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Biomedical subjects

J P Green

Publications and source records attributed to J P Green.

At least 19 recordsLinked to original sources

Pseudomemory in hypnotized and task-motivated subjects.

Highly hypnotizable hypnotized (H; n = 16) and task-motivated (TM; n = 13) subjects received pseudomemory suggestions (see Orne, 1979). TM subjects reported being more awake and motivated than did H subjects and were more likely to pass the target noise suggestion. However, 69% of subjects in both conditions who passed the noise suggestion reported pseudomemories. Pseudomemory rate (for H subjects, 69% and for TM subjects, 46%) was not reduced by informing subjects that they could distinguish reality and fantasy in a state of deep concentration. At final inquiry, after deep concentration, pseudomemories remained stable (for H subjects, 75% and for TM subjects, 54%). As predicted, H subjects reported more unsuggested noises and more pseudomemories of novel noises than did TM subjects. Subjects who reported pseudomemories were more confident in the accuracy of their memories than were subjects who reported that the suggested noises were imagined.

Adult

Finding the hypnotic virtuoso--another look: a brief communication.

Student volunteers who scored 9 (N = 20), 10 (N = 19), 11 (N = 26), and 12 (N = 15) on a live-administered Harvard Group Scale of Hypnotic Susceptibility (HGSHS:A) of Shor and E. Orne (1962) were retested with the individually administered Stanford Hypnotic Susceptibility Scale (SHSS:C) of Weitzenhoffer and Hilgard (1962). There appeared to be a break in HGSHS:A's predictive ability at 11 suggestions passed. Whereas a majority of Ss who passed at least 11 HGSHS:A suggestions retested in SHSS:C "virtuoso" range (i.e., passed at least 11 suggestions), a relatively small percentage of Ss who passed fewer than 11 HGSHS:A suggestions retested as SHSS:C virtuosos. These results are generally consistent with previous research (Register & Kihlstrom, 1986) using a standard taped-recorded HGSHS:A induction.

Amnesia

Histamine metabolites and pros-methylimidazoleacetic acid in human cerebrospinal fluid.

In cerebrospinal fluid, levels of the histamine metabolites, tele-methylhistamine and tele-methylimidazole-acetic acid, were higher in elderly than in young people, and women had higher levels than men. Therefore, age and gender should be considered in studies of histamine metabolites as exemplified by their measurements in cerebrospinal fluid of patients with Huntington's disease. Levels of pros-methylimidazoleacetic acid, an isomer of tele-methylimidazoleacetic acid and not a metabolite of histamine, were higher in cerebrospinal fluid of men than of women. Levels of pros-methylimidazoleacetic acid in cerebrospinal fluid were highly positively correlated with the severity of Parkinson's disease in a group of non-medicated, mildly to moderately affected patients.

Adult

Levels of pros-methylimidazoleacetic acid: correlation with severity of Parkinson's disease in CSF of patients and with the depletion of striatal dopamine and its metabolites in MPTP-treated mice.

The cerebrospinal fluid (CSF) levels of pros-methylimidazoleacetic acid (p-MIAA) in thirteen medication-free patients with mild to moderate Parkinson's disease were highly correlated (Spearman's rho = 0.749, p less than 0.005) with the severity of signs of the disease as scored on the Columbia University Rating Scale. Levels of p-MIAA in males (n = 8) and females (n = 5) were each significantly correlated with scores of severity (rho = 0.78, p less than 0.05 and rho = 1.0, p less than 0.05, respectively). In C57BL/6 mice treated with 1-methyl-4-phenyl-1,2,3,6-tetra-hydropyridine (MPTP), levels of p-MIAA were significantly correlated with the depleted levels of dopamine (r = 0.85, p less than 0.01), homovanillic acid (r = 0.79, p less than 0.02), 3,4-dihydroxyphenylacetic acid (r = 0.84, p less than 0.01) and norepinephrine (r = 0.91, p less than 0.002) in striatum, but not in cortex of the same mice. No such correlations were observed in either striatum or cortex of saline-treated control mice. Mean levels of p-MIAA in CSF did not differ significantly between patients and age-matched controls; and mean levels of p-MIAA in striatum did not differ between MPTP-treated mice and controls. The simplest hypothesis to account for these strong correlations in the absence of differences in mean levels of p-MIAA is that accumulation of p-MIAA [or process(es) that govern its accumulation] influences a failing nigrostriatal system. It is also possible (in analogy with findings in other diseases and with other drugs) that measurements of the putative metabolite(s) of p-MIAA may distinguish the patients and the MPTP-treated mice from their respective controls. Elucidation of the processes that regulate formation and disposition of p-MIAA in brain and information on the neural effects of p-MIAA, its precursors and its putative metabolites may yield insight into factors that regulate the progression of Parkinson's disease, and may shed additional light on the cause(s) of this disease.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine

Serotonergic modulation of the release of endogenous norepinephrine from rat hypothalamic slices.

