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S Auerbach

Publications and source records attributed to S Auerbach.

At least 37 records · Page 2Linked to original sources
PubMed1985

Serotonin turnover in raphe neurons transplanted into rat hippocampus.

Injections of the neurotoxin, 5,7-dihydroxytryptamine, into rostral raphe nuclei in rats reduced serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) in hippocampus to 35-50% of normal levels but only reduced 5-HT synthesis and catabolism by 20-35%. The small reduction in 5-HT metabolism as compared to depletion of 5-HT suggests that 5-HT turnover was increased in nerve terminals that survived the neurotoxin lesion. Transplantation of rat fetal raphe cells into the 5-HT-denervated hippocampus restored 5-HT and 5-HIAA levels and 5-HT synthesis to 125-150% of normal. This demonstrates that transplantation of fetal raphe tissue can restore metabolism to normal levels in the 5-HT denervated hippocampus.

5,7-Dihydroxytryptamine↗
PubMed1985

Activity of serotonin-containing neurons in nucleus raphe magnus in freely moving cats.

Serotonergic neurons were recorded in the nucleus raphe magnus in freely moving cats and were initially identified on-line by their characteristic slow and regular spontaneous activity during quiet waking (3.42 +/- 0.33 spikes/s; mean +/- SE). Discharge rates of these serotonergic neurons were highest during active waking (4.49 +/- 0.40 spikes/s), intermediate during slow-wave sleep (middle: 2.14 +/- 0.23 spikes/s), and lowest during REM sleep (0.20 +/- 0.03 spikes/s). Although these cells fired at a rate 31.3% higher during active waking than during quiet waking, their activity displayed no correlation with phasic elevations of the nuchal EMG or overt body movements. In addition, no relationship was observed between the activity of these neurons during slow-wave sleep and the occurrence of sleep spindles in the cortical EEG or pontogeniculooccipital waves recorded from the lateral geniculate nucleus. Serotonergic neurons of nucleus raphe magnus were also relatively unresponsive to phasic auditory and visual stimuli, with about half of the cells examined showing weak excitatory responses. These neurons did respond, however, to the administration of a small dose of the serotonin specific agonist, 5-methoxy-N,N-dimethyltryptamine (250 micrograms/kg, i.m.) with a mean decrease in unit activity of 73.6 +/- 4.5%. The results of this study are compared with those previously reported for serotonergic neurons in the dorsal raphe nucleus, nucleus centralis superior, and nucleus raphe pallidus of freely moving cats.

Acoustic Stimulation↗
PubMed1985

Response of serotonin-containing neurons in nucleus raphe magnus to morphine, noxious stimuli, and periaqueductal gray stimulation in freely moving cats.

Extracellular single-unit recordings were made in nucleus raphe magnus in unanesthetized, unrestrained cats. Discharge of serotonergic neurons in this region was increased when animals were aroused by noxious stimuli such as pinch and radiant heating of the tail, but these cells were not specifically nociceptive. Peristimulus time histograms indicated that stimulation in the periaqueductal gray was excitatory but alveolar nerve stimulation at a noxious current intensity was no more effective than nonnoxious nerve stimulation in activating serotonergic unit discharge: Similarly, stressful treatments such as physical restraint increased the discharge of some serotonergic neurons, but these cells were activated during any period of behavioral arousal whether or not arousal was the result of aversive treatment. Injection of Formalin into the paw produced pain lasting about 30 min without increasing serotonergic unit discharge above rates observed during undisturbed active waking behavior. The activity of serotonergic neurons was not increased by an analgesic dose of morphine (2 mg/kg, i.p.). These results then are not consistent with the hypothesis that morphine analgesia depends on activation of serotonergic neurons in nucleus raphe magnus or that these cells are specifically involved in modulation of nociception. These neurons may, however, be involved in nociceptive control within the context of a general modulation of sensorimotor processes by serotonin in the central nervous system. We did observe neurochemically unidentified neurons in the medulla whose discharge was more specifically activated by aversive stimuli and also by morphine. It is possible that these neurons are more directly involved in the mediation of opiate and/or stress-induced analgesia.

