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Biomedical subjects

B I Gold

Publications and source records attributed to B I Gold.

At least 19 recordsLinked to original sources
PubMed1990

Computerized volume measurement of brain structure.

Morphometric analysis of brain structures recently has become a main focus of interest in studies of some neuropsychiatric diseases. Limitations in imaging and mensuration methodology that is available currently for quantitative measurement of anatomic structures have prompted the development of a computerized system to study brain morphometry. A menudriven semi-automated computer system has been developed to assess in vivo brain morphometry using three-dimensional (3-D) magnetic resonance (MR), gradient echo, contiguous images of the whole brain. Accuracy of the system was tested with phantoms creating white on black contrast to simulate the brain tissue surrounded by subarachnoid cerebrospinal fluid (CSF), and a second set of phantoms creating black on white contrast to simulate the ventricular system in the brain tissue. The first set of phantoms was composed of three water-filled balloons (spherical, elliptical, and multiform) and a fresh postmortem brain. The second set of phantoms consisted of three rods of different diameters from a simple geometric plexiglass rod phantom and a life size cast of a human ventricular phantom. System accuracy was generally within 2.0% of the true volumes. System reliability was evaluated in three patient populations; 12 patients with Alzheimer's disease, nine with schizophrenia and nine healthy controls age-matched to the patients with Alzheimer's disease. Two independent observers measured the ventricular systems of these patients. Reliability of the system was addressed by the correlation between the two sets of measurements. For the sample as a whole, and each of the subgroups, the correlation between the two observers was 0.99. This system compares favorably with other morphometric methods reported.

Cerebral Ventricles↗
PubMed1983

Stereospecific, reversible binding of D-[3H]glucose to crude membrane fractions prepared from rat brain.

To a crude preparation of synaptic membranes prepared from rat brain, stereospecific, saturable, reversible binding was described of D-[3H]glucose. Binding showed a Kd = 0.45 microM and the fractional rate of dissociation was approximately eight times the fractional rate of association. D-[3H]glucose binding was displaced by 2-deoxyglucose and 3-O-methylglucose and it was abolished when membranes were denatured by heating.

3-O-Methylglucose↗
PubMed1983

Further studies on the role of calcium in the regulation of glutamate decarboxylase activity in brain slices.

[3H]GABA synthesis in brain slices was used as a model to study the role of Ca2+ in the regulation of GAD activity. Experimental conditions were chosen to increase and decrease the flux of Ca2+ and to promote the increase in free intracellular Ca2+. The blockade of electron transport and the inhibition of oxidative phosphorylation in the slices inhibited [3H]GABA synthesis. High K+ depolarization stimulated [3H]GABA synthesis and this effect was not blocked by lidocaine, trifluoperazine, or verapamil, but the stimulation was blocked by the intracellular Ca2+ antagonist TMB-8. The data do not differentiate between the relative contributions of extra- and intracellular Ca2+ but reflect that GAD activity is modulated by a dynamic balance between these two compartments as well as between stored and free Ca2+ within the cells.

2,4-Dinitrophenol↗
PubMed1983

Hexose transport by brain slices: further studies on energy dependence.

We studied the uptake of [3H]2-deoxyglucose [( 3H]2DG) by slices of rat cerebral cortex in vitro as a model of glucose transport by brain. Slices were incubated with [3H]2DG, or with L-[3H]glucose as a marker for diffusion; the difference between [3H]2DG uptake and L-[3H]glucose uptake was defined as net [3H]2DG transport. Net [3H]2DG transport was a function of incubation temperature, with an estimated temperature coefficient of 1.87 from 15 degrees C to 25 degrees C. The net uptake of [3H]2DG was not inhibited by phlorizin or phloretin in concentrations well above the reported Ki of these inhibitors for hexose uptake in other systems. To examine the hypothesis that [3H]2DG transport by brain slices is dependent on mitochondrial energy, we studied net [3H]2DG uptake by slices which had been preincubated in media designed to alter intracellular ATP stores. The transport process was very sensitive to inhibition by DNP, but the correlation between [3H]2DG transport and ATP levels was unclear. In contrast to our published hypothesis that the transport process required mitochondrial energy, these data indicate that dependence on energy is not absolute.

Adenosine Triphosphate↗
PubMed1981

[3H]2-deoxyglucose transport by slices of cerebral cortex: apparent dependence upon mitochondrial energy.

The transport of [3H]2-deoxyglucose by brain slices was studied. Cerebral cortex slices were incubated in vitro in the presence of [3H]2-deoxyglucose, or L-[3H]glucose as a marker for diffusion. Transport was defined as the difference between [3H]2DG uptake and L-[3H]glucose uptake. Half-maximal velocity was seen at 2.0 mM 2DG and [3H]2DG transport was not inhibited by 20-fold higher concentrations of L-glucose. Net [3H]2DG transport was unchanged in media deficient in Na+, K+, Mg2+, Ca2+ or Cl-. Uptake was significantly inhibited by 1.0 mM 2,4-DNP and a suggestion of inhibition by azide was seen. These data are consistent with a hypothesis that hexose transport in the brain depends to some extent upon mitochondrial energy.