Ca+(+)-dependent release of endogenous norepinephrine (NE) and dopamine from superfused rat hypothalamic slices was stimulated by 40 mM K+. 20 mM K+ released only NE. Two consecutive exposures to 20 mM K+ (S1 and S2, respectively) produced NE release of similar magnitude (S2/S1 = 1.03 +/- 0.08). Serotonin (5-HT), 3 to 10 microM, in the presence of methylsergide or ritanserin (antagonists at 5-HT1-like and 5-HT2 receptors), caused a concentration-dependent decrease of K(+)-evoked NE release. 5-HT alone did not alter K(+)-evoked NE release. 2-Methyl-serotonin, 2-methyl-5-hydroxytryptamine, 3 to 10 microM (a selective 5-HT3 agonist), mimicked the 5-HT response in the presence and in the absence of ritanserin. A highly selective 5-HT3 antagonist, (3 alpha-tropanyl)1H-indole-3-carboxylic acid ester (ICS 205-930), 1 nM, inhibited the effect of both agonists. The isomers of another highly selective 5-HT3 antagonist, zacopride, inhibited the effect of 2-methyl-serotonin, 2-methyl-5-hydroxytryptamine, at a concentration range, 0.03 to 20 nM, characteristic of their interaction with 5-HT3 receptors. alpha-Methyl-serotonin, alpha-methyl-5-hydroxytryptamine, a selective 5-HT1-like/5-HT2 agonist, failed to affect the K(+)-evoked NE release, but antagonized the effect of 2-methyl-serotonin, 2-methyl-5-hydroxytryptamine. These observations provide direct evidence that, in rat hypothalamus, 5-HT modulates release of endogenous NE through activation of 5-HT3 and, possibly, 5-HT1C receptors.

Animals

Pharmacological receptors: the need for a compendium of classification, nomenclature and structure.

In an attempt to contain the chaos of receptor nomenclature, the supplement distributed with this issue of TiPS catalogues cell surface receptors and their subtypes according to the most commonly used nomenclature and describes them in pharmacological, biochemical and molecular terms. This reporting of the status quo will be an invaluable aid to communication, but all scientists (not just pharmacologists) working on receptors would agree that a radical and rational classification of receptors also needs to be initiated. In this article, Jack Peter Green proposes a system of (and mechanism for) classification that should satisfy both the 'taxonomic realists' and the 'taxonomic skeptics'.

Animals

Literalism as a marker of hypnotic "trance": disconfirming evidence.

The responses given by highly hypnotizable, hypnotic subjects and those of unhypnotizable subjects who simulated hypnosis to questions of the type, "Do you mind telling me your name?" and "Do you mind standing up?" were contrasted. The purpose was to examine Erickson's (1980) assertion that literalism (answering "yes" or "no" verbally or nonverbally without any cognitive elaboration) is a marker of hypnotic "trance." Simulators exhibited a greater rate of literalism than hypnotic "virtuosos" (i.e., extreme scorers on both group and individual hypnotizability measures). Hypnotized subjects and nonhypnotized subjects approached in the campus library responded comparably. Because less than a third of hypnotic virtuosos responded literally, our results strongly refuted Erickson's assertion that literalism is a cognitive feature of hypnosis.

Cognition

Literalism and hypnosis: hypnotic versus task-motivated subjects.

To extend previous literalism research with hypnotized and simulating subjects, we compared literalism rates of hypnotized, highly hypnotizable subjects (N = 12) with nonhypnotized, task-motivated subjects (N = 12) who were also highly hypnotizable. Six questions of the type used by Erickson (e.g., "Do you mind telling me your name?") constituted tests of literalism (scored if response is "Yes" or "No," either verbally or nonverbally). Whereas Erickson claimed that 97% of his "deep trance" subjects and 90% of his "medium trance" subjects exhibited literal responses, we found that 87.5% of hypnotized, high-hypnotizable subjects' responses were nonliteral. Hypnotized and task-motivated subjects did not differ in their literal responding to the individual questions or when their scores were summed across questions. No support was secured for Erickson's assertion that literalism is a cardinal feature of hypnosis.

Adult

Manganese-binding proteins of the oxygen-evolving complex.