Analgesia↗
PubMed1985

Regulation of serotonin release from the in vitro rat hippocampus: effects of alterations in levels of depolarization and in rates of serotonin metabolism.

We analyze the time course of 5-hydroxytryptamine (5-HT, serotonin) release from K+-depolarized hippocampal slices using a two-compartment kinetic model. The model is based on the assumptions that the rate of release is dependent on the amount of 5-HT in a releasable pool and that this pool may be resupplied during depolarization by newly synthesized 5-HT. Comparisons were made between predictions of the model and observed changes in 5-HT metabolism and in 5-HT release studied under a variety of experimental conditions. In accordance with predictions of the model, experimental manipulation of 5-HT synthesis and breakdown rates did not affect release immediately after depolarization but did affect the release rate during prolonged depolarization. Increasing bath tryptophan from 0 to 10 microM approximately doubled both 5-HT synthesis and the release rate after 40 min of K+-induced depolarization while having a smaller effect on release during the first 2 min. Inhibition of 5-HT breakdown did not significantly affect release during the first 2 min of depolarization but increased it over threefold after 40 min. In contrast, altering the concentrations of K+ or Ca2+ in the incubation medium affected mainly the early phase of 5-HT release and not the late phase. Reducing Ca2+ from 2.4 to 0.4 mM reduced 5-HT release by about 30% during the first 9 min of depolarization but did not affect release during the subsequent 30 min. Increasing the concentration of K+ from 18 to 60 mM stimulated release by sixfold during the first 2 min but only twofold after a subsequent 30 min. These results support our kinetic model and suggest that regulation of 5-HT metabolism at the site of the nerve terminal could be a mechanism for modulation of 5-HT release during prolonged discharge of serotonergic neurons.

Animals↗
PubMed1982

Effect of increased oxygen affinity and anemia on cardiac output and its distribution.

Effect of increased blood O2 affinity on cardiac output and its distribution was studied in conscious sedated rats by the microsphere-reference sample method. After a preliminary measurement of cardiac output and its distribution, rats were exchange transfused with normal blood or low-P50 (PO2 at which hemoglobin is half-saturated with O2) blood; other groups were made anemic with and without a simultaneous reduction in P50. Reduction in P50 from 38 to 17 Torr did not change cardiac output, pulse, or blood pressure but caused, after allowance for changes in controls, a 102% increase in coronary blood flow and an 88% increase in cerebral blood flow. Anemia (hematocrit = 22%) produced similar changes in coronary and cerebral flow. When anemia was combined with a 12-Torr reduction in P50, coronary and cerebral flow increased by 297 and 209%, respectively. These increases in coronary and cerebral flow were not attributable to increased cardiac work or hypercapnia. It is concluded that a left shift of the O2 dissociation curve induces increased blood flow to brain and heart, probably in compensation for decreased tissue O2 pressure.

Anemia↗
PubMed1982

Vasopressin augments depolarization-induced release and synthesis of serotonin in hippocampal slices.

Vasopressin may be a neurotransmitter and in vivo experiments suggest that it acts on monoamine metabolism. The rat hippocampal slice contains serotonergic nerve terminals but not cell bodies; we studied the effect of vasopressin on the synthesis and release of serotonin from these nerve terminals during depolarization. Incubation of slices in a buffer containing 60 mM K+ (high K buffer) for 10 min stimulated the release of serotonin into bathing medium and resulted in a Ca2+-dependent depletion of tissue serotonin from about 4.2 to about 2.8 ng/mg of protein. Vasopressin (10(-7) M) inhibited this depletion by about 70% so that serotonin levels fell only to 3.8 ng/mg of protein. The peptide also augmented the high K+-induced release of serotonin into the bathing medium by about 60%. The synthesis of serotonin was measured by determining its accumulation during a period when its catabolism was inhibited by pargyline. Vasopressin augmented the synthesis of serotonin in slices incubated in high K buffer by about 60%. There are serotonergic nerve endings in both the dentate gyrus and CA1 regions of the hippocampus. The effect of vasopressin on tissue serotonin was confined to the dentate gyrus regions. The data show that vasopressin acts on a specific group of hippocampal nerve endings to increase serotonin synthesis. The resulting increase in tissue serotonin may be the factor leading to the observed increase in serotonin release.

