Depression stuff

• NIBS = non invasive brain stimulation
• tDCS = transcranial direct current stimulation
• TM = transmagnetic stimulation
• TMS is an electromagnetic induction with a pulse with a constant frequency that can increase or decrease excitability
• Anode in tDCS provokes increased cortical excitability
• Cathode in tDCS provokes decreased cortical excitability
• tDCS involves a weak current (2 mA) during 20 minutes, depending on the polarity you'll have different effects
• In depression there is a decreased reactivity to stress. This is because the over excitability of the DLPFC = meaning also an over-sensibility to stress.
• Right part brain in depression is hyper and left part is hypo
• The lasting effects depend on low/high frequency and electrode polarity (anode/cathode)
• local effect = immediate responses of brain
• local offline effect = changes in the brain that persist after stimulation has ended, aka the "neuroplastic" changes
• distal effects = changes of brain activity and connectivity occuring in areas not directly affected by stimulation
• Example of level A evidence is the anode of tDCS over the left DLPFC
• if you want to stimulate things : for mood it's on the left and for anxiety on the right
• if TMS on the motor cortex then inducing MEP aka motor evoked potentials
• Why stimulating the DLPFC ?

  Because by increasing activity in there you get more NT realsed in hippocampus and striatum which therefore will have an impact on hypothalamus and pituitary.
• NICB → DLPFC →  stimulation of hippocampus and striatum → hypothalamus → pituitary →  adrenal gland
• The DLPFC is the dorso lateral prefrontal cortex
• MDD can lead to other chronic diseases such as cardiovascular disease, diabetes, and obesity
• MDD symptoms related to the bio psycho social model
• GWAS is the genome wide association sudies is a large scale study to identify MDD genetic factors
• MDD risk factors are very polygenic (a lot of genes that have a small effects) but there are combined to the different types of MDD
• Genetic related pathways that are altered in MDD can be :

  • histocompatibility complex genes = immune system
  • calcium signalling genes in neurons
  • DA and glut neurotransmission
  • synaptic vesicle trafficking genes
• Hypoactivity of the left DLPFC in MDD
• Hyperactivity in right DLPFC, amygdala, hippocampus, ACC and thalamus in MDD
• Animal models can be created from behaviour like :

  • early life stressors
  • stress applied during adulthood
• Early life stressors in animal models can be :

  • maternal separation
  • poor mothering
• Chronic stress applied during adulthood in animal models can be :

  • social instability
  • learned helplessness
  • social defeat stress
  • social transmission of stress
• Biological modes in animal models of MDD can be :

  • LPS injection
  • Bulbectomy
  • Corticosterone drinking
  • Genetic model
  • Optogenetic manip
• Behavioral tets on rodents can be used in order to test out :

  • anhedonia = sucrose or cookie test
  • dispair = forced swim & tail suspension
  • apathy = grooming & nest building
  • anxiety = forced confrontation or motivational conflict
• To test anhedonia in mice you can use tests like sucrose or cookie test
• To test dispair in mice you can use tests like forced swiming and tail suspension test
• To test apathy in mice you can use tests like grooming and nest building
• To test anxiety in mice you can use tests like open field test or feeding suppression
• Tricylic antidepressants (TCAs) can block :

  • SERT (5HT transporter)
  • NET (NE transporter)
  • H1 and 5HT2 receptors (5HT Rc)
• Monoamine oxidase inhibitors (MAOIs) are blocking :

  MAO A or MAO B which are both targetting enzymes that degradate dopamine
• Selective serotonin-reuptake inhibitors (SSRI) block serotonin transporters
• Serotonin-norepinephrine reuptake inhibitor (SNRI) can block :

  • SERT (5HT reuptake transporter)
  • NET (NE reuptake transporter)
• Alzheimer's disease can reduce depressive behavior, anhedonia and anxiety