Biomedical subjects

D R Collins

Publications and source records attributed to D R Collins.

At least 37 records · Page 2Linked to original sources

PubMed1995

Indirect potentiation of synaptic transmission by metabotropic glutamate receptors in the rat hippocampal slice.

The role that the metabotropic glutamate receptor plays in synaptic transmission is complex due to the multiple subtypes involved, which initiate a number of intracellular mechanisms. Here we have investigated the role of the metabotropic glutamate receptor in the induction of long-term potentiation (LTP). We have shown that, providing the CA3 region remains attached to the slice, it is possible to induce potentiation by bath perfusion of the metabotropic receptor agonist (1S,3R) 1-aminocyclopentane-1,3-dicarboxylic acid (ACPD) alone. The extent of the potentiation observed showed a strong negative correlation with the age of the animal from which the slices were prepared. Perfusion of ACPD was associated with an increase in the excitability of antidromically activated CA3 neurones, the appearance of spontaneous burst firing within the CA3 region, and an increased fibre volley recorded in the CA1 region. Blockade of N-methyl-D-aspartate (NMDA) receptors prevented all these effects. We suggest that the ACPD-induced potentiation of CA1 fEPSPs is an indirect effect caused by spontaneous burst firing and/or increased excitatory drive from CA3 neurones.

2-Amino-5-phosphonovalerate↗

PubMed1995

Modeling cation/anion-water interactions in functional aluminosilicate structures.

A need for the computer simulation of hydration/dehydration processes in functional aluminosilicate structures has been noted. Full and realistic simulations of these systems can be somewhat ambitious and require the aid of interactive computer graphics to identify key structural/chemical units, both in the devising of suitable water-ion simulation potentials and in the analysis of hydrogen-bonding schemes in the subsequent simulation studies. In this article, the former is demonstrated by the assembling of a range of essential water-ion potentials. These span the range of formal charges from +4e to -2e, and are evaluated in the context of three types of structure: a porous zeolite, calcium silicate cement, and layered clay. As an example of the latter, the computer graphics output from Monte Carlo computer simulation studies of hydration/dehydration in calcium-zeolite A is presented.

Aluminum Silicates↗

PubMed1995

Prevention by the cannabinoid antagonist, SR141716A, of cannabinoid-mediated blockade of long-term potentiation in the rat hippocampal slice.

Incubation of rat hippocampal slices in the presence of the synthetic cannabinoid (-)-11-OH-delta 8-dimethylheptyl tetrahydrocannabinol (HU-210) (100 nM) prevented the induction of long-term potentiation (LTP). Slices co-incubated with both HU-210 (100 nM) and the cannabinoid antagonist, SR141716A (100 nM), exhibited tetanically induced LTP, comparable to control slices. Intriguingly, coincubation with HU-210 and SR141716A prevented the induction of the early, short-term phase of LTP.

Animals↗

PubMed1994

The action of synthetic cannabinoids on the induction of long-term potentiation in the rat hippocampal slice.

Incubation of rat hippocampal slices with the synthetic cannabinoid (-)-11-OH-delta 8-dimethylheptyl tetrahydrocannabinol (HU-210) (100 nM) prevented the induction of long-term potentiation of field excitatory postsynaptic potentials recorded in the CA1 region. However, in slices incubated with its non-psychoactive (+)-isomer HU-211 (100 nM), which is reported to be an NMDA receptor antagonist, high frequency stimulation evoked a long-lasting potentiation, comparable to control slices.

Animals↗

PubMed1994

Potentiation of synaptic transmission in the rat hippocampal slice by exogenous L-glutamate and selective L-glutamate receptor subtype agonists.

We have investigated the effects of administration of exogenous glutamate receptor agonists on the amplitude of field excitatory post-synaptic potentials (fEPSPs) evoked in the CA1 region of the rat hippocampal slice by stimulation of the Schaffer collateral-commissural fibres. L-Glutamate applied by iontophoresis or by bath perfusion (50 microM for 5 min) evoked a slowly rising increase in the amplitude of the fESPS which persisted for over 90 min. L-Glutamate induced potentiation was blocked by either D(-)-2-amino-5-phosphonopentanoic acid (40 microM) or by (RS)-alpha-methyl-4-carboxyphenylglycine (500 microM). In slices in which synaptic long-term potentiation had been saturated, iontophoretically applied L-glutamate did not induce further potentiation, but reset the fEPSP amplitude back to control levels. Iontophoretic administration of N-methyl-D-aspartate (NMDA) evoked a transient potentiation which decayed back to control levels within 90 min whereas bath perfusion of NMDA (50 microM) evoked a persistent depression. Bath perfusion of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA, 50 microM) evoked no persistent effects. Bath administration of (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD, 50 or 100 microM) caused a short term depression of the fEPSP and no significant persistent effects. Perfusion of 100 microM ACPD in medium containing 1 microM picrotoxin caused a much smaller short term depression of the fEPSP and this was followed by a gradually developing and persistent potentiation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Co-administration of (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid and arachidonic acid potentiates synaptic transmission in rat hippocampal slices.

