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Biomedical subjects

A Hamberger

Publications and source records attributed to A Hamberger.

At least 127 records · Page 7Linked to original sources
PubMed1981

Biologically active peptide-containing fractions in schizophrenia and childhood autism.

It is well documented that peptides have a major role in the effective functioning of higher animals at all levels from enzyme stabilization to homeostatic mechanisms governing essential functions such as eating, sexual behavior, and temperature regulation. The effects of exogenously administered peptides on neurotransmitter release, uptake, metabolism and behavioral consequences are also well established. We have attempted to extend these findings by postulating peptidergic neurons as transducers of multisignal inputs, and that development of pathological states may be due to genetically-determined reduced levels of activity of key peptidases, leading to excretion of regulatory peptides into the circulation. We have been able to demonstrate that, in schizophrenia and autism (in well defined clinical cases), the patterns of peptides and associated proteins from urinary samples differ considerably from each other and from normal controls. In addition to this, further purification of the material obtained has led to the discovery of a number of factors capable of modulating the function of major neurotransmitters. Some of these are in the final stages of characterization as peptides, while the remainder are also probably peptides, as purification has been followed by both biological testing and chemical analysis for peptidic material. We have outlined a number of parameters which we consider relevant in any attempt to put psychiatric disorders on a biological foundation. Any new advances in the neurochemical understanding of such disorders must take into consideration the observations of several different disciplines including genetics and psychology. However, at this stage of research it is far too early to speculate on the relevance of the various biological activities to the etiology and symptomatology of schizophrenia and childhood autism.

Autistic Disorder↗
PubMed1980

Potassium stimulated release of axonally transported radioactivity from slices of rabbit superior colliculus.

The radioactivity in the trichloroacetic acid (TCA) soluble pool in the terminals of the retinal ganglion cells in the superior colliculus (SC) was studied one month after labelling of the nerve cell bodies in the retina with different radioactive amino acids. The TCA soluble fraction in the SC represented a few per cent of the total radioactivity of the isolated tissue and was mainly derived from protein degradation. The perfused slice of the SC responded to high K+ depolarization with an increased release of TCA-soluble radioactivity, while small changes occurred for TCA-precipitable fractions. The evoked release of TCA-soluble radioactivity was particularly prominent after labelling with [3H]glycine. The release was Ca2+-dependent and the response to repetitive depolarization indicated a continuous replenishment of the releasable pool.

Amino Acids↗
PubMed1980

Hippocampal glutamate release after porta cava anastomosis: reduced sensitivity to ammonia inhibition.

In vitro measurements of basal efflux and evoked release of exogenous and endogenous glutamate from rat hippocampus showed that exposition of the tissue to pathophysiological concentrations of ammonium chloride (3 mM) for 40--60 min abolished the KCl-induced release of endogenous glutamate. Basal efflux of endogenous glutamate was elevated by ammonium chloride with a delay of 30--40 min. In an attempt to link these observations to the pathogenesis of hepatic coma, rats were subjected to porta-cava anastomosis, and the hippocampal tissue was tested for ammonia sensitivity 3--4 weeks after the operation. The results showed that ammonia perfusion of the tissue was without effect effect on either basal or KCl-evoked release of endogenous glutamate. In addition, the utilization of glutamine for glutamate formation was influenced in hippocampal but not cortical tissue form porta-cava anastomized rats. The results suggest that ammonia is an important factor for the disturbed metabolism of the neurotransmitter pool of glutamate in hepatic failure.

Ammonia↗
PubMed1980

Synaptosomal phospholipid pool in rabbit brain and its effect on GABA uptake.

Rabbit synaptosomes have been used to study the effect of the base-exchange reaction in membrane phospholipids on gamma-aminobutyric acid (GABA) transport in vitro. The uptake of GABA was measured after a base-exchange reaction with ethanolamine, choline, or L-serine and after subsequent displacement of these exchanged moieties from lipid by bases of similar or different structures which were added to the synaptosomal medium. Serine incorporation stimulated GABA transport, but its displacement from membrane lipid by choline or ethanolamine induced an inhibition of GABA transport. Ethanolamine incorporation inhibited GABA transport, but its displacement of serine or choline resulted in stimulation of GABA uptake. Choline incorporation also inhibited GABA transport, although less than ethanolamine. The pool size of synaptosomal phospholipids, presumably involved in GABA uptake, accounted for 0.2 to 10% of the total content of membrane phospholipid. Thus, alteration of phospholipid composition by exchange of the lipid hydrophilic head-groups influences the extent of GABA uptake into rabbit synaptosomes.

Animals↗
PubMed1980

Role of calcium ions in the formation and release of low-molecular-weight substances from optic nerve terminals.

Retinal proteins were labeled by intraocular injections of radioactive amino acids. Tissue slices of the superior colliculus (SC) were prepared 18-20 hr later, i.e., when the rapid phases of the axonal transport had reached the SC terminals. The effect of depolarizing pulses of high K and of Ca withdrawal on the scretion of radioactivity was studied in a perfusion system. The effluents were separated into a trichloroacetic acid (TCA) precipitable fraction and a TCA-soluble fraction. High K evoked a release of TCA-soluble radioactivity when [(3)H]glycine, [(3)H]leucine, or [(3)H]proline were used as protein precursors. Small changes occurred for TCA-precipitable fractions. The evoked release of radioactivity was Ca dependent and particularly prominent after labeling with [(3)H]glycine. Ca withdrawal increased the efflux of exogenous GABA, primary amines, and TCA-precipitable radioactivity but not of TCA-soluble radioactivity when normal media were used. The formation of TCA-soluble radioactivity was measured by incubating combined homogenates of SC and the lateral geniculate body (LGB), containing labeled proteins transported by the slow or rapid phase. The proteolytic activity was highly Ca dependent, for the rapidly transported proteins the half maximum was at approximately 0.1 mM Ca. The formation of TCA-soluble radioactivity was inhibited by p-chloromercuriphenylsulfonic acid (PCMS). Other divalent cations could not substitute for Ca. The rate of formation of TCA-soluble radioactivity and the influence of Ca ions was smaller when proteins of the slow phase were used as substrate.

