I am especially excited that V.P. Whittaker (one of the godfathers of synaptosome research) will be lecturing. The talk is listed under Cell and Molecular Neurobiology: Antecedents and Achievements. It will be in Ballroom 20 on Tuesday 16 Nov from 2:30 – 3:40PM.
Synaptosomes are artificial organelles that, in theory, represent the cellular environment present at nerve terminals. They are isolated by homogenization of brain tissue followed by a specific series of centrifugations. Essentially, the sheer force causes them to snap from the cell body and when the membrane seals back the resulting ‘synaptosome’ retains the necessary machinery to maintain functionality (i.e. uptake, storage and release of neurotransmitters). Fast-forward about 60 years from the very first isolation and the preparation is still a very useful way to study endogenous and elicited activity in this specialized region of the neuron.
Here’s an interesting paper I have come across in that field: Antioxidant strategy to rescue synaptosomes from oxidative damage and energy failure in neurotoxic models in rats: protective role of S-allylcysteine.
Elinos-Calderon. D, et al. J Neural Transm. 2010 Jan;117(1):35-44. Epub 2009 Oct 29
The authors tested S-allylcysteine (SAC), abundant antioxidant organosulfur compound from the aged garlic extract (bonus points!), as a post-treatment in different in vitro and in vivo neurotoxic rat models.
One in vivo model of Huntington’s Disease they used was mitochondrial inhibitor 3-nitropropionic acid, a micotoxin capable to selectively inhibit the mitochondrial electron transport chain through the irreversible inhibition of Complex II (succinate dehydrogenase) As a result, ATP levels are decreased leading to membrane depolarization, indirect excitotoxicity, oxidative stress, and neuronal degeneration. SAC was given to 3-NP-striatally lesioned rats for 7 consecutive days.
Elinos-Calderon suggests that SAC is able to exert some protection on biochemical markers of redox activity (elevation of lipid perioxidation and mitochondria dysfunction.) They associated the effect with preserving major physiological functions evidenced by the behavioral assessment. This supports the concept that the ongoing oxidative damage and energy depletion can be treated during the first stages of neurotoxic events.