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At least 721 records · Page 40Linked to original sources
PubMed1986

Regional distribution of high-affinity [3H]somatostatin binding sites in the human brain.

The distribution of high-affinity binding sites for [3H]somatostatin has been studied in membrane preparations from a number of regions of normal human brain. The highest densities of binding sites (greater than 48 fmol/mg protein) were found in the cerebral and cerebellar cortices and the hippocampus, with intermediate binding densities (30-46 fmol/mg protein) being present in the basal ganglia, amygdala, septum and claustrum. The lowest densities of binding sites (less than 14 fmol/mg protein) were observed in the hypothalamus, thalamus and substantia nigra. The binding of [3H]somatostatin in both the frontal cortex and cerebellar cortex demonstrated pharmacological specificity, since somatostatin-28, but not somatostatin-28(1-12) or Des AA1,2,4,5,12,13, D-Trp8-somatostatin, competed for the binding sites. Scatchard analysis of the binding in both frontal cortex and cerebellar cortex revealed the presence of two classes of high-affinity binding sites.

Aged↗
PubMed1987

Glutamate and aspartate activated channels and inhibitory synaptic currents in large cerebellar neurons grown in culture.

Patch-clamp methods were used to examine large (greater than 30 microns) cerebellar neurons of the rat, maintained in cell culture. Cells possessed voltage-activated transient inward Na+ currents which were sensitive to tetrodotoxin. Spontaneous synaptic currents, present in whole-cell recordings, were abolished by bicuculline and picrotoxin and were carried by Cl-. Cells produced inward currents in response to the transmitter candidates glutamate and aspartate and also to the glutamate agonists kainate, quisqualate, N-methyl-D-aspartate and ibotenate. Analysis of glutamate and aspartate-current noise has been used to derive characteristics of the excitatory channels. Single channel currents have also been observed directly in whole-cell and outside-out patches. Both glutamate and aspartate are able to activate channels which were blocked by Mg2+ and had a maximum conductance of 50 pS.

Animals↗
PubMed1991

The quantitative autoradiographic distribution of [3H]MK-801 binding sites in the normal human spinal cord.

The distribution of NMDA receptors in the normal human spinal cord has been investigated using the non-competitive channel blocking agent MK-801. Specific [3H]MK-801 binding was present throughout the spinal grey matter at all segmental levels, the greatest density of binding being found in the substantia gelatinosa. Focal areas of high binding were also found in a distribution corresponding to lower motor neurones in the ventral horns. This study provides anatomical evidence that NMDA receptors are likely to be important in motor as well as sensory spinal synaptic transmission. The anatomical distribution of NMDA receptors in relation to motor neurone somata may have important implications in selective vulnerability to excitotoxic injury.

Aged↗
PubMed1991

[3H]nitrendipine binding in temporal cortex in Alzheimer's and Huntington's diseases.

Specific [3H]nitrendipine binding which was shown to be calcium- and calmodulin-dependent was found to be significantly reduced in the temporal cortex in Alzheimer's disease compared to age-matched controls. Scatchard analysis revealed that this reduction was due to a loss in the number of cortical [3H]nitrendipine binding sites rather than a change in the affinity of the binding site in the Alzheimer patients. The reduction in cortical [3H]nitrendipine-specific binding was most marked in those Alzheimer's disease cases where the duration of the dementing illness was longer than two years. In contrast, no reduction in cortical [3H]nitrendipine binding was found in Huntington's disease. There was no significant correlation found between age (38-89 years) and [3H]nitrendipine binding in control cases, or between mean overall plaque counts and [3H]nitrendipine binding in the Alzheimer's disease cases. There was a significant correlation found between age (46-88 years) and [3H]nitrendipine binding in the Alzheimer's disease cases where the duration of the dementing illness was greater than two years.

Aged↗
PubMed1992

The quantitative autoradiographic distribution of [3H]MK-801 binding sites in the normal human brainstem in relation to motor neuron disease.

The distribution of N-methyl-D-aspartate (NMDA) receptors in the normal human brainstem has been investigated using MK-801. Specific [3H]MK-801 binding showed a heterogeneous distribution, the greatest density of binding sites being found in the substantia nigra, locus coeruleus, and the hypoglossal and inferior olivary nuclei. Brainstem motor nuclei subserving eye movements, which tend to be spared in motor neuron disease (MND), had significantly lower densities of binding compared to other cranial nerve motor nuclei (V, VII, X, XII) which tend to be affected. The anatomical distribution of NMDA receptors may be one factor determining selective vulnerability to excitotoxic injury.