Animals↗
PubMed1975

Metabolic stability of messenger ribonucleoprotein in HeLa cells.

The proteins bound to HeLa cell polyribosomal messenger RNA were isolated by subjecting salt-washed, puromycin-disassembled polyribosomes to a limited digestion with pancreatic ribonuclease (ref. 1, Auerbach, S. and Pederson, T. (1975) Biochem. Biophys. Res. Commun. 63, 149-153). Label-chase experiments with radioactive amino acids revealed that the in vivo decay kinetics of the messenger RNA-associated proteins were approximately first-order, with t1/2 equal 13-15 h. The results suggest that HeLa messenger RNA and its specific set of associated proteins do not behave as single units metabolically.

Drug Stability↗
PubMedDate not supplied

Protein kinase C activation induces conductance changes in Hermissenda photoreceptors like those seen in associative learning.

Phosphorylation of ion channels has been suggested as one molecular mechanism responsible for learning-produced long-term changes in neuronal excitability. Persistent training-produced changes in two distinct K+ currents (IA (ref. 2), IK-Ca (refs 3,4)) and a voltage-dependent calcium current (ICa; refs 3,4) have previously been shown to occur in type B photoreceptors of Hermissenda, as a result of associative learning. But the identity of the phosphorylation pathway(s) responsible for these changes has not as yet been determined. Injections of cyclic AMP-dependent protein kinase reduce a K+ current (IK) in B cells which is different from those changed by training, but fails to reduce IA and IK-Ca. Phosphorylase b kinase (an exogenous calcium/calmodulin-dependent kinase) reduces IA, but whether IK-Ca and ICa are changed in the manner of associative training is not yet known. Another protein kinase present in high concentrations in both mammalian brain and molluscan nervous systems is protein kinase C, which is both calcium- and phospholipid-sensitive. We now present evidence that activation of protein kinase C by the tumour promoter phorbol ester (PDB) and intracellular injection of the enzyme induce conductance changes similar to those caused by associative training in Hermissenda B cells (that is a reduction of IA and IK-Ca, and enhancement of ICa). These results represent the first direct demonstration that protein kinase C affects membrane K+ ion conductance mechanisms.

Animals↗
PubMedDate not supplied

Trauma registrar training: integrating registry functions into the trauma program--Part I.

The University of Pennsylvania Health System Trauma Network views the registry staff as key members of the trauma team and the registry as a vital component to the overall success of our programs. Trauma Registry databases are increasingly complex and require highly skilled and knowledgeable personnel to perform the functions of the job. Although the background and experience level of each registry staff member may differ, this orientation and training process provides a consistent educational experience for all. This guideline ensures that all registry functions are being performed in a standardized and consistent manner. It sets the stage for validation of not only the data, but also an individual's performance relative to abstraction and computer entry. Providing the proper learning environment for registry staff has proven to be most beneficial for our network as we strive to develop and maintain trauma registry databases which have a strong foundation and provide valid, useful and current information.

Abstracting and Indexing↗
PubMedDate not supplied

Trauma registrar training: integrating registry functions into the trauma program--Part 2.

Effective health-information management is heavily reliant upon the data-collection process of the health care program. This is also true in trauma-care systems, where healthcare providers have come to rely on timely access to complete and accurate information to support many critical functions of a trauma program. The process by which data are collected and analyzed deserves constant attention and reassessment. Data obtained in reports and analyses are only as accurate as the data abstraction and validation processes allow. The University of Pennsylvania Health System Trauma Network recognizes this, and as a result, developed this training and orientation guideline. This guideline supports the importance of the registry role in the overall trauma program, but most importantly, it fosters and supports a team approach to data collection, which in our experience has allowed us to develop and maintain trauma registry databases which provides valid, useful and current information for all.

Curriculum↗