The extrinsic 33-kDa protein (P33) was cross-linked covalently to the binding site on P33-depleted PSII preparations which is responsible for reconstitution of photosynthetic water oxidation after PSII preparations have been washed with 1 M CaCl2. Conditions were found in which more than half of the cross-linked protein complexes formed in the PSII preparations retained the ability to catalyze the oxidation of water. The complex is composed of the P33 cross-linked to the D1 and D2 proteins and a 34-kDa protein, which is present in lower abundance than the other three proteins. After solubilization of the membranes with SDS and purification by preparative SDS-PAGE, the complex retains bound manganese and can catalyze the conversion of H2O2 to O2. Calcium and chloride increased the catalase activity of the purified cross-linked complex while lanthanum or hydroxylamine abolished the activity. By use of the specific activity of the H2O2-dependent reaction to follow the extent of purification of the cross-linked complex, the most highly purified complex was determined to contain 0.34 microgram of manganese/180 micrograms of protein. The mole ratio of Mn/protein was calculated to range from 3.6 to 4.5 depending on the assumed stoichiometry of the protein subunits. The results presented here provide direct evidence that one or more of the three proteins that have cross-linked to the P33 are responsible for binding the manganese of the oxygen-evolving complex.

Catalase

Rostral-caudal concentration gradients of histamine metabolites in human cerebrospinal fluid.

The metabolites of histamine, tele-methylhistamine (t-MH) and tele-methylimidazoleacetic acid (t-MIAA), have a large concentration gradient between cisternal and lumbar CSF in the rhesus monkey. The possibility of a t-MH and/or t-MIAA gradient in man was studied in sequential samples of CSF withdrawn from the lumbar space from a healthy male. The mean levels of t-MH and t-MIAA in the 14-16 ml segment of CSF from 6 male volunteers was also measured. pros-Methylimidazoleacetic acid (p-MIAA), an endogenous isomer of t-MIAA that is not derived from histamine, was also measured. Levels of t-MH, t-MIAA and p-MIAA were measured by gas chromatography-mass spectrometry. With increasing volumes of CSF removed, t-MH and t-MIAA levels increased linearly (p less than 0.01) when plotted against the midpoints of each volume segment. Levels of t-MH and t-MIAA from the volunteers showed little variation; the means of the levels were within 15% of the respective regression lines of the points from the single subject. In contrast, p-MIAA levels showed no gradient (p greater than 0.6) in serially removed CSF; the individual levels in CSF from the volunteers on unrestricted diets varied widely, suggestive of a dietary influence on p-MIAA levels in the CNS. The concentration gradient of histamine metabolites in CSF confirms the rostral-caudal gradient observed in monkey and argues against plasma or spinal cord as major sources of these metabolites.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Diurnal fluctuation in levels of histamine metabolites in cerebrospinal fluid of rhesus monkey.

In samples of ventricular cerebrospinal fluid (CSF) that were collected from a conscious, restrained rhesus monkey at intervals of 30 90 min, levels of the histamine metabolites, tele-methylhistamine (t-MH) and tele-methylimidazoleacetic acid (t-MIAA), were determined by gas chromatography-mass spectrometry. Levels of t-MH and t-MIAA each showed time-related fluctuations. Peak and trough concentrations of t-MIAA, the product of t-MH, paralleled, but lagged about 2 h behind, the levels of t-MH. Within the first 3 h of illumination, metabolite levels increased more than 3-fold; they fell sharply within the first 3 h of darkness. Mean levels of t-MH and t-MIAA were significantly higher during periods of illumination than of darkness. Fluctuations in the levels of pros-methylimidazoleacetic acid (p-MIAA), an endogenous isomer of t-MIAA that is not a histamine metabolite, were markedly different from those of t-MH or t-MIAA; p-MIAA levels peaked only at the middle of the dark period. The time-related fluctuations in levels of t-MH and t-MIAA, but not p-MIAA, are similar to the daily rhythmic changes observed in monkey CSF for the levels of other central neurotransmitters and peptide neurohormones.

Animals

Presence and measurement of imidazoleacetic acid, a gamma-aminobutyric acid agonist, in rat brain and human cerebrospinal fluid.

Imidazoleacetic acid (IAA) was unequivocally demonstrated in rat brain, human CSF, and human plasma by a gas chromatographic-mass spectrometric method that can reliably quantify as little as 8 pmol, i.e., 1 ng. Owing to tautomerism of the imidazole ring, IAA and [15N, 15N]IAA, the internal standard, each formed two chromatographically distinct isomers after derivatization of the ring nitrogens with either ethyl chloroformate or methyl chloroformate. The isomers of n-butyl(N-ethoxycarbonyl)imidazole acetate and n-butyl(N-methoxycarbonyl)imidazole acetate were identified by analysis with methane chemical ionization and electron impact ionization of molecular and fragment ions. The levels (mean +/- SEM) of free IAA were 140 +/- 14 pmol/g and 2.7 +/- 0.2 pmol/ml in brains of untreated rats and human lumbar CSF, respectively. Mean levels of IAA in brains of anesthetized rats, perfused free of blood, did not differ significantly from mean levels of anesthetized, nonperfused controls or from untreated rats. The source or sources of IAA in brain and CSF are unknown. Because IAA is a potent agonist at gamma-aminobutyrate receptors, it merits examination as a regulator in brain.

