Hippocampal Neurogenesis: Proof of Long Term Rewiring

Scientists from Tubingen, Germany have been able to demonstrate long term plastic change in the learning centers of the brain — specifically they focused on an area involved in memory and spacial awareness. The study used stimulation and magnetic resonance imaging to show that changes in the hippocampus resulted in changes in the activation of broad areas of the brain.

I’m posting this here because it connects yet another link in the chain of growing evidence supporting the idea that brain training can lead to long term brain change. The recent Swedish study by the team from the Karolinska Institutet showed that working memory training results in neurogenesis. And now we have the conclusion that plastic change (intrinsically linked to neurogenesis) leads to long term restructuring in large areas of the brain.

Long Term Brain Restructuring - Before and After

Brain Activity Before And After Plastic Change

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3 Responses to “Hippocampal Neurogenesis: Proof of Long Term Rewiring”

  1. Will says:

    That’s interesting…what actual activity/brain exercises induced the change?

  2. martin says:

    Hi Will.

    It’s not exactly clear. I think that there was direct electrical stimulation which would mean that this wasn’t a study on people !

    Martin

  3. martin says:

    Hey Will.

    Found out some more:

    “Santiago Canals of the Max Planck Institute for Biological Cybernetics in Tübingen and his colleagues first anesthetized 14 rats, then made small openings in the animals’ skulls so that electrodes could be implanted into the hippocampus. The electrodes were fixed to the sides of the opening in the skull with dental cement and plastic screws. The rats were then fitted into a custom-made fMRI-compatible frame which prevented them from moving their heads, and placed in the scanner. In this way, the researchers could induce LTP in their experimental animals and simultaneously monitor the global changes in brain activity induced by it.

    “Following induction of LTP, stimulation of neurons in the perforant path was found to activate cells in the hippocampus which receive inputs from them, as measured by an increase in blood flow to that region of the brain. Unexpectedly though, it also led to increased activity in the subiculum and entorhinal cortex, areas which surround the hippocampus, and to activation of these same regions in the opposite hemisphere. In fact, the acitivity in the opposite hemisphere was found to be higher than that of the activity of cells in the hemisphere in which LTP had been induced. But the effects went even further afield than the hippocampus and adjacent regions – activation of neurons in the prefrontal cortex, nucleus accumbens and olfactory nucleus was also observed. Application of MK-801, a compound which blocks the NMDA receptor, inhibited this activity, confirming that it was occurring in response to the LTP induced in the perforant path-hippocampus synapses.

    “Earlier studies have shown that LTP induces a series of biochemical changes within individual neurons. These can eventually lead to structural changes in the microscopic organization of neurons which enable the potentiated connections to persist for longer periods of time. Cells can not only strengthen existing synapses, but they can form de novo connections, by sprouting new dendritic spines, the tiny finger-like projections at which synapses are located. However, these changes have until now been thought to occur only at the level of single potentiated synapses.

    “This new research provides the first evidence that the local modifications in synaptic connections induced by LTP lead to long-lasting changes in the activity of a diffuse network of brain regions, and even to facilitated communication between the two hemispheres. The fMRI data showed that hippocampal LTP recruits higher order association areas, as well as regions involved in emotions and others subserving different sensory modalities, all of which are known to be involved in memory formation. ”

    Martin

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