Glial cells and schizophrenia?!

Glial cells…..neurons…nope. Glial cells.

I keep coming back to glial cells, no matter how I keep rationalizing things, I find myself always coming back to wondering what role glial cells have in all of the disorders we have been discussing. In particular (of course) I am interested in the role of glial cells in schizophrenia. It just seems to make so much sense. For instance, if someone was sick we wouldn’t assume it was just them getting sick. There must be some cause. We might assume the food. However, when we discuss neural issues, I feel like we always just assume neurons as the cause for everything. But what if the issues with neurons is the version of ‘sick’ in this case? Then what is the tainted food? I’d posit that it would be glial cells. They form the structural stability for the neurons, and they provide the neurons with everything they need to function. Take that away, and you don’t have too much. Imagine–taking away your skeleton and trying to function as a bag of skin. Yeah…structure is important!

During all of my research on glial cells this semester during my free time (yeah..i don’t know where I found this free time either..)I found many papers on glial cells and depression, glial cells and addiction..glial cells and everything. However, I always had a hard time finding anything relating glial cells to schizophrenia. I did manage to find an article recently that I think is really interesting. I have included the abstract below:

Glial-neuronal interactions are impaired in the schizophrenia model of repeated MK801 exposure.
Kondziella et al., 2006

Schizophrenia-mimicking compounds such as phencyclidine (PCP) and MK801 are antagonists at the N-methyl-D-aspartate (NMDA) receptor and produce the whole spectrum of positive, negative, and cognitive symptoms. This is one of the most important pillars of the hypoglutamatergic hypothesis of schizophrenia. Since the synthesis of glutamate and GABA in neurons is closely connected to astrocyte metabolism, the study of astrocytic function is essential in this context. Dizocilpine-maleate (MK801) (0.5 mg/kg) was injected into rats every day for 6 days. The last dose was given together with [1-(13)C]glucose and [1,2-(13)C]acetate. Extracts from frontal, retrosplenial, and cingulate cortices (CRFC) and temporal lobes were examined by (13)C nuclear magnetic resonance spectroscopy, high pressure liquid chromatography, and light microscopy. In CRFC, significant increases in the levels of glutamate, glutathione, and taurine were seen, whereas amounts and turnover of noradrenaline, dopamine, and serotonin were unchanged. Glutamate and glutamine, derived from [1,2-(13)C]acetate and thus astrocytes, were significantly decreased in CRFC as compared to controls. Labeling from [1-(13)C]glucose and thus mostly neuronal metabolism was affected in the same brain region with decreased labeling of glutamate and GABA. The present model mimics the increased glutamate/glutamine activity found in drug-naive patients with first episode schizophrenia. Moreover, the decreased labeling indicates the transition to lower glutamatergic function seen in chronic schizophrenia patients. The disturbance in astrocytic function and the glutamine-glutamate-GABA cycle are of significant importance and might add to the malfunction of the cortico-striato-thalamo-cortical loop caused by NDMA receptor blockade.

So what is the issue with glial cells and schizophrenia? Some papers seem to suggest an over-activation, some that there aren’t enough. Which makes sense based on the symptoms of the disorder? What do you think? It could be possible that a lack of glial cells could provide issues, but what if too much structure, or too much glial expression, could also be an issue?

I suppose we can always go back to ‘everything in moderation’.

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