PubMed Health⌕ Search

Biomedical subjects

N Schechter

Publications and source records attributed to N Schechter.

At least 73 records · Page 4Linked to original sources
PubMed1984

Induction of immune alterations and successful renal transplantation with a simplified method of donor-specific blood transfusion.

We developed a new and simplified donor-specific blood transfusion (DSBT) protocol for prospective kidney transplant recipients from one-haplotype-mismatched related donors. Prospective kidney donors gave 450 ml of blood in a quad-pack unit, and the blood was stored in a blood bank. Twenty-five patients were transfused with 100 ml of the respective donor's whole blood at 1, 8, and 15 days after its storage. After DSBT, only three (12%) developed donor-specific lymphocytotoxic antibodies. Following DSBT, donor-specific mixed lymphocyte culture (MLC) was significantly suppressed, without any accelerated (secondary-type) response in early MLC. In addition, sera obtained after DSBT also suppressed donor-specific MLC significantly. Sixteen recipients subsequently received a kidney transplant from the donor, and all had functioning grafts at three months, but one lost the graft thereafter (graft survival rate: 94% at 12 months). This study indicates that (1) 100 ml of stored whole-blood DSBT three times at weekly intervals is a practical, less immunizing, and effective approach to enhance graft survival in recipients of a one-haplotype-mismatched graft; and (2) immune consequences of DSBT include induction of donor-specific cellular and humoral adaptive responses that might be conducive to successful graft outcome.

Adolescent↗
PubMed1984

58,000 dalton intermediate filament proteins of neuronal and nonneuronal origin in the goldfish visual pathway.

A group of proteins in the goldfish optic nerve with a molecular weight of 58K daltons was analyzed by two-dimensional gel electrophoresis. Results show that the proteins are differentially phosphorylated and found exclusively in a cytoskeletal-enriched fraction. The proteins from this fraction can be reconstituted into typical intermediate filament structures, as shown by electron microscopy. Two components which are of neuronal origin are transported within the slow phase of transport. The 58K proteins are the most abundant proteins in the optic nerve, and they are distinct from actin and tubulin. It was concluded that they are intermediate filament proteins. Cytoskeletal preparations of rat spinal cord, rat optic nerve, and goldfish optic nerve were compared by one-dimensional gel electrophoresis. The rat spinal cord contains glial fibrillary acidic protein (GFAP), and the rat optic nerve contains vimentin and GFAP, in addition to the neurofilament triplet. A typical mammalian neurofilament triplet is not detected in the goldfish optic nerve, while the major cytoskeletal constituent is a 58K band which coelectrophoreses with vimentin in the rat optic nerve by one-dimensional gel electrophoresis.

Animals↗
PubMed1984

Experimental febrile convulsions in the developing rat: effects on the cholinergic system.

The effects of hyperthermia-induced convulsions (HCs) on nicotinic and muscarinic receptor sites, choline acetyltransferase (ChAT), and acetylcholinesterase (AChE) in the rat were investigated. A series of 10 convulsions, evoked between 5 and 16 days of age, had marked effects on the development of the cholinergic system in the cerebellum and frontal cortex, but not in the hippocampus or hypothalamus. The concentration of muscarinic receptor sites in the cerebellum of the HC group was similar to that in controls at 2 days, greater than in controls at 8 days, but less than in controls at 55 days after the last convulsion. ChAT and AChE activities were increased at 2 days, similar at 8 days, and less than those in controls at 55 days. A decrease in muscarinic receptors and a decline in ChAT activity in the frontal cortex of the HC group were observed at 55 days after the last convulsion. The concentration of nicotinic receptor sites did not distinguish HC from control groups. A simple relationship between the experimental febrile convulsion and the cholinergic system was not found. The greatest effects were noted at 55 days after the last HC, which suggests that these may reflect secondary and possibly transsynaptic influences of the convulsion on cholinergic activity.

Acetylcholinesterase↗
PubMed1984

Myocardial cholinergic receptor sites and enzyme activity in the Dahl model of essential hypertension.

The density of muscarinic receptor sites, choline acetyltransferase (ChAT), and acetylcholinesterase (AChE) activity in the myocardium of the Dahl salt-sensitive (DS) and salt-resistant (DR) rat was investigated. Both normotensive and hypertensive (as a result of 8.0% NaCl added to the diet) DS rats displayed a lower concentration of muscarinic receptors and less ChAT and AChE activity in myocardial tissue than normotensive DR rats. Lower receptor site density and enzyme activity in the myocardial of the DS line may reflect decreased vagal tone. If true, this may produce dificits in the ability to appropriately adjust heart rate (HR) in response to elevations in blood pressure (BP). Therefore, the present results may be viewed as exacerbational factors in the pathogenesis of hypertension in the DS line.