Animals

pros-methylimidazoleacetic acid in rat brain: its regional distribution and relationship to metabolic pathways of histamine.

pros-Methylimidazoleacetic acid (p-MIAA; 1-methylimidazole-5-acetic acid), an isomer of the histamine metabolite, tele-methylimidazoleacetic acid (t-MIAA), is present in brain and CSF. Its relationship to histamine synthesis and catabolism was assessed in brains of rats. p-MIAA distribution in brain regions was heterogeneous although the concentrations in regions with the highest (hypothalamus) and the lowest (medulla-pons) levels differed less than four-fold. There was no significant correlation between the regional distributions of p-MIAA with those of histamine or its metabolites. pros-Methylhistidine (1 g/kg, i.p.) produced a 20-fold increase in mean levels of p-MIAA and up to a 50-fold increase in levels of pros-methylhistamine (p-MH), a putative intermediate; levels of histamine and its metabolites were unaltered. L-Histidine (1 g/kg, i.p.) or alpha-fluoromethylhistidine (100 mg/kg, i.p.), the irreversible inhibitor of histamine synthesis, did not alter the levels of p-MIAA in brain. Like the levels of t-MIAA, the levels of p-MIAA were unaltered after probenecid administration. Contrary to its effects in lowering t-MIAA levels, pargyline (75 mg/kg, i.p.) produced a slight rise in levels of p-MIAA in all regions. These findings suggest that, in brain, the metabolic pathways of histamine are independent of pathways that generate p-MIAA. Further, since brain is capable of p-MH formation, its use as an internal standard in analytical methods merits caution.

Animals

Release of endogenous dopamine by stimulation of 5-hydroxytryptamine3 receptors in rat striatum.

5-Hydroxytryptamine (5-HT) caused a persistent, concentration-dependent increase of spontaneous release of endogenous dopamine (DA) from superfused rat striatal slices. 2-Methyl-5-HT, a selective 5-HT3 agonist, mimicked the 5-HT response with a potency only slightly less than that of 5-HT. A highly selective 5-HT3 antagonist, ICS 205-930 [(3-alpha-tropanyl)1H-indole-3-carboxylic acid ester], inhibited the effect of both agonists with a pKB value characteristic of 5-HT3 receptors. 5-HT-evoked DA release was resistant to antagonism by methiothepin and methysergide, antagonists at 5-HT 1-like and 5-HT2 receptors. Neither (2,5-dimethoxy-4-iodophenyl)-2-aminopropane, the selective 5-HT2 receptor agonist, nor 5-carboxamidotryptamine, the selective 5-HT 1-like receptor agonist, altered DA release. The release of DA by 5-HT3 stimulation was Ca++-dependent and partially sensitive to tetrodotoxin. 5-HT and 2-methyl-5-HT also increased K+-evoked DA release. These observations constitute direct, unambiguous evidence that in rat striatum 5-HT3 receptors modulate release of DA.

Animals

Stimulation of histamine H2 receptor in rat hypothalamus releases endogenous norepinephrine.

The effect of histamine (HA) on the release of endogenous norepinephrine (NE) from superfused rat hypothalamic and striatal slices was assessed. Measurements were made by high-performance liquid chromatography with electrochemical detection. Superfusion with HA (0.1-80 microM) resulted in a concentration-dependent increase (10-220%) of NE release from hypothalamus but was ineffective in the striatum. The process was Ca++-dependent and was unaffected by blockade of monoamine oxidase. The H2 agonists, dimaprit (50 microM) and impromidine (10 microM), increased NE release from hypothalamic slices 3-fold and 2-fold, respectively. Tiotidine (10 microM), an H2 antagonist, did not alter the spontaneous release of NE but completely abolished the effect of dimaprit. To increase the ability of the tissue to sustain NE release on repeated stimulation, tyrosine was added to the perfusion medium. Under these conditions 10 microM HA produced, in two consecutive stimuli, a 1.9-fold increase. Two consecutive stimuli by 80 microM HA elicited a 3.2- and a 2.9-fold increase. Under the same conditions, 50 microM ranitidine, another H2 antagonist, but not pyrilamine, an H1 antagonist, completely blocked the effect of 10 microM HA. Although NE release was increased in the presence of tyrosine, tyrosine did not increase the tissue levels of NE. These experiments imply that H2 receptor activation increases release of NE from the rat hypothalamus. Since in the hypothalamic slice, noradrenergic nerve endings are cut from their cell bodies, the modulatory event must have occurred at the nerve terminals.

Animals