Biomedical subjects

M E Trulson

Publications and source records attributed to M E Trulson.

At least 19 recordsLinked to original sources

PubMed1988

Ethanol alters microvasculature enzymes in the rat forebrain.

Forebrain arterioles were analyzed histochemically to determine the effects of an acute administration of ethanol on key enzymes of aerobic and anaerobic metabolism as well as on the hexose monophosphate shunt in rats. The enzymes were glucose 6-phosphate dehydrogenase, cytochrome oxidase, lactate dehydrogenase, beta-hydroxybutyrate dehydrogenase, and isocitrate dehydrogenase. All enzymes were quantified under two conditions: 1 h and 2 days after ethanol administration. Significant changes were noted in four of the five enzymes measured after 1 h and in all five enzymes when measured 2 days after ethanol administration. Our data suggest that ethanol may cause impaired metabolism in the forebrain microvasculature, which, in turn, may account for some of the characteristic behavioral effects of acute ethanol administration.

Animals↗

PubMed1987

Low doses of L-tryptophan are lethal in rats with adrenal insufficiency.

Adrenalectomy decreased the LD50 value for L-tryptophan from greater than 1000 mg/kg in normal rats to 11.6 mg/kg. The LD50 in adrenalectomized rats was restored to normal by corticosterone replacement therapy. Administration of metyrapone, which blocks the synthesis of adrenal steroids, to normal rats decreased plasma corticosterone levels by approximately 50% and decreased the LD50 from greater than 1000 mg/kg to 24.9 mg/kg. Neurochemical analysis revealed a large increase in tissue tryptamine levels following administration of L-tryptophan in rats with adrenal insufficiency. Therefore, it appears that death due to L-tryptophan in animals with adrenal insufficiency is due to formation of excess tryptamine and, consequently, an elevation in blood pressure and other cardiovascular dysfunctions.

Adrenal Insufficiency↗

PubMed1987

Dopamine neuron transplants: electrophysiological unit activity of intrastriatal nigral grafts in freely moving cats.

Fetal transplants of substantia nigra dopamine (DA)-containing neurons into the caudate nucleus in cats produced functional synaptic connections, as measured by behavioral analysis. Electrophysiological activity of single units from the intrastriatal nigral grafts revealed that these neurons displayed some of the characteristic electrophysiological parameters of DA neurons, i.e., long duration action potentials and tri-phasic waveform. However, these neurons discharged at a faster rate and never displayed the characteristic decremental burst pattern seen in intact, non-grafted animals. These data are the first electrophysiological recordings of grafted DA neurons in freely moving animals.

Action Potentials↗

PubMed1987

Phencyclidine suppresses the activity of midbrain dopamine-containing neurons recorded from mouse brain slices in vitro.

Phencyclidine produced a dose-dependent decrease in the activity of dopamine-containing neurons in the substantia nigra and ventral tegmental area recorded from mouse brain slices in vitro. The suppression of dopamine neuronal activity by phencyclidine was blocked by pretreatment of the animals with alpha-methyl-para-tyrosine or haloperidol. These data are in contrast with previous studies which reported that the activity of many midbrain dopamine neurons is increased by phencyclidine, while others are decreased and yet others showed no change.

Animals↗

PubMed1987

Recording of mouse ventral tegmental area dopamine-containing neurons.

