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M Segal

Publications and source records attributed to M Segal.

At least 271 records · Page 15Linked to original sources
PubMed1982

Changes in neurotransmitter actions in the aged rat hippocampus.

Intracellular activity was recorded from pyramidal cells in region CA1 of young and aged rat hippocampal slices. There were no apparent differences between the two age groups in the passive or active membrane properties tested. These included resting membrane potential, input resistance, spike size and overshoot, after potentials, and EPSP's. There were marked differences between the two age groups in reactivity to chemical stimulation. The response to acetylcholine (ACh) in young rat hippocampal cells consisted of an initial hyperpolarization followed by a late, slow depolarization. These were accompanied by a decrease in reactivity of the recorded cell to afferent stimulation. In the old cells the initial hyperpolarization and late depolarization were markedly reduced, yet the decreased reactivity to afferent stimulation was maintained. Both young and old cells were depolarized by GABA to the same magnitude, yet the recovery was slower in the old cells. 5-HT evoked a smaller response in old compared to young cells. These data indicate that some specific physiological processes which are not paralleled by reported biochemical changes are affected by aging. The mechanisms underlying these changes are subject to further investigations.

Acetylcholinesterase↗
PubMed1982

The phosphorylation of proteins in hippocampal slices: effects of noradrenaline and of pretreatment with kainic acid.

Hippocampal slices were incubated in the presence of [32P]P1, and protein phosphorylation was examined by means of sodium dodecyl sulfate-gel electrophoresis. Incubation for at least 30 min with 300 muCi of [32P)P1/brain slice gave rise to the phosphorylation of 8-10 protein bands. Most of these bands showed enhanced phosphorylation in response to noradrenaline. The basal phosphorylation of kainic acid-pretreated hippocampal slices was enhanced two- to threefold compared with controls. There was also an additional increase in kainic acid-pretreatment slices in the response to noradrenaline. 8-Br-Cyclic AMP and phosphodiesterase inhibitors, such as papaverine or isobutylmethylxanthine, had no effect on the phosphorylation patterns.

Animals↗
PubMed1982

Visualization of the spread of electrical activity in rat hippocampal slices by voltage-sensitive optical probes.

1. Voltage-sensitive membrane-bound dyes and a matrix of 100 photodetectors were used to detect the spread of evoked electrical activity at the CA1 region of rat hippocampus slices. A display processor was designed in order to visualize the spread of electrical activity in slow motion.2. The stimulation of the Schaffer collateral-commissural path in the stratum radiatum evoked short latency (2-4 msec) fast optical signals, followed by longer latency (4-15 msec) slow signals which decayed within 20-50 msec. Multiple fast signals were frequently detected at the stratum pyramidale; they propagated toward the stratum oriens with an approximate conduction velocity of 0.1 m/sec.3. The fast signals were unaltered in a low Ca(2+) high Mg(2+) medium but were blocked by tetrodotoxin. These signals probably represent action potentials in the Schaffer collateral axons. Their conduction velocity was about 0.2 m/sec and their refractory period about 3-4 msec.4. The slow signals were absent in a low Ca(2+) medium and probably represent excitatory post-synaptic potentials (e.p.s.p.s) generated in the apical dendrites of the pyramidal cells. They were generated in the stratum radiatum, where the presynaptic signals were seen, and spread into somata and basal dendrites (the stratum pyramidale and oriens, respectively).5. The timing of the signals with fast rise-time, which were detected at the statum pyramidale, approximately coincided with the timing of the extracellularly recorded field potentials. These multiple discharges probably represent action potentials of the pyramidal cells. They spread back into the apical dendrites but with significant attenuation of the amplitudes of the high frequency components of the pyramidal action potentials.6. Hyperpolarizing potentials could be detected when strong stimuli were applied to the stratum radiatum or alveus. The net hyperpolarizations were detected only in the stratum pyramidale and the border region between the stratum pyramidale and radiatum. Frequently the inhibition was masked by the large e.p.s.p.s. However, its existence could be demonstrated by treatment of the slice with picrotoxin or a low Cl(-) medium. Under these conditions a long-lasting depolarization of the apical dedrites was evoked by the stimulation. This was associated with an increase of the multiple discharges in the stratum pyramidale and oriens.7. These studies illustrate the usefulness of voltage-sensitive dyes in the analysis of passive and active electrical properties, pharmacological properties and synaptic connexions in mammalian brain slices, at the level both of small neuronal elements (dendrites, axons) and of synchronously active neuronal populations.

Action Potentials↗
PubMed1982

Schedule-induced defecation.

