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Biomedical subjects

J M Cott

Publications and source records attributed to J M Cott.

17 recordsLinked to original sources
PubMed2000

Valerian as a hypnotic for Hispanic patients.

Valerian is a botanical used for its sedative effects whose central nervous system activity is ascribed to multiple constituents. Twenty-three established outpatient symptomatic Hispanic volunteers receiving mental health services at a large urban hospital participated in this case study. All complained of insufficient sleep. They were asked to try a popular national brand of valerian ("Nature's Way", 470 mg valerian root) and completed sleep questionnaires at baseline and at the end of Weeks 1 and 2. They were instructed to take 1 capsule each night before retiring and were allowed to increase their dose to a maximum of 3 capsules after Week 1. Twenty patients completed the trial. On an ordinal scale of 1 (no effect), 3 (moderately helpful), and 5 (extremely helpful), 16 patients rated their insomnia as at least "moderately improved" at the end of Week 1. By Week 2, 16 still rated themselves at least "moderately improved," but 15 of them now described their response as either a 4 or a 5. Global improvement at Week 2 was significantly better than at Week 1 (Wilcoxon ranks test p = .005), perhaps reflecting a time-dependent or dose-response relationship. This case study suggests that valerian can be a supplement for improving insomnia in a symptomatic population.

Adult↗
PubMed1998

Is St. John's wort (Hypericum perforatum) an effective antidepressant?

SJW is a remarkably safe antidepressant with an apparently unique mode of action. Although it has demonstrated efficacy in mild and moderate depression when compared with placebo or tricyclic antidepressants, several research areas beg to be explored. Its effects should be compared with serotonin reuptake inhibitors. Studies in severely depressed patients are lacking, as are studies on its utility as a therapeutic adjunct to standard antidepressants.

Animals↗
PubMed1997

In vitro receptor binding and enzyme inhibition by Hypericum perforatum extract.

Hypericum perforatum L. Hypericaceae (St. John's wort), has been used since the time of ancient Greece for its many medicinal properties. Modern usage is still quite diverse and includes wound healing, kidney and lung ailments, insomnia and depression. This plant has been known to contain a red pigment, hypericin, and similar compounds, which have been assumed to be the primary active constituent(s) in this plant genus. A crude Hypericum extract was tested in a battery of 39 in vitro receptor assays, and two enzyme assays. A sample of pure hypericin was also tested. Hypericin had affinity only for NMDA receptors while the crude extract had significant receptor affinity for adenosine (nonspecific), GABAA, GABAB, benzodiazepine, inositol triphosphate, and monoamine oxidase (MAO) A and B. With the exception of GABAA and GABAB, the concentrations of Hypericum exact required for these in vitro activities are unlikely to be attained after oral administration in whole animals or humans. These data are consistent with recent pharmacologic evidence suggesting that other constituents of this plant may be of greater importance for the reported psychotherapeutic activity. Alternative pharmacologic mechanisms for Hypericum's antidepressant activity are critically reviewed and the possible importance of GABA receptor binding in the pharmacology of Hypericum is highlighted. Some of these results have been previously reported.

Animals↗
PubMed1993

Psychotherapeutic Medications Development Program (PMDP).

The Psychotherapeutic Medications Development Program (PMDP) of the National Institute of Mental Health was established in 1990. The purpose of the PMDP is to improve, enhance, and speed the development of new medications and improve the therapeutic usefulness of existing medications for the treatment of mental illness. The PMDP will fulfill this mission by implementing four initiatives. In the drug discovery and development initiative, the PMDP will aid in the development of promising new drugs. This initiative will also include improving the therapeutic usefulness of existing medications. In the technology transfer initiative, PMDP will improve the technology transfer from academic and government researchers to the pharmaceutical industry; improve the dissemination of information concerning technology transfer opportunities as it pertains to psychotherapeutic medications; and enhance technology transfer by acting as a broker to bring interested parties together. For the third initiative, the PMDP will develop and maintain a capability to clinically evaluate psychotherapeutic medications. The PMDP will also act to facilitate the development and testing of new concepts and models of mental illness. There is a detailed description of the steps that are involved in developing a new chemical entity (NCE) from the conceptual stage to a medication that is approved for the treatment of a particular illness. The pharmaceutical industry estimates that this medication development process costs $238 million.

