Biomedical subjects

Farid F Youssef

Publications and source records attributed to Farid F Youssef.

3 recordsLinked to original sources

PubMed2006

NMDA-induced preconditioning attenuates synaptic plasticity in the rat hippocampus.

It was recently demonstrated that glutamate could precondition hippocampal slices against the damaging effects of hypoxia, and we have now extended this observation by investigating (i) the ability of glutamate receptor agonists to act as preconditioning agents and (ii) the effects of preconditioning on synaptic plasticity. Using rat hippocampal slices, 15 microM NMDA applied for 10 min (chemical insult) caused abolition of the population spike potentials (PS) followed by approximately 33% recovery at 60 min post-insult. In comparison, a 5 min preconditioning exposure of 10 microM NMDA given 30 min prior to the insult significantly improved the recovery to 69%. Preconditioning did not alter paired pulse facilitation; however, it significantly enhanced paired pulse depression and reduced population spike long-term potentiation (PS-LTP) and LTP in field recordings. This effect on PS-LTP appeared to be NMDA receptor dependent and was blocked by the nitric oxide synthase inhibitors nitro-L-arginine methyl ester (L-NAME) and 7-nitro indazole (7-NI) but not by the adenosine receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). We conclude that preconditioning by NMDA can improve recovery following acute insults but may have deleterious effects on neuronal plasticity.

Action Potentials↗

PubMed2003

LTP-induced depression of response to hypoxia in hippocampus: effects of adenosine receptor activation.

Previous work has shown that long-term potentiation (LTP) can reduce the effects of hypoxia in depressing population spikes in rat hippocampal slices. We have now investigated the role of adenosine in this phenomenon. There is no mutual inhibition between the depressant effects of hypoxia and adenosine, but LTP reduces responses to both hypoxia and adenosine, as does application of an A1 receptor antagonist. The effect of LTP is not due to a change in the balance of activation of A1 and A2A adenosine receptors since a selective A2A receptor antagonist did not prevent the interaction. We suggest that LTP may reduce the response to hypoxia by attenuating neuronal sensitivity to adenosine A1 receptors.

Adenosine↗

PubMed2003

Neuroprotective role of learning in dementia: a biological explanation.

Several epidemiological studies have found an association between low educational level (or low cognitively demanding occupations) and dementia. Although other studies have not found evidence to support such an association, there has been a general trend toward a "use it or lose it" concept which attempts to promote a neuroprotective role of intellectual activity against the development of dementia. Formation of amyloid-beta peptide (Abeta) in the brain plays a key role in the development of Alzheimer's disease whilst glutamate has been implicated in the pathophysiology of a number of neurological disorders including Alzheimer's disease and vascular dementia. Abeta can mediate neurodegeneration by a complex interaction of neurodegenerative processes that involve increasing extracellular concentration of glutamate, increasing intracellular Ca2+ concentration, and apoptosis. Long-term potentiation (LTP, a biological correlate of learning and memory) increases the sensitivity of hippocampal neurons to synaptically released glutamate whilst decreasing responses of neurons to bath applied glutamate receptor agonists and to hypoxia/ischemia in vitro. The effects of LTP are likely to involve changes in intracellular Ca2+ concentration. Based on these findings we are proposing that the LTP-induced neuroprotection in vitro may help explain the epidemiological evidence of a possible neuroprotective role of high intellectual activity against dementia.

Amyloid beta-Protein Precursor↗