Excessive defecation, typically considered to be a concomitant of stress, was experimentally induced or eliminated under specific schedules of positive reinforcement of lever pressing by rats. The schedules were, by and large, those under which polydipsia is typically induced. In the first of three experiments, rats under fixed-interval 32-second schedules and variable interval 32-second schedules for food and water reinforcers defecated profusely, but not under fixed-interval one-second schedules or other small interval schedules. Somewhat higher rates of defecation were observed on variable interval 32-second schedules than on fixed-interval 32-second schedules. In a second experiment, fixed-ratio schedules were used, some of which resulted in responding such that reinforcement densities were similar to those on the interval schedules that induced defecation. Defecation was not systematically induced by these ratio schedules. In a third experiment, fixed-time schedules of food presentations were utilized. High rates of defecation were induced comparable to those induced by interval schedules of the same time parameter. No other behavior commonly termed "emotional" was observed in any of these experiments.

Animals↗
PubMed1982

Constriction of the umbilical cord by an amniotic band after midtrimester amniocentesis.

Constriction of the umbilical cord by an amniotic band after previous midtrimester amniocentesis is an extremely rare entity. A case report of fetal asphyxia caused by partial occlusion of the umbilical cord by an amniotic band is presented. Clinical and experimental evidence strongly suggests that the pathogenesis of this defect is related to early rupture of the membranes during gestation with subsequent encirclement and ligation of fetal umbilical cord, or extremities. In this case, formation of the amniotic band caused by midtrimester amniocentesis is strongly suggested. Obstetricians should be aware of this hazardous complication during pregnancy and labor in women who had had a midtrimester amniocentesis.

Adult↗
PubMed1981

Reformation in adult rats of functional septo-hippocampal connections by septal neurons regenerating across an embryonic hippocampal tissue bridge.

Implants of embryonic hippocampus, placed into a cavity transecting the septo-hippocampal pathway in adult rats, have previously been shown to promote the regeneration of the lesional septo-hippocampal axons across the cavity. The present study provides electrophysiological evidence that these regenerating acetylcholinesterase-containing axons are able to re-establish atropine-sensitive excitatory synaptic connections in the grafted hippocampus as well as in the dorsal part of the initially denervated host hippocampus, thus demonstrating that intracerebral tissue implants can promote true, functional regeneration across a major tissue defect in the adult mammalian CNS.

Acetylcholinesterase↗
PubMed1981

Cyclic AMP-generating systems in rat hippocampal slices.

Properties of the norepinephrine (NE) stimulated, cAMP-generating system were studied in rat hippocampal slices. NE but not other putative neurotransmitters, caused a 3--4-fold rise in cAMP levels in the slices. All 3 main subdivisions of the hippocampus (HPC), the dentate gyrus, areas CA3 and CA1, possessed the capacity to produce cAMP. The latency to the NE stimulation of cAMP formation was about 20 sec but maximal stimulation was reached only after 5--10 min of incubation. Intrahippocampal injection of kainic acid (KA) caused a nearly complete destruction of hippocampal neurons and a marked increase in number of glial cells. NE caused a 12--15-fold rise in cAMP levels in KA-treated HPC. Compared to normal HPC where potency order of noradrenergic agonists indicated activation of a beta-1 receptor type, the pattern for the KA-treated HPC indicated the dominance of beta-2 receptors. The beta-1 antagonist, practolol, and the beta-2 antagonist, H35/25, were about equipotent in blocking the NE-stimulated cAMP formation in normal HPC. In KA-treated HPC, on the other hand, H35/25 was much more potent than practolol in inhibiting NE-stimulated cAMP formation. It is suggested that in the HPC beta-1 adrenergic receptors are primarily neuronal and beta-2 receptors, glial, and that activation of both receptor species results in activation of a cAMP-generating system.

Adenosine↗
PubMed1981

Histamine modulates reactivity of hippocampal CA3 neurons to afferent stimulation in vitro.

Intracellular activity was recorded from hippocampal CA3 pyramidal cells maintained in vitro. Histamine (HA) produced a slow depolarization associated with minimal conductance changes. In addition, there was an increase in action potential discharge rates and the emergence of bursting firing patterns. EPSP size increased by about 50% and spontaneous dendritic spikes were observed. These effects were markedly reduced by tetrodotoxin. Extracellular recording of population spikes revealed a marked difference between CA1 and CA3 regions; in the former HA produced an increase in population spike size whereas in the latter this increase was larger and was associated with the appearance of secondary and tertiary population spikes. It is suggested that HA produces its effects by enhancing release of neurotransmitters from excitatory synapses on the recorded neurons.

Afferent Pathways↗
PubMed1981

Opiate receptor binding in the brain of the hypertensive rat.

Experimental and genetic hypertension in male rate is accompanied by a lower specific [3H]naloxone binding in the dorsal horn of the spinal cord, and in the hippocampus as compared to controls. Rats which are genetically resistant to hypertensive stimuli have a higher specific [3H]naloxone binding in the nucleus tractus solitarius and lower opiate receptor binding in the dorsal horn. Together with previous studies which demonstrated a correlation between blood pressure and pain sensitivity, these results support the notion that specific brain loci participate in co-regulation of pain perception and blood pressure.

Animals↗
PubMed1981

Mechanisms of norepinephrine actions on hippocampal pyramidal cells in vitro.