We examined the electrophysiologic and pharmacologic properties of dopamine-containing ventral tegmental area neurons in the mouse using extracellular single-unit recording techniques in both chloral hydrate-anesthetized mice and in vitro mouse midbrain slices. In vivo the ventral tegmental area neurons had long-duration action potentials (2 to 5 ms) and discharged at 1 to 9 spikes/s with either a decremental burst pattern or a regular pattern. Systemic administration of the dopamine agonist, apomorphine, decreased their firing rate, and the dopamine receptor blocker, haloperidol, reversed this effect. Similarly, systemic administration of the dopamine-releasing agent, d-amphetamine, suppressed their discharge rate, an effect blocked by pretreatment of the animals with alpha-methyl-p-tyrosine. When recorded in vitro from midbrain slices, ventral tegmental area neurons showed electrophysiologic properties similar to those found in vivo; however, the neurons recorded in vitro fired at a significantly faster rate and their firing pattern tended to be more pacemaker-like, especially when recordings were made in an incubation medium that blocked synaptic transmission (i.e., low calcium/high magnesium). The activity of most of these neurons was suppressed by addition of apomorphine to the incubation medium, an effect reversed by haloperidol. Pretreatment with alpha-methyl-p-tyrosine produced no significant change in the discharge pattern or rate for cells recorded in vitro. These data indicate that mouse ventral tegmental area dopamine neurons in vivo exhibit the same electrophysiologic and pharmacologic properties as do rat and cat dopamine-containing neurons and that in vitro they fire with pacemaker regularity in a low-calcium/high-magnesium medium. The in vitro preparation offers an approach to examining the fundamental properties of ventral tegmental area dopamine-containing neurons in the absence of afferent inputs.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1987

Chronic cocaine administration decreases dopamine synthesis rate and increases [3H] spiroperidol binding in rat brain.

Chronic administration of cocaine HCl (10 mg/kg, IP, every 12 hours for 10 consecutive days) resulted in a significantly decreased rate of accumulation of 3,4-dihydroxyphenylalanine following decarboxylase inhibition (-27 to -33%) and of homovanillic acid following probenecid treatment (-25 to -34%) in rat striatum, limbic forebrain and midbrain. In addition, the Bmax for [3H]-spiroperidol receptor binding was significantly increased (+24 to +36%) in these brain regions following chronic cocaine administration. These changes were observed 60 days following termination of the chronic cocaine treatment regimen. These data suggest that cocaine produces long-term, if not permanent, effects on central dopamine synthesis.

Animals↗

PubMed1987

Chronic cocaine administration depletes tyrosine hydroxylase immunoreactivity in the meso-limbic dopamine system in rat brain: quantitative light microscopic studies.

Chronic administration of cocaine (10 mg/kg, IP, every 12 hours for 10 consecutive days) produced a large decrease in tyrosine hydroxylase staining axons and terminal boutons in the frontal cortex and nucleus accumbens in rats. This treatment also produced a depletion of tyrosine hydroxylase immunoreactivity in the ventral tegmental area of the midbrain when examined 60 days following the final cocaine injection. These effects were quantitated using a Leitz Data Acquisition and Display System. This analysis revealed a 59% and 65% decrease in tyrosine hydroxylase positive staining terminal processes in the frontal cortex and nucleus accumbens, respectively. Furthermore, quantitative light microscopic analysis showed a 52% decrease in tyrosine hydroxylase positive material in the ventral tegmental area. These data demonstrate that chronic administration of cocaine produces a long-term, if not permanent, loss of tyrosine hydroxylase enzyme in both the cell bodies of the midbrain ventral tegmental area as well as in the nerve terminals in post-synaptic target regions of the forebrain.

Animals↗

PubMed1987

A comparison of the electrophysiological and pharmacological properties of serotonin-containing neurons in the nucleus raphe dorsalis, raphe medianus and raphe pallidus recorded from mouse brain slices in vitro: role of autoreceptors.