Humans↗
PubMed1981

Sedative/anxiolytic effects of antidepressants in animals.

The sedative effects of several different structural types of antidepressants were investigated in mice. Six different models of sedation were used and the results were averaged. The rank order of sedative potency was: amitriptyline greater than mianserin greater than maprotiline greater than imipramine greater than desipramine greater than clomipramine greater than alaproclate greater than zimelidine greater than norzimelidine. Sedative potency of the antidepressants was found to be significantly correlated with their affinity for four different brain amine receptors. The rank order of correlation of sedation with receptor affinity was: histamine (H1) greater than serotonergic greater than muscarinic greater than alpha 1-adrenergic. These findings appear to be associated with clinical side effects observed during treatment with antidepressants. While scant literature is available concerning specific anxiolytic effects of antidepressants, pharmacological evidence for the role of central 5-HT systems in the anxiolytic effect is plentiful. Our preliminary findings show a marked antagonism of isolation-induced aggression by low doses of the specific 5-HT uptake inhibitor, zimelidine, and the 5-HT releasing agent, p-chloramphetamine, thus supporting the hypothetical importance of 5-HT in the pharmacology of anxiolytic agents.

Aggression↗
PubMed1980

Antidepressant drugs and ethanol: behavioral and pharmacokinetic interactions in mice.

The interactions between ethanol and antidepressant drugs (both tricyclics and newer non-tricyclics) were studied in mice. The ability of these drugs to enhance the sedative effects of ethanol at two different doses (3.2 and 4.0 g/kg) was measured. The percentage of mice losing the righting-reflex was used for the lower dose, and the duration of ethanol-induced sleep was used at the higher dose. The relative order of potency was amitriptyline greater than or equal to imipramine > maprotiline = mianserin > desipramine greater than or equal to chlorimipramine > iprindole greater than or equal to alaproclate > norzimelidine greater than or equal to zimelidine. Amitriptyline (60 mg/kg) caused death in all mice when combined with 4.0 g/kg ethanol. Clinically established antidepressants which enhanced ethanol sedation only at doses considerably above therapeutic levels were zimelidine and iprindole. The relative potency of the antidepressants to enhance ethanol sedation is correlated with their inherent sedative properties which are in turn related to their ability to block central 5-HT, alpha-NA, muscarinic and H1-receptors. Amitriptyline (20 mg/kg) was found to increase ethanol plasma levels to 202, 167 and 132% of control values at 30, 60 and 90 min after ethanol administration, respectively. Desipramine, mianserin and alaproclate also increased ethanol plasma levels initially, but to a lesser extent. These findings suggest that in addition to their sedative effect, several antidepressants, particularly amitriptyline, are likely to interact with ethanol by increasing its concentration in plasma.

Animals↗
PubMed1976

Investigations into the mechanism of reduction of ethanol sleep by thyrotropin-releasing hormone (TRH).

Thyrotropin-releasing hormone (TRH), administered intraperitoneally, was found to antagonize ethanol-induced sleep and hypothermia in mice without affecting brain ethanol content. This reduction of the actions of ethanol was also apparent after oral or intracisternal administration of TRH. In addition, TRH reduced ethanol-induced sleep in rats, hamsters, gerbils and guinea pigs. Evidence that the pituitary-thyroid axis is not necessary for the effects of TRH was provided by observations that hypophysectomy did not reduce TRH antagonism of ethanol narcosis and findings that neither triiodothyronine nor thyrotropin mimicked its action. Certain analogs of TRH, which have little effect on the pituitary, were also found to antagonize ethanol-induced sleep and hypothermia. Pretreatment with the antiadrenergic drugs, alpha-methyltyrosine, phentolamine and propranolol did not antagonize the ability of TRH to reduce sleep induced by ethanol. However, after intracisternal administration of atropine methyl nitrate, TRH no longer caused a significant reduction of sleep, even though TRH antagonism of the ethanol-induced hypothermia was still apparent. In contrast, central administration of other anticholinergic drugs, such as delta-tobocurarine and hexamethonium, reduced ethanol-induced sleep and this effect was additive with TRH. Carbachol also reduced ethanol sleeping time and this effect was also blocked by atropine methyl nitrate. The antagonism of ethanol-induced sleep by dibutyryl cyclic adenosine 3', 5'-monophosphate was significantly reduced but not blocked by atropine methyl nitrate. Results provide evidence that TRH has a direct extrapituitary action on brain and that both TRH and ethanol may interact with central cholinergic systems.

