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Biomedical subjects

D E Schmidt

Publications and source records attributed to D E Schmidt.

At least 55 records · Page 3Linked to original sources
PubMed1989

A longitudinal study of the effect of different social rearing conditions on cerebrospinal fluid norepinephrine and biogenic amine metabolites in rhesus monkeys.

The purpose of this study was to determine whether disruption of early social attachment alters the activity of brain biogenic amine systems in rhesus monkeys (Macaca mulatta). Male rhesus monkey infants were deprived of maternal interaction, peer interaction, or both, during the first 22 months of life. Cerebrospinal fluid (CSF) was collected under rigorously controlled conditions approximately every month and assayed for levels of norepinephrine (NE), its major metabolite, and the metabolites of dopamine and serotonin. Mother-Deprived infants had lower levels of CSF NE than Mother-Reared infants. Mother-Deprived infants also failed to develop the same pattern of intercorrelations between compounds and month-to-month stability in levels of neurotransmitter and metabolites in CSF as the Mother-Reared infants. Finally, there were changes in CSF NE levels associated with social separation and social group formation. The brain NE system appears to be sensitive to changes in the social environment. Its level of activity, as reflected in levels of NE in CSF, appears to depend on both the prevailing social environment and the prior rearing environment.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1983

Strain specific cholinergic changes in response to stress: analysis of a time-dependent avoidance variation.

Investigators have established that the performance of an incompletely learned avoidance task is a U shaped function of the time since the original partial acquisition. Thus rats perform more poorly when retested at intermediate time intervals (1-8 hr) after training than they do when tested at longer post-acquisition intervals (24-48 hr). Studies have suggested that such time-dependent deficits are not related to changes in learning ability, but rather result from shock-induced motor suppression which interferes with active avoidance responding. Pharmacological studies utilizing drugs which effect cholinergic function have indicated that an inhibitory cholinergic system may be involved in mediating post-shock motor suppression. To obtain direct biochemical evidence for possible cholinergic mediation of post-shock motor suppression, measurements of high affinity choline uptake and acetylcholine turnover were made at varying time intervals following partial active avoidance training in F-344 rats. An increase in cholinergic function was found in the dorsal, but not the ventral hippocampus 30 min, 1 hr and 4 hr following acquisition training. These biochemical alterations were temporally correlated with deficits in active avoidance responding. We have reported that the immediate behavioral suppression observed in another rat strain (Sprague-Dawley, Zivic Miller Laboratories), which exhibits inferior active avoidance performance, is similarly correlated with cholinergic activation in the dorsal hippocampus [17]. These data support the hypothesis that the dorsal-hippocampal cholinergic system is involved in the mediation of stress-induced behavioral suppression.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1983

Effects of dietary lecithin on hormonal and neurobehavioral profiles in normal subjects.

Four normal subjects received lecithin supplements sufficient to elevate serum choline levels 3-fold. Despite persistent hypercholinemia over 48 hours of close observation, no increase was observed in serum ACTH, cortisol, and insulin concentrations, or in free urinary catecholamine excretion. Screening of a large group of other pituitary and gonadal hormones also failed to reveal any influence of lecithin supplements. EEG patterns and results of psychometric tests were also unaltered.

Acetylcholine↗
PubMed1982

Exogenous choline enhances the synthesis of acetylcholine only under conditions of increased cholinergic neuronal activity.

The effect choline (60 mg/kg, i.p.) on fluphenazine- and pentylenetetrazol-induced alterations in the concentration of acetylcholine (ACh) and/or the rate of sodium-dependent high-affinity choline uptake (HACU) in rat striatum and hippocampus was studied. Systemic administration of the dopamine receptor blocking agent fluphenazine hydrochloride (.05 mg/kg, i.p.) decreased the concentration of ACh in the striatum; this effect was prevented by the prior administration of choline. The central nervous system stimulant pentylenetetrazol (30 mg/kg, i.p.) reduced the concentration ACh in both striatum and hippocampus and increased the velocity of HACU in the hippocampus. Pretreatment with choline totally prevented the depletion of ACh induced by pentylenetetrazol in the striatum. In the hippocampus, prior administration of choline prevented the pentylenetetrazol-induced increase in the rate of HACU and attenuated the effect of pentylenetetrazol on the levels of ACh. Results indicate that the acute administration of choline antagonizes pharmacologically induced alterations in cholinergic activity as assessed by the rate of HACU and the steady-state concentration of ACh. Furthermore, data support the hypothesis that the administration of choline increases the ability of central cholinergic neurons to synthesize ACh under conditions of increased neuronal activity.

Acetylcholine↗
PubMed1981

Tuftsin, a natural activator of phagocytic functions including tumoricidal activity.