The potential role of autoreceptors in regulating the activity of serotonin-containing nucleus raphe dorsalis (RD), raphe medianus (RM) and raphe pallidus (RPA) neurons was examined by recording the activity of these neurons under a variety of conditions both in vivo and in vitro. Raphe neurons recorded in vivo displayed the characteristic slow, rhythmic discharge pattern previously described for rat and cat raphe cells. The activity of these neurons was suppressed in a dose-dependent manner by tryptophan, LSD and chlorimipramine administered intravenously. There were no significant changes in the spontaneous discharge rate of raphe neurons over time when recorded in vitro, even though tissue serotonin and its metabolite, 5-hydroxyindoleacetic acid, decreased dramatically. RPA neurons fired significantly faster than either RD or RM neurons both in vivo and in vitro. Prior depletion of brain serotonin by p-chlorophenylalanine administration resulted in no significant change in raphe unit activity recorded in vitro. Elevation of brain serotonin by monoamine oxidase inhibition produced a total inhibition of raphe unit activity in vitro. Similarly, increasing the concentration of serotonin in the tissue slice by adding serotonin directly to the incubation medium resulted in a profound, though transitory, depression of unit activity. This depressant effect of serotonin was rapidly reversible upon drug wash-out. Serotonin receptor blockers, methiothepin, cypoheptadine, and methysergide, produced no significant change in unit activity. The serotonin reuptake blocker, fluoxetine, produced a total inhibition of raphe unit activity in all three nuclei in vitro. These data suggest that excess serotonin suppresses the activity of raphe neurons, apparently by an action on autoreceptors, but that a deficiency, or normal concentration, of serotonin does not influence the spontaneous activity of these cells. The data also show that RD and RM are much more sensitive to the depressant effects of serotonin than the caudal RPA neurons. More generally, these studies provide a data base for examining the electrophysiological and pharmacological characteristics of serotonergic neurons in the three major serotonin-containing nuclei in mouse brain. The mouse has proven to be a much easier species than the rat to use in these types of studies, based on the finding that mouse brain slices are more viable in vitro than are rat brain slices.

Action Potentials↗

PubMed1987

Tyrosine hydroxylase immunochemistry and quantitative light microscopic studies of the mesolimbic dopamine system in rat brain: effects of chronic methamphetamine administration.

Long-term treatment of rats with methamphetamine (20 mg/kg, IP, every 12 hours for 10 days) resulted in a large decrease in tyrosine hydroxylase staining axons and terminal boutons in the nucleus accumbens and frontal cortex, as well as the ventral tegmental area of the midbrain, when examined 60 days following termination of the drug treatment regimen. Quantitative analysis showed a 71 and 78% decrease in tyrosine hydroxylase staining processes in the nucleus accumbens and frontal cortex, respectively, and a 90% decrease in tyrosine hydroxylase positive material in the ventral tegmental area. Thus, tyrosine hydroxylase enzyme in both the cell bodies of the midbrain ventral tegmental area as well as in the nerve terminals in post-synaptic target regions of the forebrain is depleted by chronic methamphetamine administration.

Animals↗

PubMed1987

Mesencephalic arteriolar and neuronal metabolic profiles from fresh and in vitro incubated tissue sections in the mouse: a histochemical approach.

Neuronal perikarya and arterioles of slices of mouse midbrain were examined histochemically to determine their metabolic profiles. No differences in reactivities of key metabolic enzymes were observed between fresh 400-micron tissue sections and sections undergoing in vitro incubation for 4 h at 35 degrees C. Both neurons and arterioles appear capable of aerobic and anaerobic metabolism, while fatty acid utilization is limited. An operative hexose-monophosphate shunt occurs in midbrain neurons and arterioles. These data strongly suggest that electrophysiological and neurochemical studies using the in vitro preparation yield similar data to those obtained from fresh tissue.

Animals↗

PubMed1987

Cocaine: long-term administration depletes cardiac enzymes in the rat.

Arterioles and myocytes of the cardiac ventricle were examined histochemically to determine their metabolic profiles in normal rats and in rats treated either acutely or chronically with cocaine. Following long-term, but not acute, cocaine administration, enzymes involved in both aerobic and anaerobic metabolism as well as in hexosemonophosphate shunt were greatly decreased. These data suggest that long-term usage of cocaine leads to severely impaired coronary metabolism.

Adenosine Triphosphatases↗

PubMed1987

Acute administration of chloral hydrate depletes cardiac enzymes in the rat.

The arterioles of the left cardiac ventricle were analyzed histochemically to determine the effects of an acute administration of chloral hydrate on key enzymes of aerobic and anaerobic metabolism, as well as the hexosemonophosphate shunt in rats. Significant changes were noted in three of the 5 enzymes examined. Our data suggest that nontoxic levels of chloral hydrate can cause impaired coronary metabolism.

Aerobiosis↗

PubMed1987

Halothane anesthesia alters cerebral enzymes: a histochemical study in the rat.

