Stress-induced increases in brainstem amino acid levels are prevented by chronic sodium hydrosulfide treatment.

Neurotransmitter amino acid levels were measured in select brain regions of rats and mice after chronic treatment with sublethal doses of sodium hydrosulfide (NaHS). Brainstem aspartate, glutamate, glutamine, taurine and GABA levels increased in chronically but not acutely saline-treated rats. These increases may have been due to stress from frequent handling, and were prevented by chronic NaHS treatment (7.

Dithiothreitol liberates non-acid labile sulfide from brain tissue of H2S-poisoned animals.

Acid-labile sulfide measured by conventional gas dialysis and ion chromatography with electrochemical detection accounts for only a proportion of the total sulfide present in brain tissue after poisoning with NaHS, an H2S precursor. Dithiothreitol (DTT) displaced additional measurable sulfide not detectable by the conventional techniques from NaHS-poisoned brain tissue. Sulfide liberation by DTT was dose-dependent and maximal at higher DTT concentration (10 and 30 mM) and was thought to represent non-acid labile sulfide.

Decreases in behavioral and striatal neuronal responses to dexamphetamine with aging.

Striatal neurons of mature rats responded to 2.5 mg/kg dexamphetamine with increased multiple unit activity that followed the time course of drug-increased behavior. In contrast, in older (middle-aged) rats striatal neurons failed to respond to dexamphetamine with excitation.

Brain sulfide levels in anaesthesia: a comparison with hydrogen sulfide intoxication.

Although sublethal concentrations of hydrogen sulfide produce a state not unlike anaesthesia, measurement of rat brain sulfide levels by gas dialysis and IC with electrochemical detection after either 1.5 g/kg urethane or 42 mg/kg pentobarbital failed to demonstrate any changes as compared with endogenous brain sulfide levels of saline-injected controls. This suggests that the mechanisms underlying anaesthesia are not directly linked to endogenous cerebral sulfide levels.

Acute hydrogen sulfide poisoning. Demonstration of selective uptake of sulfide by the brainstem by measurement of brain sulfide levels.

The possibility of measuring sulfide levels in the central nervous system (CNS) opens up many avenues for exploration. In acute hydrogen sulfide (H2S) poisoning, death results from loss of central respiratory drive. To date, however, measurement of brain sulfide has not been possible.

Determination of sulfide in brain tissue by gas dialysis/ion chromatography: postmortem studies and two case reports.

An analytical method for the determination of sulfide in human and rat brain is described. It utilizes a continuous flow gas dialysis pretreatment and quantitation by ion chromatography with electrochemical detection. Rat brain sulfide levels were reliably measured after fatal intoxication by intraperitoneal injection of NaHS.

Monoamine oxidase inhibition as a sequel of hydrogen sulfide intoxication: increases in brain catecholamine and 5-hydroxytryptamine levels.

Administration of sodium hydrosulfide (NaHS), an alkali salt of hydrogen sulfide (H2S) at doses of 10 and 30 mg/kg, corresponding to sublethal and lethal doses (0.66 and 2.0 X LD50) resulted in significant increases in regional catecholamine levels of the rat brain only after the dose of 2.

Pharmacological activity profiles of dopamine D-1 and D-2 reception agonists and antagonists on striatal neuronal activity and the response to dexamphetamine in freely moving rats.

1. The effects of dopamine D-1 and D-2 receptor agonists and antagonists were investigated by recording extracellular striatal action potentials in freely moving rats. Dopamine receptor antagonist effects were also evaluated on dexamphetamine-induced excitation of striatal neurons.

Hydrogen sulfide in combination with taurine or cysteic acid reversibly abolishes sodium currents in neuroblastoma cells.

Patch clamp studies of neuroblastoma cells have shown that in the presence of sodium hydrogen sulfide (NaHS; the in vitro precursor of H2S), addition of the sulfonated amino acids, taurine or cysteic acid resulted in reversible abolition of the inward sodium currents. This effect could also be demonstrated by preincubating cells for 3-20 min with 5-10 mM NaHS followed by replacement of the solution with taurine or cysteic acid in sulfide-free saline. Neither NaHS, taurine nor cysteic acid alone had any effect.

Excitation of striatal neurons by dexamphetamine is not abolished by either chloral hydrate or urethane anaesthesia.

In order to understand differences between studies maintaining that dopamine actions are significantly reduced as a result of chloral hydrate anaesthesia or not affected to any appreciable extent, striatal neuronal responses to the indirect dopamine agonist, dexamphetamine, were examined in rats anaesthetized with either chloral hydrate (400 mg/kg) or urethane (1.5 g/kg). Striatal neuronal activity was markedly depressed by chloral hydrate and urethane.

Effects of acute intoxication with hydrogen sulfide on central amino acid transmitter systems.