Acetylcholinesterase↗
PubMed1983

In vitro protein synthesis in the goldfish retinotectal pathway during regeneration: evidence for specific axonal proteins of retinal origin in the optic nerve.

Four proteins with molecular weights of 58,000 can be separated as a linear array by two-dimensional gel electrophoresis. They are highly concentrated in the goldfish optic nerve and are designated as ON1, ON2, ON3, and ON4. Proteins ON1 and ON2 are undetectable in the optic nerve after disconnection and their concentration is gradually restored during regeneration. In vitro incubations of retinas, optic nerves, or tecta in the presence of [35S]methionine indicate that proteins ON1 and ON2 are of retinal origin. The labeling rate of these proteins in the retina increases fourfold after optic nerve crush whereas the overall labeling rate in the retina remains largely constant. Their synthesis cannot be detected in tissues devoid of retinal ganglion cells. This is consistent with the view that ON1 and ON2 are synthesized by retinal ganglion cells and are consequently of neuronal origin in the optic nerve. In contrast, similar experiments indicate that ON3 and ON4 are of nonneuronal origin. They are synthesized in the optic nerve in the absence of retinal ganglion cells.

Animals↗
PubMed1983

Cholinergic receptor site binding, choline acetyltransferase, and acetylcholinesterase activity in the forebrain and brainstem of the Dahl rat model of essential hypertension.

Muscarinic and nicotinic receptor site binding and the activity of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) in the forebrain and brainstem of Dahl salt-sensitive (DS) and salt-resistant (DR) rats was investigated. The DS line had a greater density of muscarinic sites in the cortex, hypothalamus, and medulla. Hypertensive DS rats had a greater density of sites than normotensive DS rats. ChAT activity was also higher in the cortex and hypothalamus of the DS line than the DR line. No significant differences were found in the activity of AChE or the concentration of nicotinic sites. These results suggest that the central muscarinic cholinergic system may participate in the pathogenesis of hypertension in the DS rat. The data indicate that central cholinergic activity is possibly greater in the DS than the DR rat and that this may help to explain the enhanced pressor response in the DS line after pharmacological activation of the central cholinergic system.

Acetylcholinesterase↗
PubMed1982

Long-term deficits in passive avoidance responding following experimental febrile convulsions during infancy.

Human infantile febrile convulsions are occasionally associated with later deficits in cognitive and motor performance. In the present report, experimental febrile convulsions during various stages of infancy in the rat were investigated. Infant rats that were subjected to a single hyperthermia-induced convulsion at 10, 15, or 20, but not 5, days of age required more trials than controls to acquire a step-down passive avoidance response when tested as adults (50-60 days of age). Although rats that were subjected to a series of convulsions during infancy also evinced deficits in passive avoidance responding at adulthood, the magnitude of the effect was not appreciably greater than that following a single convulsion. The present results indicate that a single experimental febrile convulsion during infancy can have long-term effects on subsequent behavior.

Age Factors↗
PubMed1982

Experimental febrile convulsions: long-term effects of hyperthermia-induced convulsions in the developing rat.

The susceptibility of infant rats to experimental febrile convulsions was investigated. Rats were subjected to a single hyperthermia convulsion at 5, 10, 15, or 20 days of age or the a series of convulsions from 5 to 20 days of age. Susceptibility to the experimental febrile convulsion decreased with age in all rats except those subjected to multiple convulsions. In this group, susceptibility tended to increase. This results is discussed in terms of its similarity to the kindling phenomenon and to the incidence of recurrent febrile convulsions in the human infant. Sex differences in susceptibility to the convulsion were examined, but none were found. Mature rats that had been subjected to experimental febrile convulsions as infants were found to be significantly more susceptible to a convulsive dose of pentylenetetrazol than controls. The results of this study indicate that even a single experimental febrile convulsion during infancy can exert a long-lasting, if not permanent, enhancement in seizure susceptibility. The similarities between the present findings and human infantile febrile convulsions are discussed.

Age Factors↗
PubMed1981

Glutamic acid binding in goldfish brain and denervated optic tectum.

The binding of L-glutamic acid to goldfish brain membranes and changes in tectal binding following optic nerve denervation and regeneration were investigated. Saturable, reversible, and specific binding occurred to sodium-free washed membranes from goldfish brain at a single population of sites having an apparent Kd of 3.4 microM and a capacity of 10 pM/mg original tissue. Binding was enriched in crude synaptosomal (P2) subcellular fractions. There was a 10-fold regional variation in the concentration of binding sites. In pharmacological studies protection constants (Kp) (the concentration which resulted in a 50% inhibition of binding) ranged from 4 microM for glutamate to greater than 10 mM for GABA. Following eye removal, the total number of tectal glutamic acid binding sites was stable for 4 days, followed by a rapid loss in binding, reaching 40% of control at 24 days. After optic nerve crush and optic nerve regeneration, the number and concentration of binding sites was not different from control. The relationship between glutamate, nicotinic, and muscarinic receptor sites in the retinotectal pathway is discussed.