Perfusion of the 1S,3R isomer of trans-aminocyclopentane-1,3-dicarboxylic acid (t-ACPD, 50 microM), or arachidonic acid (10 microM), for 5 min produced only depression of the field excitatory postsynaptic potential recorded in the CA1 region of rat hippocampal slices from which the CA3 region had been removed. However, perfusion of t-ACPD and arachidonic acid in combination induced a rapid potentiation of the response which in 4/6 slices was maintained for at least 90 min.

Animals↗

PubMed1993

Early diagnosis of acute myocardial infarction with use of a rapid immunochemical assay of creatine kinase MB isoenzyme.

In 195 patients presenting with chest pain and referred acutely for cardiological assessment, blood was taken immediately for assay of creatine kinase (CK; EC 2.7.3.2) MB isoenzyme by an immunochemical method and results [mass units of enzyme per liter of plasma (microgram/L)] were obtained within 30 min of sampling. Diagnosis of acute myocardial infarction in the patients was made independently, based on electrocardiograms and conventional cardiac enzyme profiles. The administration of any thrombolytic therapy in response to the CK-MB concentration result was also noted, allowing assessment of the assay's potential influence on patient management in addition to the diagnostic efficiency evaluation. The study demonstrated that, when blood samples were collected on admission to hospital and the decision level suggested by the manufacturers was utilized, the assay had an immediate sensitivity of 52% and a specificity of 97%. Of the 81 patients who were shown by conventional means to have had acute myocardial infarction, 8 (10%) had equivocal electrocardiograms but positive CK-MB concentration results. In four of these patients (5%), thrombolytic therapy was given on the basis of the clinical features and a positive CK-MB concentration result alone.

Creatine Kinase↗

PubMed1988

Truncated variants of apolipoprotein B cause hypobetalipoproteinaemia.

Familial hypobetalipoproteinaemia is a rare autosomal dominant disorder in which levels of apo-B-containing plasma lipoproteins are approximately half-normal in heterozygotes and virtually absent in homozygotes. Here we describe mutations of the apo-B gene that cause two different truncated variants of apo-B in unrelated individuals with hypobetalipoproteinaemia. One variant, apo-B(His1795----Met-Trp-Leu-Val-Thr-Term) is predicted to be 1799 amino acids long and arises from deletion of a single nucleotide (G) from leucine codon 1794. This protein was found at low levels in very low density and low density lipoprotein fractions in the blood. The second, shorter variant, apo-B(Arg1306----Term), is caused by mutation of a CpG dinucleotide in arginine codon 1306 converting it to a stop codon and predicting a protein of 1305 residues. The product of this allele could not be detected in the circulation. The differences in size and behaviour of these two variants compared to apo-B100 or apo-B48 point to domains that may be important for the assembly, secretion or stability of apo-B-containing lipoproteins.

Amino Acid Sequence↗

PubMed1988

Genetic evidence from two families that the apolipoprotein B gene is not involved in abetalipoproteinemia.

Abetalipoproteinemia (ABL) is a recessive disorder in which affected individuals have extremely low or undetectable levels of serum apo B-containing lipoproteins. Using restriction fragment length polymorphisms, we have studied two families, each with two children with classical ABL born of normal parents. In each of these families, the two affected children have inherited different apo B alleles from at least one parent, whereas the siblings would be anticipated to share common alleles if this disorder were due to an apo B gene mutation. This linkage study shows that in these families, the apo B gene is discordant with ABL and therefore the disorder is caused by a defect in another gene, which is important for the normal synthesis or secretion of apo B-containing lipoproteins from both the liver and intestine.

Abetalipoproteinemia↗

PubMed1985