The acute effects of hydrogen sulfide (H2S) on brain amino acid levels were examined in five regions of the rat brain following administration of either saline (controls), or 10 or 30 mg/kg i.p. of sodium hydrosulfide (NaHS).

The effects of cortical ablation on multiple unit activity in the striatum following dexamphetamine.

Bilateral removal of the fronto-parietal cortex of the rat resulted in decreased spontaneous multiple-unit activity recorded in the striatum of freely-moving rats. Cortical ablations changed the neuronal response in the striatum to systemic administration of dexamphetamine (2.5 mg/kg i.

Activation of striatal neurons by dexamphetamine is antagonized by degeneration of striatal dopaminergic terminals.

Unilateral degeneration of nigrostriatal dopaminergic terminals by the intranigral infusion of 6-OHDA produced a decrease in spontaneous multiple unit activity (MUA) in both the ipsilateral and contralateral striata of freely moving rats. Nigral lesions also attenuated the dexamphetamine-induced increase in MUA in the ipsilateral but not in the contralateral striatum. The magnitude of the attenuation in the ipsilateral striatum was directly proportional to the percent depletion of dopamine.

Immobilization of rats modifies the response of striatal neurons to dexamphetamine.

The effect of dexamphetamine (DEX) on striatal multi-unit activity was examined in freely moving rats and again 24 or 48 hr later during immobilization. Animals which in the freely moving state responded with striatal activation following DEX, 1 mg/kg IP, did not respond to this dose of DEX after immobilization. Similarly with DEX 2.

The role of afferents from the parafascicular-centromedian complex in the excitatory striatal neuronal response to dexamphetamine in freely moving animals.

The striatal neuronal response to dexamphetamine, 2.5 mg/kg, was studied in normal freely moving animals and in freely moving animals with unilateral lesions of the parafascicular-centromedian complex. Whereas dexamphetamine produced predominantly excitation of striatal neurons in control animals, the predominant response in lesioned animals was inhibition.

Responses of striatal neurons to anesthetics and analgesics in freely moving rats.

The effects of anaesthetics and analgesics on striatal neurons were examined in freely moving rats by recording extracellular action potentials of neurons in the striatum. Spontaneous multiple unit activity was reduced to less than 20% of control firing rates following either pentobarbital 35 mg/kg i.p.

Bilateral ablation of the corticostriatal projection: behavioral, biochemical and electrophysiological correlates.

Striatal neuronal responses to dexamphetamine, 2.5 mg/kg i.p.

The effects of the ionophore A-23187 on the rat vas deferens.

The calcium ionophore A-23187 induced spontaneous, rhythmic contractions in the rat isolated vas deferens in a concentration-dependent manner. Contractions were blocked by phentolamine and were abolished following pretreatment with reserpine. In tissues preloaded with [3H]noradrenaline, A-23187 (10 microM) caused a time-dependent increase in the release of tritium.

Immobilization-induced changes in the response of striatal neurons to dexamphetamine.

Bipolar multiple unit recording electrodes were implanted in the striata of male Long-Evans rats 5-7 days prior to experimentation. In subsequent experiments, striatal neuronal activity in response to dexamphetamine (1.0 or 2.

Specific immune gammaglobulin in the control of Mycoplasma meleagridis.

Turkey embryos naturally infected with Mycoplasma meleagridis were treated with different fractions of turkey immunoglobulins obtained from either abattoir or hyperimmune sera. The whole crude globulin fraction, IgG or IgM, were injected directly into the yolk sac of infected embryos. Embryos that died during incubation were broken out, aged, and the yolk sac contents cultured for M.

Effects of biotin, folic acid, and pantothenic acid on the growth of Mycoplasma meleagridis, a turkey pathogen.

The biotin, folic acid, and pantothenic acid requirements of Mycoplasma meleagridis were determined in vitro by examining the growth and survival of the organism in the presence of varying concentrations of these factors. Growth and survival were also studied in the presence of aminopterin and methotrexate which prevent utilization of folic acid, and in the presence of avidin, a known biotin antagonist. Whereas pantothenate appeared to have no obvious effect on growth or survival, folate was marginally stimulatory at only the highest concentration tested.

Identification of Trypanosoma theileri as a contaminant in primary cultures of bovine retina.

T. theileri has been isolated from primary cultures of bovine retina and subcultered successfully for 2 passages in sub-confluent cultures. When cultures reached confluency no trypomastigotes or epimastigotes could be detected and attempts to recover trypanosomes from these cultures were unsuccessful.

Modification of the contractile responses of rabbit mammary strips to oxytocin by prostaglandin E1.

PGE1 administration to isolated strips from pregnant and lactating rabbit mammary gland resulted in different effects on oxytocin-induced contractions. In strips from pregnant animals, oxytocin action was enhanced; in those from lactating animals, it was reduced and threshold doses for oxytocin were markedly higher.