This morning I virtually attended this conference:
Majia here:You can download the speakers/lectures here
The first two speakers focused on chemicals and autism. They were particularly interested in PCBs and neuro-toxicity.
I was personally most interested in the first speaker, Dr. Pamela Lein's presentation: Environmental Risk Factors in the Development of ASD, which focused on PCBs.
She says that efforts to link PCBs to autism have addressed three possible exposure effects:
1. Decreased dopamine content
2. Interference with thyroid hormone signaling
3. Increased levels of intracellular calcium
She focused on levels of intracellular calcium in her presentation. She postulates that PCBs affect neuronal growth, by impacting intracellular calcium:
Here is a slide from her presentation on the importance of calcium-ion channels in neural development (adopted from Krey and Kolmetsch 2007):
Here research has found that PCBs 'hijak' calcium-ion signaling pathways that control activity dependent dendritic growth
Majia here: Alterations to dendritic growth have adverse effects for 'normal' neurological development.
Her findings support her hypothesis that PCBs adversely impact dendritic growth and synpatic development, which may pose one causal pathway towards autism.
Studies on PCBs are critically important because of their ubiquity in our environment.
However, her findings suggest that any chemical or element that can be uptaken into the brain's calcium-ion channels may have similar, or worse, impacts on dendritic growth and synaptic development.
I would like to challenge autism researchers to look at radiocesium and radiostrontium which are long lived radio-isotopes that can be upaken into the brain's calcium-ion channels.
I'll focus on strontium, which the body confuses with calcium. Brain cells have calcium stores and radiostrontium would be stored in these sites, where it would decay. Decay inside the brain would, no doubt, have all sorts of problematic influences beyond chemical effects on dendritic growth processes.
See the abstract at the end of this post about how strontium enters the brain's calcium-ion channels.
Consider all the cesium and strontium in our environment from atmospheric testing, nuclear accidents (ranging from known to classified).
These radioactive elements will be in our bodies, just as lead and mercury are. Environmental science has examined lead and mercury so effectively. Why aren't scientists studying radio-isotopes and autism? Radioisotopes could also explain the DNA microdeletions found in autism!
Radio-iodine should also be studied. It could explain the 'Interference with thyroid hormone signaling' hypothesis for autism.
I love environmental science but I don't understand why the environmental scientists won't study radiation!
Here is an abstract documenting how strontium enters brain's calcium-ion channels.
M. A. Xu-Friedman and W. G. Regehr (1999) Presynaptic strontium dynamics and synaptic transmission Biophys J. 1999 April; 76(4): 2029–2042. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1300177/
Strontium can replace calcium in triggering neurotransmitter release, although peak release is reduced and the duration of release is prolonged. Strontium has therefore become useful in probing release, but its mechanism of action is not well understood.
Here we study the action of strontium at the granule cell to Purkinje cell synapse in mouse cerebellar slices. Presynaptic residual strontium levels were monitored with fluorescent indicators, which all responded to strontium (fura-2, calcium orange, fura-2FF, magnesium green, and mag-fura-5).
When calcium was replaced by equimolar concentrations of strontium in the external bath, strontium and calcium both entered presynaptic terminals. Contaminating calcium was eliminated by including EGTA in the extracellular bath, or by loading parallel fibers with EGTA, enabling the actions of strontium to be studied in isolation.
After a single stimulus, strontium reached higher peak free levels than did calcium (approximately 1.7 times greater), and decayed more slowly (half-decay time 189 ms for strontium and 32 ms for calcium). These differences in calcium and strontium dynamics are likely a consequence of greater strontium permeability through calcium channels, lower affinity of the endogenous buffer for strontium, and less efficient extrusion of strontium.
Measurements of presynaptic divalent levels help to explain properties of release evoked by strontium. Parallel fiber synaptic currents triggered by strontium are smaller in amplitude and longer in duration than those triggered by calcium. In both calcium and strontium, release consists of two components, one more steeply dependent on divalent levels than the other.
Strontium drives both components less effectively than does calcium, suggesting that the affinities of the sensors involved in both phases of release are lower for strontium than for calcium. Thus, the larger and slower strontium transients account for the prominent slow component of release triggered by strontium
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