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S L Almond

Publications and source records attributed to S L Almond.

4 recordsLinked to original sources
PubMed2006

Behavioral and biochemical characterization of a mutant mouse strain lacking D-amino acid oxidase activity and its implications for schizophrenia.

D-amino acid oxidase (DAO) degrades D-serine, a co-agonist at the NMDA receptor (NMDAR). Hypofunction of the NMDAR has been suggested to contribute to the pathophysiology of schizophrenia. Intriguingly, DAO has been recently identified as a risk factor for schizophrenia through genetic association studies. A naturally occurring mouse strain (ddY/DAO-) has been identified which lacks DAO activity. We have characterized this strain both behaviorally and biochemically to evaluate DAO as a target for schizophrenia. We have confirmed that this strain lacks DAO activity and shown for the first time it has increased occupancy of the NMDAR glycine site due to elevated extracellular D-serine levels and has enhanced NMDAR function in vivo. Furthermore, the ddY/DAO- strain displays behaviors which suggest that it will be a useful tool for evaluation of the clinical benefit of DAO inhibition in schizophrenia.

Acoustic Stimulation↗
PubMed2003

Pseudoainhum in chronic psoriasis.

Pseudoainhum is a term used to describe the presence of constricting bands of the extremities due to a variety of underlying causes. Progression of the lesions can cause irreversible damage and autoamputation of the affected digit. This report documents a rare association of pseudoainhum and psoriasis and emphasizes the importance of recognizing this condition.

Adult↗
PubMed1996

Characterisation of the rat cerebella CB1 receptor using SR141716A, a central cannabinoid receptor antagonist.

We describe the use of SR141716A, a central cannabinoid antagonist, in radioligand binding and adenylyl cyclase (AC) inhibition studies in rat cerebella membranes. The binding of [3H]SR141716A was dose-dependent and saturable, with Kd and Bmax of 0.61 +/- 0.12 nM and 1752 +/- 294 fmol/mg protein, respectively. Kinetic analysis of [3H]SR141716A binding afforded a Kd of 0.72 nM. In addition [3H]SR141716A was displaced dose-dependently by unlabelled SR141716A yielding a pKi of 8.37 +/- 0.07. Cannabinoid receptor agonists displaced [3H]SR141716A in a dose-dependent manner, (pKi) nabilone (8.29 +/- 0.08), WIN 55,212-2 (7.75 +/- 0.15), delta 9-tetrahydrocannabinol (7.29 +/- 0.21), delta 8-tetrahydrocannabinol (6.53 +/- 0.09) and anandamide (5.92 +/- 0.04). The affinity of anandamide was increased (6.26 +/- 0.13) by co-incubation with a serine protease inhibitor. A range of 13 commonly used non-cannabinoid ligands included at 100 microM were unable to displace [3H]SR141716A. WIN 55,212-2 inhibited basal cAMP formation dose-dependently with a pIC50 of 7.61 +/- 0.12 (24.3 nM) in an SR141716A (1 microM) reversible manner.

Animals↗