Some of the properties of the tetrapeptide tuftsin, Thr-Lys-Pro-Arg, are discussed. We describe three phases of tuftsin activation of the macrophage. Tuftsinyltuftsin, the octapeptide Thr-Lys-Pro-Arg-Thr-Lys-Pro-Arg, was synthesized with a view of minimizing the formation of Lys-Pro-Arg, from tuftsin by tissue aminopeptidases. The tripeptide is a tuftsin inhibitor. The octapeptide proved to be quite effective in prolonging the life of syngeneic mice injected with L1210 leukemia cells. Its effect in our laboratory, was considerably better than we could obtain with tuftsin. A simple method for purifying tuftsin by high performance liquid chromatography is described using 0.75% trifluoroacetic acid in water. The tuftsin sequence Thr-Lys-Pro-Arg is present in P12 protein of Rausher murine leukemia virus. A close analog Thr-Arg-Pro-Lys appears in yet another virus protein the haemagglutinin of influenza virus. A second close analog Thr-Arg-Pro-Arg forms the penultimate carboxyterminal of a pancreatic polypeptide found in human and several animals.

Animals↗
PubMed1981

Effects of pH and sulfhydryl specific reagents on 4-fumarylacetoacetate fumarylhydrolase.

The pH-dependence of fumarylacetoacetase (4-fumarylacetoacetate fumaryl-hydrolase, EC 3.7.1.2) activity was studied in the pH range 6.25-8.50. After correction of the substrate concentration for enolate formation, the Michealis constant was found to be pH independent in this range. Likewise, the Ki values for the competitive inhibitors chloride and fluoride were found to be independent of pH between 6.25-8.50. A bell-shaped curve described the log V vs. pH dependence, and ionization constants of 6.5 and 8.2 were calculated. Tentatively an imidazole group and a sulfhydryl group were assigned to the constants 6.5 and 8.2, respectively. Both p-hydroxymercuribenzoate and 5,5'-dithiobis(2-nitrobenzoic acid) react with both sulfhydryl groups per subunit in the native protein and three sulfhydryl groups per subunit in the denatured protein. Substrate protects one sulfhydryl group in the native protein from reaction with 5,5'-dithiobis(2-nitrobenzoid acid). Substrate or the competitive inhibitor, fluoride, protect the enzyme from inactivation by p-hydroxymercuribenzoate. In addition p-hydroxymercuribenzoate shows saturation kinetics. Neither sulfhydryl inhibitor completely inactivates the enzyme. The enzyme is described as having three sulfhydryl groups per subunit, one of which is inaccessible to the sulfhydryl specific reagents when the protein is in the native state. One of the two accessible sulfhydryl groups is either near the active site or essential in maintaining the structure of the protein.

Acetoacetates↗
PubMed1981

Failure of muscarinic blockade to antagonize analepsis induced by thyrotropin-releasing hormone and MK-771 in the rat.

In the rat, the antimuscarinics atropine and scopolamine failed to block the reduction in pentobarbital-induced sleep time produced by either thyrotropin-releasing hormone (TRH) or MK-771 (a TRH analog). Previous reports have indicated that the marked analeptic effect produced by TRH is antagonized by such agents. It is not clear at this time whether the difference between our findings and these previous studies indicates a reduced sensitivity of cholinergic receptors in the rat to muscarinic blockade, a different neurochemical mechanism of action of TRH in the rat, or other unknown factors.

Animals↗
PubMed1979

Scaling current and energy with body weight: requirements for the transthoracic ventricular defibrillation of calves as they grow from 50 to 150 kg.

To test the hypothesis that the effectiveness of a shock in achieving ventricular defibrillation is relatively independent of body weight if electrode diameter is proportional to the one-third power and current is proportional to the two-thirds power of weight, we studied defibrillation rates in 10 calves as they increased weight. At 50 kg, each calf was subjected to 20 fibrillation-defibrillation episodes using 10.3-cm diameter electrodes and 32-amp, 4-msec rectangular pulses for defibrillation. Two days after the original study, each calf underwent 20 additional episodes involving 44-amp pulses. With the specified scaling of electrode diameter and pulse amplitude, the two studies were repeated at weight intervals of 25 kg as the animals grew. Six calves survived. In the study that started with 32-amp pulses, first-shock success values of 28%, 49%, 66%, 51% and 23% were found in the six surviving calves at 50, 75, 100, 125 and 150 kg, respectively. The corresponding values were 93%, 96%, 93%, 94% and 91% in the study that started with 44-amp pulses. While the results of the 32-amp study fail to support our initial hypothesis, those obtained in the 44-amp current study appear compatible with the hypothesis.

Animals↗