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D Benjamin

Publications and source records attributed to D Benjamin.

At least 181 records · Page 10Linked to original sources
PubMed1993

Naltrexone reverses ethanol-induced dopamine release in the nucleus accumbens in awake, freely moving rats.

The effect of the opioid receptor antagonist, naltrexone, on ethanol-induced changes in extracellular dopamine and serotonin in the nucleus accumbens was investigated using in vivo microdialysis in awake, freely moving rats. Locally applied ethanol (5% infused transprobe) resulted in substantial increases in dopamine in dialysate. Administration of naltrexone (cumulative dosing with 0.25-1.0 mg/kg i.p.) during ethanol administration dose-dependently reversed ethanol-induced increases in extracellular dopamine and its metabolite homovanillic acid but not serotonin. These data demonstrate an essential role for the endogenous opioid system in stimulation of dopamine release by ethanol in a brain area associated with reward and support the opioid system as a prime target for pharmacological modulation of the rewarding effects and consumption of ethanol.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1993

Characteristics of endogenous peptides eluted from the class I MHC molecule HLA-B7 determined by mass spectrometry and computer modeling.

Microcapillary HPLC electrospray ionization tandem mass spectrometry was used to sequence 15 peptides eluted from HLA-B7. Sequence alignment implicated four peptide positions in specific interactions with the class I molecule, and their importance was confirmed using synthetic peptides. Because no crystal structure for HLA-B7 was available, computer-assisted modeling was used to understand novel aspects of peptide binding specificity and to accurately predict the effect of defined changes in peptide structure. The results demonstrate that mass-spectrometric sequencing coupled with computer-assisted modeling can be used in the absence of a crystal structure to make accurate predictions concerning requirements for peptide binding to class I molecules. These techniques may be valuable to predict or engineer T cell epitopes.

Amino Acid Sequence↗
PubMed1993

Increased protein kinase C activity in human memory T cells.

A number of T cell surface antigens including CD45R0, CD58, CD11 alpha, CD29, CD44, and CD26 are present on differentiated T cells and identify T cell populations that respond to recall antigens. To further study the biochemical basis for this immune memory, we used an anti-CD26 mAb to identify the memory T cell population. We have previously shown that CD26+ T cells display an increased proliferative response to anti-CD3 and anti-CD2 mAbs and furthermore have significantly greater PMA-induced phosphorylation of the invariant gamma and delta chains of the T cell receptor (TCR)/CD3 complex when compared to CD26-T cells. This suggested that differential distribution of protein kinase C (pkC) in the CD26 subsets may be related to the reduced activation requirements observed in memory T cells upon recall antigen challenge. We now directly demonstrate that when peripheral blood T cells are sorted into CD26+ and CD26- T cells the majority of pkC activity can be recovered from the cytosol fraction of the memory (CD26+) T cell population. When activated through the TCR/CD3 pathway, the CD2 pathway, or directly by the phorbol ester, PMA, the memory (CD26+) T cells showed an increased proliferative response that was inhibited by the pkC inhibitor, staurosporine. When CD26+ T cells were cultured in the presence of PMA, which depletes pkC activity, CD26 antigen expression was down-regulated. PMA was also able to inhibit phytohemagglutinin (PHA)-induced expression of the CD26 antigen in CD26- T cells. These data demonstrate a relation between CD26 expression and pkC activity and suggest that enhanced pkC activity is associated with memory T cell function.

Alkaloids↗