Cerebral forebrain arterioles and neuropil were analyzed histochemically to determine the effects of halothane anesthesia on key enzymes of aerobic and anaerobic metabolism, as well as the hexose monophosphate shunt in rats. Significant changes were noted in all five enzymes examined in arterioles, while no changes were observed in the two enzymes involved in aerobic metabolism in the neuropil. Our data suggest that surgical anesthetic levels of halothane can impair forebrain metabolism and lead to altered electrophysiological responses.

Anesthesia↗

PubMed1987

Chloral hydrate anesthesia alters cerebral enzymes in the rat. A histochemical study.

Cerebral forebrain arterioles and neuropil were analyzed histochemically to determine the effects of chloral hydrate anesthesia on key enzymes of aerobic and anaerobic metabolism, as well as the hexose monophosphate shunt in rats. Significant decreases were observed in cytochrome oxidase, and beta-hydroxybutyrate dehydrogenase in arterioles, while glucose-6-phosphate dehydrogenase and isocitric dehydrogenase showed a significant increase and lactate dehydrogenase showed no significant change. In the neuropil, cytochrome oxidase, isocitrate dehydrogenase and glucose-6-phosphate dehydrogenase showed significant increases following chloral hydrate administration, while beta-hydroxybutyrate dehydrogenase and lactate dehydrogenase showed no significant changes. These data suggest that surgical anesthetic levels of chloral hydrate can impair forebrain metabolism which may lead to altered electrophysiological responses.

Anesthesia↗

PubMed1987

Halothane depletes cardiac microvasculature enzymes in the rat.

Left ventricular arterioles from Sprague-Dawley rats were analyzed histochemically to determine the effects of halothane administration on key enzymes of aerobic and anaerobic metabolism, as well as on key enzymes of the hexose monophosphate shunt. Significant decreases occurred in cytochrome oxidase (-42%) and beta-hydroxybutyrate dehydrogenase (-57%). No significant changes were observed in isocitrate dehydrogenase, glucose-6-phosphate dehydrogenase, or lactate dehydrogenase. These data suggest that anesthetic levels of halothane can cause impaired metabolism in the coronary microvasculature.

Animals↗

PubMed1986

Effects of dopamine and amphetamine on mouse caudate neurons recorded in vitro.

Mouse caudate neurons recorded from brain slices in vitro displayed one of three different types of electrophysiological activity. These were: (a) a regular, pacemaker-like firing pattern; (b) an irregular discharge pattern, and (c) a bursting pattern. Both dopamine and D-amphetamine produced a dose-dependent increase in the activity of the regularly and irregularly firing caudate neurons when placed in the incubation bath, but had no effect on the bursting neurons. These studies demonstrate that the excitatory effect of amphetamine on caudate neurons is due to a direct action on these cells.

Amphetamine↗

PubMed1986

Morphine increases locus coeruleus noradrenergic neuronal activity in vitro.

Morphine produced a dose-dependent increase in the activity of norepinephrine-containing locus coeruleus neurons recorded from mouse brain slices in vitro. The response was not changed in a low calcium-high magnesium incubation medium, indicating that the observed effects are the result of a direct action of morphine on locus coeruleus neurons. When the mice were anesthetized with chloral hydrate prior to preparation of tissue slices, morphine produced a dose-dependent suppression of noradrenergic neuronal activity. These studies suggest that previous data showing a decrease in activity of locus coeruleus neurons following incubation with morphine in vitro are due to the use of anesthesia.

Animals↗

PubMed1986

A histochemical examination of the metabolic profiles of rat ventral tegmental area and substantia nigra arterioles.

To determine the metabolic profiles of arterioles of the rat ventral tegmental area and zona compacta and zona reticulata of the substantia nigra (SN), the distribution of selected enzymes, or by-products, of key metabolic pathways were examined histologically. Arterioles of all three regions expressed the enzymes required for aerobic and anaerobic metabolism. However, the relative abundance of the enzymes and byproducts suggests a lower metabolic capacity for the SN than the ventral tegmentum, while lipid catabolism in both regions appears non-operative. Moreover, the larger ventral tegmental arterioles possess a greater potential for nucleic acid and protein synthesis. Together, these results suggest the larger ventral tegmental arterioles possess a greater capacity for proliferation and repair.

Animals↗