Animals↗
PubMed1980

Electrophoretic analysis of specific proteins in the regenerating goldfish retinotectal pathway.

Proteins in the goldfish retinotectal pathway were analyzed by 2-D gel electrophoresis, under conditions of optic nerve crush or eye removal. A specific cluster of proteins was detected, consisting of 4 components, all of which are highly concentrated in the intact optic nerve. Two components were not detectable in non-visual areas of the goldfish brain. The total cluster was diminished by about 80% in the denervated optic tectum, and its level was restored during optic nerve regeneration. These data were interpreted as evidence for visual system-specific proteins in the goldfish retinotectal pathway.

Animals↗
PubMed1980

The effect of kainic acid on cholinergic enzymes and receptors in the amygdala complex of the rat.

Kainic acid (KA) was injected into the amygdala (AM) complex of the rat and its effect on the cholinergic enzymes, choline acetyltransferase (CAT) and acetylcholinesterase (AChE), and the binding of the muscarinic ligand, [3H]quinuclidinyl-benzilate (QNB) and the nicotinic ligand [125I]alpha-bungarotoxin (aBuTX) was investigated. Ka produced a loss of approximately 35% of the CAT activity in the AM. However, no effect on AChE activity was observed. A 30--50% decrease in the number of muscarinic and nicotinic receptor sites was also found. CAT, AChE and QNB binding in the AM contralateral to the injection did not change. However, the binding of aBuTX was found to decrease by approximately 40%. The present results suggest that the loss of CAT activity in the AM after treatment with KA is due to the destruction of cholinergic neurons within the AM. The lack of effect on AChE suggests that the major cholinergic input to the AM is not affected by KA. In addition, the loss of nicotinic receptors in the contralateral AM may reflect anterograde degeneration of terminals that have nicotinic sites located on them, or may be secondary to the elicitation of intense seizure activity evoked by the KA.

Acetylcholinesterase↗
PubMed1980

Analysis of protein levels and synthesis after learning in the split-brain pigeon.

A series of experiments were performed to study the effects of learning upon proteins in the split-brain pigeon. With this preparation, one side of the brain was trained in a color discrimination task while the other side served as a naive control. Proteins from both sides of the brain were separated by one- and two-dimensional polyacrylamide gel electrophoresis and analyzed to measure protein levels or protein synthesis. No differences were found between trained and naive telencephalic hemispheres or between trained and naive optic lobes in the steady-state protein levels or in protein synthesis.

Animals↗
PubMed1980

Stability of muscarinic-cholinergic receptor activity in the deafferented retinotectal pathway.

The high-affinity antagonist, 3-quinuclidinyl benzilidate (QNB), was used to analyze muscarinic-cholinergic receptor activity in the optic tectum of goldfish and optic lobe of developing chicks and adult pigeons after deafferentation. After deafferentation no significant loss of total or specific muscarinic receptor binding activity was observed in contrast to prior experiments where there was a marked and rapid loss of nictonic-cholinergic receptor binding activity, as measured by alphabungarotoxin binding. The relative stability of the muscarinic site as opposed to the instability of the nicotinic site in these experiments is discussed.

Animals↗
PubMed1979

Rapid loss of nicotine-cholinergic receptor binding activity in the deafferented avian optic lobe.

The levels of alpha-bungarotoxin (alpha-BuTX) sensitive receptor sites were investigated in the optic lobe after optic deafferentation in the neonatal and adult chicken. Within two days a 30% loss of alpha-BuTX binding sites per optic lobe is observed in the neonatal chick after enucleation. The results are similar with the adult chicken in experiments where the receptor binding activity is measured in the optic lobe and in the optic tectum after enucleation. The possibility that acetylcholine is a neurotransmitter in the vertebrate retinotectal pathway is discussed.

Age Factors↗
PubMed1979

Recovery of tectal nicotinic-cholinergic receptor sites during optic nerve degeneration in goldfish.

The concentration of cholinergic nicotinic-like sites as measured by alphabungarotoxin (alphaBuTX) binding, decreased in the goldfish (Carassius auratus) optic tectum after optic nerve disconnection. Initially, the rate of loss of sites is greater than the rate of tissue or protein degradation in experiments where disconnection was achieved either by unilateral optic nerve crush or by enucleation of one eye. When the crushed optic nerve is allowed to regenerate and form behaviorally potent connections, the number and concentration of these sites appears restored. Pharmacological studies indicate that the alphaButTX binding site in the goldfish optic tectum has a drug binding profile similar to that seen at central or peripheral alphaBuTX sites in other species.

Animals↗