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Y Dudai

Publications and source records attributed to Y Dudai.

At least 73 records · Page 4Linked to original sources
PubMed1981

beta-Carboline binding to deoxycholate solubilized benzodiazepine receptors from calf cerebral cortex.

The beta-carbolines harmane and norharmane competitively inhibit [3H]flunitrazepam ([3H]FNZ) binding to deoxycholate-solubilized benzodiazepine receptors from calf cerebral cortex, with Ki in the micromolar range [3H]Propyl-beta-carboline-3-carboxylate ([3H]PrCC) binds to the soluble receptors with an affinity similar to its binding to particulate receptors (0.41 nM vs 0.48 nM, respectively). The component that binds [3H]PrCC displays a sedimentation profile on sucrose gradient centrifugation similar to that of [3H]FNZ binding component (sedimentation coefficient about 11S).

Alkaloids↗
PubMed1981

In vivo modulation of the number of muscarinic receptors in rat brain by cholinergic ligands.

Administration of the muscarinic agonist oxotremorine led to a decrease in the number of muscarinic receptors, as determined by specific binding of [3H]quinuclidinyl benzilate ([3H]QNB), in several rat brain regions both during development and at maturity. In contrast, administration of the muscarinic antagonist scopolamine led to an increase in the number of [3H]QNB-binding sites in various brain regions. Scopolamine also prevented the decrease in the number of [3H]QNB-binding sites induced by administration of an organophosphorus drug. The results are compatible with the hypothesis that the number of brain muscarinic receptors, or at least of a sub-class of them, is regulated by their transmitter.

Acetylcholinesterase↗
PubMed1981

Benzodiazepine receptors in chick retina: development and cellular localization.

Benzodiazepine receptors are present in high concentration in the chick retina. Their pharmacological properties are similar to those of the benzodiazepine receptors present in the brain. The retina receptors appear prior to, as well as during, the period of synaptogenesis. In the newborn chick retina the receptors are localized in the inner synaptic layer, probably on or close to synaptic connections.

Aging↗
PubMed1980

Solubilization and properties of a benzodiazepine receptor from calf cortex.

A putative benzodiazepine receptor was solubilized from calf cortex by the use of sodium deoxycholate as an 10.9S entity containing subunits of which at least part are of 51 K molecular weight. The solubilized receptor retains its high affinity for [3H]flunitrazepam. The affinity for various other drugs, including benzodiazepines and xanthine derivatives, was also not significantly altered. GABAergic modulation of the receptor affinity for [3H]flunitrazepam was diminished but still detectable.

Animals↗
PubMed1980

Early septal lesion: effect on the development of the cholinergic system in rat hippocampus.

The development of the cholinergic system in the rat hippocampal formation was studied following lesion of the septal region at an age 2--4 days postnatal (i.e. the lesion was performed prior to the establishment of the septohippocampal connections). The steep increase in acetylcholinesterase (AChE) level, that under normal conditions takes place during the second and the third week postnatal, was not observed in early lesioned animals, and AChE level at maturity was about 30% of control. AChE level of adult-lesioned animals was about 15% of control, suggesting an age-dependent plasticity in response to the lesion. Early deafferentation did not seem to alter the pattern of development of muscarinic binding sites as measured by specific binding of [3H]quinuclidinyl benzilate ([3H]QNB). Total [3H]QNB bound per hippocampus of adult, early-lesioned animals was about 70% of control, but this reduction could be accounted for by the atrophy observed in the hippocampal formation following early lesion. Binding of [3H]QNB per protein in early lesioned animals did not differ from normal. Thus the development and the level of muscarinic binding sites in the hippocampal formation do not seem to depend upon normal establishment of presynaptic contacts.

Acetylcholinesterase↗
PubMed1980

Studies on the properties of benzodiazepine-binding sites from calf cortex.

[3H]Flunitrazepam ([3H]FNZ) specifically binds to a single class of sites in calf cortex homogenate at a level of about 1 pmol/mg protein. Essentially all binding sites sediment after a 30 min centrifugation at 20,000 X g. The affinity of the sites decreases with increasing temperature both in a homogenate and in a washed membranes preparation. Binding sites in the washed membranes preparation display lower affinity than those in the homogenate (e.g., KD of 14.8 nM vs. 7.6 nM respectively at 37 degrees C), but membrane-sites affinity can be increased by aliquots of high-speed supernatant as well as by GABA (> 10(-7) M). GABA has only a small effect on the on-reaction but slows the off-reaction. The binding sites require chloride ions (approximately 100 mM) for optimal activity, are inhibited by Hg+2, and are partially released into a high-speed supernatant by several detergents.

Animals↗
PubMed1979

Cholinergic binding sites in rat hippocampal formation: properties and ontogenesis.

The hippocampal formation of the rat contains two types of membrane-bound cholinergic binding sites, as revealed by specific binding of [3H]quinuclidinyl benzilate (QNB) or of a-[125I]bungarotoxin (a-Btx). The sites differ in pharmacological profile, sensitivity to detergents and ontogenesis. The major binding site (about 17 pmol per adult hippocampus) is of a muscarinic nature, and binds [3H]QNB with an on-rate of 2 x 10(6) M-1 sec-1 and an apparent KD of 0.4 nM. This binding is displaced by low concentrations of muscarinic ligands but not of nicotinic ligands. The earliest increase in binding level is detected at about day 4 postnatal and a sharp increase in total binding takes place between days 10 and 15. Total binding continues to increase gradually about 3-fold until an age of about 7 weeks, at a rate resembling that of acetylcholinesterase. a-Btx-binding sites (about 0.6 pmol per adult hippocampus) display a nicotinic profile with an on-rate constant for a-[125I]Btx of 6 x 10(4) M-1 sec-1 and an apparent KD of 2 nM. Ontogenesis of these sites clearly differs from that of muscarinic sites and acetylcholinesterase. Absolute binding reaches mature levels at an age of 12--14 days postnatal, and binding per tissue protein is higher during the first postnatal days than at maturity. It appears that the level of toxin-binding sites attains mature values before the major synaptogenetic events in the area are completed.

Age Factors↗
PubMed1978

Distribution of an alpha-bungarotoxin-binding cholinergic nicotinic receptor in rat brain.

Cholinergic nicotinic receptors in rat brain were demonstrated by the use of the potent nicotinic antagonist [125I]alpha-bungarotoxin [125I]alpha-Btx). Biochemical studies on binding of [125I]alpha-Btx to rat hippocampal homogenates revealed saturable binding sites which are protected by nicotine, D-tuborcurarine and acetylcholine but not by atropine or oxotremorine. The hippocampus and hypothalamus displayed relatively high [125I]alpha-Btx specific binding whereas the cerebellum was devoid of specific binding. Other regions displayed intermediate binding levels. Analysis of the regional distribution of [125I]alpha-Btx binding by autoradiography of frontal brain sections revealed high labeling in the hippocampus, hypothalamic supraoptic, suprachiasmatic and periventricular nuclei, ventral lateral geniculate and the mesencephalic dorsal tegmental nucleus. It is suggested that the limbic forebrain and midbrain structures as well as sensory nuclei are the main nicotinic cholinoceptive structures in the brain.

Animals↗