum stimulation occurred within 2.5 min of incubation with these agents and lasted for at least 30 min. Regional studies demonstrated that the maximal accumulation of cyclic AMP occurred to a greater degree in tissue slices from the dorsal section of spinal cord from both rat and guinea pig. Whereas the ouabain and veratridine stimulatory responses are completely dependent on extracellular Ca++, the K+ response is only partially dependent. Stimulation due to ouabain and veratridine is dependent, and K+ is independent, of release of neurohumoral substances such as norepinephrine or adenosine from spinal neurons. These experiments indicate the possible modulatory role of depolarization-linked events in regulating the spinal cord cyclic AMP system.

Animals↗
PubMed1982

Adrenergic receptors in rat spinal cord.

Radioligand binding assays were used to demonstrate the presence of alpha 1, alpha 2 and beta receptors in rat spinal cord. Specific and saturable binding was exhibited for [3H]-WB 4101 (alpha 1), [3H]-aminoclonidine (alpha 2) and [3H]-dihydroalprenolol (beta). Binding was of high affinity and the total number of binding sites (Bmax) were: alpha 1, 66.5 +/- 1.0 fmol/mg protein; alpha 2, 20.0 +/- 0.6 fmol/mg protein; beta, 10.2 +/- 0.3 fmol/mg protein. The data confirms the existence of adrenergic receptors in spinal cord and provides further evidence of the role of catecholaminergic neurons in regulating spinal cord physiology

Adrenergic alpha-Antagonists↗
PubMed1982

Adrenergic receptors in rat spinal cord.

Radioligand binding assays were used to demonstrate the presence of alpha 1, alpha 2 and beta receptors in rat spinal cord. Specific and saturable binding was exhibited for [3H]-WB 4101 (alpha 1), [3H]-aminoclonidine (alpha 2) and [3H]-dihydroalprenolol (beta). Binding was of high affinity and the total number of binding sites (Bmax) were: alpha 1, 66.5 +/- 1.0 fmol/mg protein; alpha 2, 20.0 +/- 0.6 fmol/mg protein; beta, 10.2 +/- 0.3 fmol/mg protein. The data confirms the existence of adrenergic receptors in spinal cord and provides further evidence of the role of catecholaminergic neurons in regulating spinal cord physiology.

Animals↗
PubMed1981

Parental perceptions of enuresis. A collaborative study.

Of 1,379 children 4 years of age and older who were patients in nine medical centers across the country, 346 (25.1%) were found to be enuretic. Their parents considered heavy sleeping and emotional problems as the main causes of enuresis in children; physical causes rarely were believed to be important. "Waking up the child" from sleep to urinate and "talking about the problem" were the main methods that parents used to treat enuresis. Very few used medication. Parents with a grade school level of education punish bed-wetting children at twice the rate of high school- and college-educated parents. Physicians need to be more aware that enuresis is an important problem for parents and that there are many widely held beliefs about cause and management.

Adolescent↗
PubMed1981

Adenosine regulation of cyclic 3',5'-adenosine monophosphate formation in rat spinal cord.

Adenosine stimulates the formation of cyclic 3',5'-adenosine monophosphate (cyclic AMP) in rat spinal cord tissue slices in a concentration-dependent manner with maximal accumulation (30 pmol/mg of protein) at a concentration of 1 mM (Ec50 50 microM). 2-Chloroadenosine (EC50 1 microM) produced a maximal accumulation to 50 pmol/mg of protein. The adenosine antagonists, theophylline and isobutylmethylxanthine, block the increase, and the phosphodiesterase inhibitor, RO 20-1724, potentiates the increase in cyclic AMP accumulation. Adenosine deaminase eliminated the adenosine-dependent increase. Cyclic AMP accumulation was also enhanced by ATP, ADP and 5'-AMP. However, the stimulation due to these nucleotides was dependent upon conversion to adenosine. The increase in cyclic AMP accumulation was more than additive when adenosine was combined with norepinephrine. This potentiation effect is blocked by theophylline, isobutylmethylxanthine and alpha adrenergic antagonists. Additional experiments revealed that only postsynaptic alpha adrenergic agonists were capable of potentiating the response to adenosine. The interaction is concentration-dependent, is also observed with phosphorylated nucleotides of adenosine and is blocked specifically by alpha receptor antagonists. Receptor binding assays revealed that adenosine does not alter the number of alpha adrenergic receptors. Both the alpha receptor and adenosine-stimulated cyclic AMP accumulation were Ca++-dependent. These results suggest that adenosine-dependent cyclic AMP formation in rat spinal cord is mediated through two types of receptors, one of which is independent, and the other coupled to the alpha adrenergic receptor.

Adenosine↗
PubMed1981

Enuresis: a contrast of attitudes of parents and physicians.

Questionnaires were used to survey 1,435 parents and 446 physicians in order to determine and compare attitudes and beliefs about enuresis. Although both groups thought that bed-wetting is a maturational problem, the parent group thought emotional causes were important and were less likely to accept small bladder size as an etiology. Parents thought that children should be dry at a much younger age than did the physicians (2.75 vs 5.13 years, respectively). Only 63% of parents thought that medical intervention is a good way to deal with a child's bed-wetting, yet 87% of the physicians suggested medical evaluation. A comparison of the various methods used to stop bed-wetting indicated that parents use waking the child, reassurance and talking with the child, restricting fluids, and punishment significantly more often than physicians. Although many physicians prescribe medication, only 6.6% of the parents thought that medicines are a "very good way" to treat enuresis. When developing a treatment plan for a child with enuresis, the physician should recognize the wide differences between parental and physician attitudes toward this common problem of childhood.

Attitude to Health↗
PubMed1980

Epidemiology of anorexia nervosa in Monroe County, New York: 1960-1976.

The Monroe County Psychiatric Case Register and hospital records were used to investigate the incidence of anorexia nervosa in Monroe County, New York, during the periods 1960-1969 and 1979-1976 to determine whether the number of newly diagnosed cases has increased over time. The results support the general clinical impression of a recent increase in the incidence of anorexia nervosa. This pattern of overall change was accounted for by the sharp increase in the number of females with the disorder, particularly those aged 15-24. The data also suggest that the disorder occurs more often in the higher socioeconomic levels.

Adolescent↗
PubMed1980

Alpha adrenergic receptor mediated formation of cyclic AMP in rat spinal cord.

Methoxamine and phenylephrine (PE), postsynaptic alpha adrenergic agonists stimulated the accumulation of cyclic AMP in spinal cord tissue slices. Naphazoline, oxymetazoline and clonidine, previously shown to have greater efficacy at presynaptic alpha receptors did not alter accumulation and, in fact, blocked the PE response. The PE-stimulation was completely inhibited by postsynaptic alpha antagonists, incompletely by agents which bl ock presynaptic alpha receptors, and slightly by the beta blocker propranolol. Pe-stimulated accumulation was potentiated by phosphodiesterase inhibition (RO 20-1724). In contrast to previous reports on the requirement of the copresence of adenosine for alpha receptor stimulated accumulation of cyclic AMP in neuronal tissue, the PE-stimulation in spinal cord slices was unchanged by adenosine receptor blockade (theophylline), hydrolysis of endogenous adenosine (adenosine deaminase), inhibition of adenosine deaminase (EHNA) or blockade of adenosine uptake (dipyridamole). Added adenosine increased basal accumulation and produced a marked potentiation of the PE response. From this data it is evident that, in spinal cord tissue slices, there occurs a postsynaptic alpha adrenergic receptor linked to cyclic AMP accumulation which does not require the presence of other neurohumoral agents for activation.

4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone↗