Animals↗
PubMed1981

Cerebrospinal fluid GABA and cyclic nucleotides in alcoholics with and without seizures.

Cerebrospinal fluid levels of gamma-aminobutyric acid (GABA) and cyclic nucleotides were measured in alcoholic and control patients. Alcoholics without seizures had higher GABA levels than either alcoholics with seizures or controls. Levels of cyclic AMP and cyclic GMP in cerebrospinal fluid of controls and alcoholics with and without seizures were not significantly different.

Alcoholism↗
PubMed1980

CSF GABA in psychotic disorders.

CSF GABA levels were not significantly different in a group of drug-free psychotic patients compared to a group of psychotic patients at two points during haloperidol treatment or a neurological comparison group. In the untreated group, CSF GABA was significantly negatively correlated with clinical ratings of anxiety and agitation. Early in haloperidol treatment CSF GABA was significantly positively correlated with CSF HVA.

Adolescent↗
PubMed1980

GABA levels in CSF of patients with psychiatric disorders.

The authors measured gamma-aminobutyric acid (GABA) levels in the lumbar CSF of patients with depression, with psychosis, or undergoing evaluation for a neurologic disorder. GABA levels in the CSF from depressed patients were significantly decreased compared with neurologic control patients. CSF GABA levels in psychotic patients were not different from those in neurologic patients, although the data suggested a decrease in CSF GABA levels in patients with schizoaffective disorder.

Adult↗
PubMed1979

Denervation supersensitivity to serotonin in rat forebrain: single cell studies.

To investigate the development of denervation supersensitivity to serotonin (5-hydroxytryptamine, 5-HT) in the amygdala (AMYG) and the ventral lateral geniculate nucleus (vLGN), single cell recordings, microiontophoretic, histochemical and biochemical techniques were used in the present study. 5-HT projections to the vLGN and the AMYG were destroyed by 5,7-dihydroxytryptamine (5,7-DHT, a relatively selective toxin for 5-HT neurons) injected directly into the lateral ventricle or the ascending 5-HT pathway in the ventromedial tegmentum area. Enhanced responsiveness of cells to the inhibitory effect of microiontophoretically applied 5-HT (ionto-5-HT) began to develop within 24 h and approached a maximum 7 days after 5,7-DHT pretreatment. In general, the time courses for the reduction in both the density of 5-HT fluorescent varicosities and synaptosomal 5-HT uptake activity paralleled the time course for the development of denervation supersensitivity to 5-HT. During the first 2 days after 5,7-DHT, the enhanced sensitivity was selective for 5-HT; responses to D-lysergic acid diethylamide (LSD), norepinephrine (NE) and gamma-aminobutyric acid (GABA) were unchanged. Seven or more days after 5,7-DHT there was a marked increase of the responsiveness of neurons in the vLGN and the AMYG to both 5-HT and LSD (a 5-HT agonist which is not a substrate for the high affinity 5-HT uptake system). At these later times, the responsiveness of cells in the AMYG to NE and to a lesser extent GABA was also increased. In contrast to the marked supersensitivity seen after 5,7-DHT induced denervation, chronic administration of parachlorophenylalanine, a 5-HT synthesis inhibitor, failed to induce 5-HT supersensitivity.

5,7-Dihydroxytryptamine↗
PubMed1977

Effect of ethanol on the cyclic AMP system in rat brain.

The effects of ethanol on adenylate cyclase and phosphodiesterase activity in vitro, and on cyclic AMP, ATP and adenosine levels in vivo were studied. Ethanol appeared to affect the cyclic AMP system indirectly, probably through its effect on neurotransmitter release or on adenosine formation.

Adenosine↗
PubMed1975

Interactions of ethanol with cyclic AMP.

Ethanol and other alcohols stimulate adenylate cyclase activity in various tissues and potentiate its stimulation by some hormones. This effect, however, usually requires a high alcohol concentration. In some cases, an unknown substance, different from cyclic AMP, was formed from ATP in the presence of an alcohol and mimicked stimulation of adenylate cyclase. Ethanol inhibits phosphodiesterase activity in some tissues. In the brain, only the low affinity enzyme of pons-medulla region is inhibited. ATP levels and ATPase activities are affected by ethanol treatment and this can lead to secondary changes of the cyclic AMP levels. Cyclic AMP levels in the brain and liver are decreased by acute ethanol administration while levels in other organs are unchanged. High doses of ethanol inhibit the postdecapitation-induced rise of cyclic AMP level in the brain while low ethanol doses potentiate the postdecapitation rise of cyclic AMP in the lower brain stem. Chronic ethanol administration increases basal adenylate cyclase activity and cyclic AMP levels, and decreases stimulation of adenylate cyclase by norepinephrine in the brain. In contrast, the stimulation of cyclic AMP formation by norepinephrine and other biogenic amines is increased in the brain of ethanol-withdrawn animals. Chronic administration of ethanol affects also cyclic AMP levels and cyclic AMP formation in some peripheral organs. Cyclic AMP might be involved in ethanol-induced fatty liver, since it activates hepatic lipase and might also participate in the fatty acid oxidation.

3',5'-Cyclic-AMP Phosphodiesterases↗