viernes, 28 de diciembre de 2012

Synaptic plasticity in depression: Molecular, cellular and functional correlates

Progress in Neuro-Psychopharmacology and Biological Psychiatry
22 December 2012

  • Highclere Court, Woking, Surrey, GU21 2QP, UK


Synaptic plasticity confers environmental adaptability through modification of the connectivity between neurons and neuronal circuits. 

This is achieved through changes to synapse-associated signaling systems and supported by complementary changes to cellular morphology and metabolism within the tripartite synapse. 

Mounting evidence suggests region-specific changes to synaptic form and function occur as a result of chronic stress and in depression. 

The prefrontal cortex (PFC) and hippocampus represent the best studied regions where functional and structural findings are consistent with a deficit in long-term potentiation (LTP), and neuronal and glial growth at excitatory synapses. 

Correlating these changes may be those to glutamate receptors (AMPARs and NMDARs), growth factor signaling (BDNF-TrkB) and several signal transduction pathways (NOS-NO, cAMP-PKA, Ras-ERK, PI3K-Akt, GSK-3, mTOR and CREB). 

In contrast other brain regions such as the amygdala may feature a somewhat opposite synaptic pathology including reduced inhibitory tone. 

Deficits in synaptic plasticity may further correlate disrupted brain redox and bioenergetics in stress and depression. 

Moreover, at a functional level region-specific changes to synaptic plasticity in depression may relate to maladapted neurocircuitry and parallel reduced cognitive control over negative emotion.

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