Animals↗
PubMed1975

Parameters of alteration of pentobarbital response by hypothalamic polypeptides.

Both thyrotropin-releasing hormone (TRH) and amphetamine antagonize pentobarbital. They are more effective in the day than at night. This is true for TRH even when the dose of pentobarbital is increased at night to prolong sedation. Under this condition the day-night difference is lost for amphetamine. Both substances are more effective in cold ambient temperatures (18 degrees C) and less effective in warm temperatures, but their activity at warmer temperatures (37 degrees C) is still substantial. In contrast, somatotropin release-inhibiting factor (SRIF) augments the effects of pentobarbital at room temperature. This action is unaffected by time of day. However, the increase in sleeping time is lost in both a warm environment and in a cold environment.

Amphetamine↗
PubMed1975

Effects of thyrotropin-releasing hormone (TRH) on the actions of pentobarbital and other centrally acting drugs.

Thyrotropin-releasing hormone (TRH) was found to antagonize pentobarbital-induced sleeping time and hypothermia. While 3 to 100 mg/kg of TRH reduced pentobarbital sleeping time when administered prior to the barbiturate, a dose-response relationship to TRH could not be established. However, doses of 10 to 100 mg/kg of TRH enhanced the lethality of pentobarbital when these compounds were administered simultaneously. Thyrotropin or L-triiodothyronine did not imitate and hypophysectomy did not reduce the effects of TRH, indicating that the pituitary is not essential for its antagonism of pentobarbital. Studies of TRH analogs provided further support of this view. In addition, TRH reduced the sleep and hypothermia produced by thiopental, amobarbital, secobarbital and phenobarbital, and it antagonized the hypothermia and reduced motor activity produced by chloral hydrate, reserpine, chlorpromazine and diazepam. Intracisternally administered TRH also reduced pentobarbital sleeping time and hypothermia, but melanocyte-stimulating hormone release-inhibiting factor and somatostatin administered by this route did not. While reduction of pentobarbital sleeping time by TRH could not be attributed to an affect on monoamine systems or to deamidated TRH, this action was reduced by intracisternally administered atropine, suggesting that cholinergic mechanisms may contribute to the effects of TRH. Thus, the results provide evidence that TRH acts on brain independent of an effect on the pituitary.

Animals↗
PubMedDate not supplied

Dietary supplements and natural products as psychotherapeutic agents.

Alternative therapies are widely used by consumers. A number of herbs and dietary supplements have demonstrable effects on mood, memory, and insomnia. There is a significant amount of evidence supporting the use of Hypericum perforatum (St. John's wort) for depression and Ginkgo biloba for dementia. Results of randomized, controlled trials also support the use of kava for anxiety and valerian for insomnia. Although evidence for the use of vitamins and amino acids as sole agents for psychiatric symptoms is not strong, there is intriguing preliminary evidence for the use of folate, tryptophan, and phenylalanine as adjuncts to enhance the effectiveness of conventional antidepressants. S-adenosylmethionine seems to have antidepressant effects, and omega-3 polyunsaturated fatty acids, particularly docosahexaenoic acid, may have mood-stabilizing effects. More research should be conducted on these and other natural products for the prevention and treatment of various psychiatric disorders.

Amino Acids↗