Amino Acids↗
PubMed1980

Differences in attachment between herpes simplex type 1 and type 2 viruses to neurons and glial cells.

Fractions of nerve cell perikarya, synaptosomes, and astrocytic glia were prepared from human, monkey , rabbit, rat, and mouse brain tissue. The herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) binding capacity of these fractions was studied. Pretreatment of fractions with one type of HSV and the subsequent testing of adsorption of homotypic and heterotypic virus ws employed to reveal type selectivity of virus binding receptors. A higher density of HSV-1 than of HSV-2 selective receptors was found on synaptosomes and glial cells, except with mouse-derived preparations. Synaptosomal and glial cell preparations of mouse brains adsorbed both types of HSV well. Little or no adsorption was observed with HSV-1 and HSV-2 to neuronal perikarya. The type selectivity of HSV binding receptors on brain cells ws demonstrated on preparations of human synaptosomes and mouse glial cells. Some possible implications of the observations on the HSV infection of the nervous system are discussed.

Animals↗
PubMed1980

Effects of undernutrition on nucleic acid synthesis in neuronal and glial cells from different regions of developing rat brain.

Rats were undernourished by being given half their normal diet from the 10th day of pregnancy, 10-, 15- and 30-day-old rats were studied. Incorporation of labelled precursors into brain DNA and RNA was carried out in vitro with slices from cerebral cortex, brain stem and cerebellum. Neuronal and glial cells were subsequently isolated and analyzed for specific radioactivity. The proliferation and differentiation of all brain cells were affected by undernutrition. Glial cells in particular and the small neuronal cells appeared most vulnerable probably because of their intense postnatal development.

Animals↗
PubMed1979

Glutamate as a CNS transmitter. II. Regulation of synthesis in the releasable pool.

Slices of the molecular layer of the dentate gyrus of rat hippocampus were used to study the regulation of glutamate synthesis and release. Net glutamate synthesis increased dramatically during conditions which stimulated the release of glutamate. The rate of glutamine incorporation into glutamate released into the medium was increased almost immediately upon stimulation with a 56 mM KCl, 3 mM CaCl2 medium. Synthesis appeared to be regulated both by glutamine uptake and the activity og glutaminase. Glutamine uptake was stimulated in the presence of 56 mM KCl and 3 mM CaCl2. The increased glutamine uptake was not due to a decrease in efflux, was unrelated to tissue glutamate levels, and could be dissociated from the rate of glutamate biosynthesis. The presence of Ca2+ ions and depolarization seemed necessary. Glutaminase activity was regulated by end product inhibition: increased levels of tissue glutamate resulted in a decrease in glutamate synthesis. Glutamine in the presence of 56 mM KCl increased the rate of glucose incorporation into glutamate over that seen without glutamine.

Animals↗
PubMed1979

Comparison of rat brain membrane antigens by complement mediated release of neurotransmitters from brain fractions using antisera against S-100 and Thy-1.

Synaptosomal, glial and neuronal fractions were prepared from rat brain and incubated to accumulate radioactively labelled neurotransmitters. Treatment of these fractions with antisera and complement showed that anti-(Thy-1) serum gave good release (50-75% of total uptake) of all neurotransmitters tested from synaptosomal and glial fractions. GABA and glutamate were released from neuronal perikarya, but not norepinephrine or serotonin. Anti-(S-100) serum gave no significant release of any neurotransmitter tested from any of the fractions, although all of them had previously been shown to contain this protein. These results are compatible with the membrane nature of Thy-1 and the mainly soluble nature of S-100 protein. They permit a selection for membrane antigens and neurotransmitters from different brain fractions. Antigenic differences between neuronal and glial plasma membranes were suggested by results with antiserum raised against bulk-isolated rat neuronal perikarya.

Animals↗
PubMed1978

Glutamate secretion and NAD(P)H levels during calcium-dependent depolarization of slices of the dentate gyrus.

Evidence from studies involving release, postsynaptic responses, inactivation, storage and synthesis etc. support the contention that glutamate may be the transmitter of the perforant input to the granule cells in the dentate gyrus of the hippocampus. In the present report the release of endogenous glutamate and the levels of reduced pyridine nucleotides (NAD(P)H) has been measured in parallel experiments on slices from the dentate gyrus of the hippocampus. A Ca-dependent release of glutamate is evoked by tissue depolarization caused either with electrical field stimulation or with elevated KC1. Electrical stimulation induced a transient increase in tissue NAD(P)H levels, the increase being inhibited by approximately 50% during Ca-free conditions. KC1 stimulation, on the other hand, produced a long-lasting decrease in NAD(P)H, the decrease being halved in the absense of Ca. A metabolic relation between stimulus secretion and energy utilization is discussed.

Animals↗