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[RazB]

Hey Guys

I've been following this forum since my early days as a master student (in psychology), and currently I'm conducting my PhD research in neurosciences in Helsinki university.

 

My research project is dealing directly with neuro-plasticity; or more specifically, how to use neuroplasticity in order to treat depression and Alzheimer. We have developed an optogenetic model that allows us to induce plasticity in a localized place in the brain & to a specific type of cell linage with blue laser. My specific specialization observing the brain of a living, awake animal (mice) under a specialized microscope (two-photon microscopy) with different degrees of induced neuroplasticity. This microscope allows us to study how the neurons 'talks' with each other in real time, much like fMRI, but unlike fMRI- we can observe these interaction on the cellular level. For those that interested, how this 'magic' is happening, you can read about calcium imaging here.

 

I have acquired some knowledge, and hopefully some useful insights in the field while working and designing my PhD project. If you have questions that are dealing with neuroplasticity and\or SSRI medications, please do ask.

 

Just to get the conversation going, I wish to share with you couple of insights about neuroplasticity that really surprised me.. and should be considered here on the forum:

 

1. Synaptogenesis & increased connectivity aren't always a good news for cognition

       >Two famous examples of brain disorder that induces over-connectivity and are bad for cognition, is autism & Down-syndrom

 

2. Over-stimulate your brain will not necessarily result  in healthy or efficient brain

       > Over secretion of NMDA/ glutamate is the neuronal basis of many psychiatric disorders, Schizophrenia for example.

 

3. Decreased connectivity might mean more efficient brain, and better cognition 

  

 

Now I'm not bringing up all this information in order to be a party-destroyer for the common nootropic user. However, I do bring it up in order for us to cultivate better and deeper understanding of the tissue and structures we try to "hack" and enhance =]

 

[Galaxyshock]

Good, hope you contribute more here. Isn't Schizophrenia considered a hypoglutamatergic (not excess) disorder though? As PCP-site NMDA-antagonists mimic the symptomatology. Or is there inital excess of glutamate/NMDA signalling in development of the disorder that exhausts the glutamatergic system or something.