Adult↗
PubMed1994

N-methyl-D-aspartate (NMDA) receptors in the spinal cord and motor cortex in motor neuron disease: a quantitative autoradiographic study using [3H]MK-801.

The distribution and density of NMDA receptors in spinal cord and motor cortex was compared in motor neuron disease (MND; 10 cases) and controls (8 cases) using [3H]MK-801 autoradiography. In the spinal ventral horn of MND cases, [3H]MK-801 binding was reduced and there were fewer focal hot spots of binding. These changes are likely to reflect loss of motor neurons (MN) bearing NMDA receptors. [3H]MK-801 binding was increased in intermediate spinal grey matter and deeper layers of the motor cortex in MND cases compared to controls. This may represent either an adaptive response to MN loss or a pathophysiological phenomenon contributing to MN degeneration.

Aged↗
PubMed1976

The role of endogenous catecholamines in the regulation of electrocortical activity in the encephale isole cat.

Experiments were performed on encephale isole cats. The cats were either untreated or pretreated with reserpine, alpha-methyl-p-tyrosine (AMPT) or FLA 63, and the depletion of endogenous noradrenaline was determined by fluorescence microscopy. Pretreatment with reserpine reduced waking and spindle sleep while the synthesis inhibitors did not. A combined pretreatment with reserpine and AMPT or FLA 63 was necessary to deplete totally brain stem noradrenaline. Under these circumstances, behavioural arousal was abolished and all electrocortical activity except spindling was also abolished. Injection of L-DOPA into cats pretreated with reserpine and AMPT produced behavioural alerting and low voltage, high frequency electrocortical activity. In cats pretreated with reserpine and FLA 63, the minimum effective dose of L-DOPA was often elevated, and when the low voltage, high frequency activity occurred, it was accompanied by spindling. It was accompanied by spindling. It is suggested that dopamine and noradrenaline independently modulate electrocortical activity, dopamine mediating spindling, and noradrenaline inhibiting spindling but mediating low voltage, high frequency activity.

Animals↗
PubMed1985

Human cerebellar cortex possesses high affinity binding sites for [3H]somatostatin.

Somatostatin binding sites have been identified in the human brain using [4-3H-(Phe6)]-somatostatin-14. In contrast to that of the rat, the human cerebellar cortex possesses a high density of somatostatin binding sites, comparable to that found in either the rat or human cerebral cortex. Autoradiographic localisation of somatostatin binding sites in the human cerebellum reveals that the highest density is associated with the granule cell layer.

Aged↗
PubMed1987

Autoradiographic visualization of binding sites for [3H]somatostatin in the rat brain.

[4-3H][Phe6]somatostatin-14 was used to localize somatostatin binding sites in the rat brain by tritium-film autoradiography. The distribution of binding sites using 0.7 nM [3H]somatostatin confirmed that previously described for iodinated tyrosyl analogues of somatostatin, with highest densities of sites in the cerebral cortex (particularly in laminae III-V), amygdala, lateral septal nucleus, hippocampus and claustrum. Investigation of the pharmacological specificity of the binding sites showed that somatostatin-28, but not its N-terminal dodecapeptide, somatostatin-28 (1-12) or des-Ala1[Gly2,Lys4,Asn5,Thr12,Ser13]somatostatin displaced [3H]somatostatin. Further examination of the binding inhibition characteristics, using a homogenate assay, suggested the presence of two classes of binding sites in the cerebral cortex, hippocampus, midbrain and striatum. The existence of sub-populations of somatostatin binding sites in the rat brain has implications for future studies on the physiological and pharmacological significance of somatostatin receptors in the central nervous system.

Animals↗
PubMed1992

Effects of substitution of aspartate-440 and tryptophan-487 in the thiamin diphosphate binding region of pyruvate decarboxylase from Zymomonas mobilis.

A tryptophan residue at position 487 in Zymomonas mobilis pyruvate decarboxylase was altered to leucine by site-directed mutagenesis. This modified Z. mobilis pyruvate decarboxylase was active when expressed in Escherichia coli and had unchanged kinetics towards pyruvate. The enzyme showed a decreased affinity for the cofactors with the half-saturating concentrations increasing from 0.64 to 9.0 microM for thiamin diphosphate and from 4.21 to 45 microM for Mg2+. Unlike the wild-type enzyme, there was little quenching of tryptophan fluorescence upon adding cofactors to this modified form. The data suggest that tryptophan-487 is close to the cofactor binding site but is not required absolutely for pyruvate decarboxylase activity. Substitution of asparagine, threonine or glycine for aspartate-440, a residue which is conserved between many thiamin diphosphate-dependent enzymes, completely abolishes enzyme activity.

Amino Acid Sequence↗