Neuro: Depression Flashcards
How do genetics and the environment affect behaviour?
- The brain is a product of our genetics
- The environment can interact with the genetics of our brain which can affect brain function and as a result behaviour
Depression is a type of affective disorder. What is an affective disorder?
- They are disorders of mood rather than thought or cognition
- Depression is most common affective disorder
What are the 2 main types of depression?
- Unipolar depression
- Bipolar depression
What are some of the characteristics of unipolar depression?
- Mood swings in one direction
- Most common type of depression
- Environmental factors induce this type of depression more than genetic factors
What are some of the characteristics of bipolar depression?
- Switching between depression and mania
- Mania - state of enhanced emotions. E.g. excessive self-confidence/enthusiasm as well as excesive aggression/irritability
- Less common than unipolar depression
- Much higher genetic contribution compared to bipolar depression
What is the difference between a depressive disorder and a major depressive disorder?
- A depressive disorder a low state marked by significant levels of sadness, lack of energy and self-worth
- A major depressive disorder is a severe pattern of all the characteristics of a depressive disorder and is disabling
How is depression diagnosed?
- The diagnosis for depression is based on a person having the following symptoms in the same 2 week period:
- Depressed mood - most of the day, everyday
- Greatly reduced interest/pleasure in most activities
- Signifcant weight loss (when not dieting) or weight gain
- Insomnia or hypersomnia
- Loss of energy
- Recurring thoughts of death
- One of these symptoms has to be depressed mood or loss of interest/pleasure
What are the 2 categories of symptoms of depression? For each type name a few examples
- Emotional symptoms
- Loss of motivation
- Low self esteem
- Pessimism/negativity
- Biological symptoms
- Reduced activity
- Loss of libido
- Loss of appetite
Depression is often found co-morbid (occuring with) other psychiatric and non-psychiatric disorders. Name of the disorders that often occur with depression
- Terminal illness - e.g. cancer
- Chronic pain
- Drug abuse
- Parkinson’s disease
- Anxiety
Explain the monoamine theory of depression
- Theory states that depression is caused by low levels of monoamine synaptic transmission within the brain
- Specifically low levels of Noradrenaline and Serotonin (5-HT)
What pieces of evidence are there that support the monoamine theory of depression?
- Resperine causes depletion of Noradrenaline and Sertonin stores in the brain by preventing uptake into vesicles - this eventually leds to it all leaking out into synaptic cleft
- Depression is induced in mice which are injected with reserpine
- Also, all major antidepressant drugs increase noradrenaline and/or serotonin levels in the brain
What pieces of evidence go against the monoamine theory of depression?
- Samples of Cerebrospinal fluid (CSF) and blood taken from people with depression has shown levels of NA and 5-HT to be normal - levels should be low based on monoamine theory
- Low serotonin levels more linked with increased aggression rather than depression
- Most antidepressant drugs take weeks to induce therapeutic effects - based on monoamine theory therapeutic effects should occur staright away as increase in NA and 5-HT due to antidepressants occurs straight away
Explain the neuroendocrine theory of depression
Theory states that depression is caused by hyperactivity of the HPA-axis
- Not-normally stressful stimuli will cause almost constant activation of the Noradrenergic and Serotonergic neurons in the hypothalamus
- This causes hypothalamus to release Corticotrophin-releasing hormone (CRH) into hypophyseal-portal circulation where it’ll bind to receptors on corticotroph cells on anterior pituitary
- This will cause corticotroph cells to secrete Adrenocorticotropic hormone (ACTH) into circulation
- ACTH will bind to receptors on adrenal glands leading to secretion of cortisol
- Because HPA-axis is hyperactivated cortisol levels will remain very high in the blood for an extended period of time
- This leads to symptoms of depression
What two brain areas input into the HPA-axis and what effect do they have on the HPA-axis?
- Amygdala - Activates HPA-axis
- Hippocampus - Inhibits HPA-axis
Apart from producing negative feedback on the hypothalamus and anterior pituitary, how else does cortisol prevent its own release?
- Cortisol binds to glucocorticoid receptors on hippocampus causing activation of hippocampus
- Actiavtion of hippocampus will cause the inhibition of the HPA-axis
- Inhibition of the HPA-axis will result in cortisol not being secreted
Explain the mechanism of how monoamine oxidase inhibitors work
- Monoamine oxidase inhibitors inhibit monoamine oxidase
- This means less Noradrenaline/serotonin is broken down when it’s taken back up into pre-synaptic neuron so there’s increased levels in the pre-synaptic neuron
- This leads to greater release of NA/5-HT into synaptic cleft which leads to more activation of post-synaptic noradrenergic and serotonergic neurons
Explain the mechanism for how selective serotonin reuptake inhibitors (SSRIs) work
- They inhibit the Serotonin reuptake transporter (SERT) which leads to more Serotonin in the synaptic cleft as it can’t be transported back into pre-synaptic neuron
- This leads to increased activation of serotonergic neurons
- They also inhibit 5-HT1A and 5-HT1D receptors which are autoreceptors for serotonin
- This leads to increased Sertonin release into synaptic cleft via exocytosis