Responses of pyramidal cells to topical application of norepinephrine (NE) were studied by intracellular recording in hippocampal slices in vitro. Norepinephrine hyperpolarized CA1 cells. Simultaneously, there was a decreased response to constant hyperpolarizing and depolarizing current pulses. The number of spikes evoked by constant depolarizing pulses was reduced. Spontaneous activity, when present, was reduced or abolished. The response to depolarizing current pulses was reduced more than the response to hyperpolarizing current pulses. The reduction of the depolarizing response was minimal for the first 6-8 msec of the pulse, whereafter it increased. The effects persisted after blocking synaptic transmission with low calcium-high magnesium concentrations in the incubation fluid. We conclude that the hyperpolarization is most likely due to a conductance increase. The mechanism behind the reduced response to depolarizing current pulses is discussed.

Animals↗
PubMed1981

The action of norepinephrine in the rat hippocampus: intracellular studies in the slice preparation.

The ionic basis of norepinephrine (NE) action was studied with intracellular recording techniques in the rat hippocampal slice. Topical application of NE caused, in CA1 neurons, a 3-4 mV hyperpolarization associated with a 10-20% decrease in input resistance. This effect was accompanied by a decrease in spontaneous action potential discharges and, in some cells, by a reduction in EPSPs produced by stimulation of the excitatory Schaffer collateral-commissural pathway. An analysis of the voltage and concentration dependency revealed that NE may activate two different mechanisms. Experiments performed to test this hypothesis have demonstrated that a short duration hyperpolarizing action of NE was still present in a low Cl- medium. The hyperpolarizing responses to NE were absent in ouabain-treated slices and in low temperature. Cyclic AMP produced a 3-4 mV hyperpolarization associated with minimal changes in input resistance. This effect of cAMP was blocked by ouabain. IBMX potentiated responses to low concentrations of NE. It is proposed that NE activates two mechanisms; one involves activation of Cl- conductance and the other activation of a Na+-K+ pump. This latter effect might be mediated by cAMP.

Animals↗
PubMed1981

Electron transfer between azurin from Alcaligenes faecalis and cytochrome c551 from Pseudomonas aeruginosa.

The electron transfer equilibrium and kinetics between azurin from Alcaligenes faecalis and cytochrome c551 from Pseudomonas aeruginosa have been studied. The equilibrium constant K = ([Cyt(III)] . [Az(I)])/([Cyt(II)] . [Az(II))]) = 0.5 at 25 degrees C is about seven times smaller than that observed between the cytochrome c551 and the titrations confirmed a 43-mV difference between the mid-point potentials of +266 mV and +309 mV for the Alcaligenes and Pseudomonas azurins respectively. The kinetics of the reaction between Alcaligenes azurin and Pseudomonas cytochrome c551 were investigated by the temperature-jump chemical relaxation method. Only a single relaxation mode was observed throughout the range of concentrations and temperatures examined. Thus, the slow relaxation time observed in the reaction between P. aeruginosa azurin and cytochrome c551 is not observed with the Alcaligenes azurin. The simplest mechanism that can therefore be ascribed to the investigated system is: [formula: see text]. This scheme is similar to that proposed earlier for the reaction between P. aeruginosa azurin and cytochrome c551 but does not involve the conformational transition proposed for azurin. The specific rates for the electron transfer are still fast: 1.8 x 10(6) M-1 . s-1 and 3.0 x 10(6) M-1 . s-1 respectively at 25 degrees C.

Alcaligenes↗
PubMed1981

Malignant external otitis: early histopathologic changes and pathogenic mechanism.

The histopathologic changes during the early stage of malignant external otitis (MEO) were studied in two patients, one a non-diabetic. The specimens were obtained by an en bloc excision of the diseased tissue of the external ear canal through a retroauricular approach. The most prominent histologic features of the early stage of MEO consist of a thick layer of almost acellular, partly degenerated, collagen extending from the cartilage into the dermis, which most likely existed prior to the penetration of the microorganism. This finding supports our concept that MEO is a disease which develops as a results of invasion of opportunistic organisms into tissue previously devitalized, probably due to vascular compromise and that these latter features constitute the basic mechanism of the entire disease process.

Aged↗
PubMed1981

Regional differences in neuronal responses to 5-HT: intracellular studies in hippocampal slices.

1. Intracellular recordings were obtained from cells in the regions CA1, CA3 and the dentate gyrus (DG) of rat hippocampal slices. 2. Topical application of 5-HT induced a 2-10 mV hyperpolarization in all cells tested. 3. The hyperpolarization was accompanied by a marked reduction in input resistance in CA1 and DG cells, but by a much smaller resistance change in CA3 cells. 4. These effects of 5-HT were not abolished by tetrodotoxin. 5. It is suggested that 5-HT causes an increase in K+ conductance in regions CA1 and DG and that this results in hyperpolarization. A different mechanism might be activated by 5-HT in cells of the CA3 region.

Animals↗