Neuroscience Sem 2 Flashcards
(35 cards)
What is the incidence rate of Schizophrenia?
- Effects 1% of population (fairly common)
- Means ‘splitting of psychic functions’
- 45% concordance in monozygotic twins
- 10% concordance in dizygotic twins
What are the symptoms (positive + negative) of Schizophrenia
Positive symptoms:
- Bizarre delusions
- Inappropriate affect (emotions)
- Odd behaviour
- Incoherent thought
Negative symptoms
- Social withdrawal
- Depression
What are some drugs that are prescribed to treat schizophrenia/psychosis
- Reserpine (agonist)
- Chlorpromazine (antagonist)
- Haliperidol
Explain how Reserpine works to treat Schizophrenia
Reserpine
- Depletes dopaminergic vesicles
- Reducing the amount of DA that can be released (agonist)
Explain how Chlorpromazine works to treat Schizophrenia
Chlorpromazine
- It’s a false transmitter (antagonist)
- Binds to receptors, but has no effect
- As a result, it stops DA from working as DA is blocked from getting to receptors
Explain how Haliperidol works to treat Schizophrenia
Haliperidol
- Very potent anti-psychotic drug
- Little evidence for binding with DA receptors until D1/D2 receptors found
- Higher potency binding to D2 receptors
Explain these keywords:
Agonist
Antagonist
Enzyme
Adenylate cyclase
Agonist - Drug that elicits an effect on receptors (depletes dopaminergic receptors
Antagonist - Drug that binds to receptor with no effect, blocking other chemicals from binding (blocks)
Enzyme - speeds up a chemical process
Adenylate cyclase - Enzyme that helps send messages within a cell
Explain the Dopamine Theory of schizophrenia
- Drugs that increase dopamine neurotransmission (cocaine, amphetamines) produce psychotic symptoms
- Drugs that reduce dopamine neurotransmission (chlorpromazine, haliperidol) reduce psychotic symptoms (too little leads to Parkinson’s)
- This leads to DA theory of schizophrenia
What is the difference between Contingent drug tolerance and Conditioned drug tolerance?
Contingent drug tolerance
- Tolerance only develops to experienced drug effects
Conditioned drug tolerance
- Maximal tolerance is experienced in the environment in which the drug is usually taken (toilet cubicle etc.)
What are the three main ways in which drugs can be consumed
Ingestion (orally)
- Easy + relatively safe, although absorption via digestive tracts is unpredictable
Injection (bypasses digestive tract)
- Subcutaneously (SC) - under the skin
- Intramuscularly (IM) into large muscles
- Intravenously (IV) - into veins - drug delivered straight to the brain
Inhalation (tobacco/marijuana)
- Absorbed through capillaries in the lungs
- Absorbed through mucous membranes (nose/mouth)
Explain the case of HM
27 year old male suffered extreme epilepsy
Had a bilateral removal of temporal lobes in 1953
Temporal lobes = amygdala + hippocampus
What is retrograde/anterograde amnesia
Anterograde amnesia - past memories before the brain lesion
Retrograde amnesia - Future memories disrupted after brain lesion (can’t form new memories)
What type of tasks did HM fail at?
/
What was his main problem
Digit span +1 task (he never got past 6 digits)
Most got to 15
He didn’t get past 6 in the colour block challenge either
- His main problem was memory consolidation: transfer of STM into LTM
Which long term memory tasks could HM do?
Implicit (unconscious learning tasks)
- Rotary pen (procedural memory task)
- Incomplete picture task (priming)
- Tone with air blown in eye (classical conditioning)
Explain the case of patient R.B
Product of a bungled operation
- Interruption to blood supply to brain during heart surgery
- Damage to pyramidal cell layer of CA1 subfield in hippocampus
- Indicates small damage to hippocampus is enough to get amnesia symptoms
Explain Korsakoff’s syndrome
- Too much alcohol
- Vitamin B1 deficiency
- Similar to medial temporal lobe amnesia (retrograde)
- As disease progresses it becomes anterograde as well
What is the delayed non-matching to sample task
Tests object recognition memory + explicit LT memory
- Monkey removes sample object to get food underneath
- Delay period (screen lowered)
- Monkey shown same object + novel object
- Monkey must choose novel object to get food
Monkey’s performance greatly diminished after medial temporal lobe is lesioned
Is there a specific part of the medial temporal lobe involved in memories
Was originally thought that the hippocampus was responsible for memory deficits, however the rhinal cortex was also damaged in the lesions
Mumby box task with rats showed that the rhinal cortex was actually involved
What is ischemia and how is it involved in memory deficits?
Ischemia is loss of oxygen and glucose to the brain
- Damage is severe from later effects of glutamate over excitement
- Hippocampus susceptible because it has a lot of glutamate receptors
- Sends glutamate to other areas of the brain, possibly killing other regions
Explain the LTP Hebb proposed learning at the synapse study
Brain taken out + hippocampus activity recorded
- Input into hippocampus is through the perforant path
- First group of cells are in the dendate gyrus
- Single electrical pulse into perforant path + recorded
- Trains on high frequency stimulation into perforant path
- 1 day + 1 week after induction, a single pulse will give a bigger response
- This is known as Long Term Potentiation (LTP)
What can calcium trigger inside cell
Calcium can trigger cascades inside the cell that can lead to LT changes
Nitric oxide triggered by calcium
What is one critical factor for LTP
Co-occurence of firing in pre and post synaptic neurons is the critical factor for LTP
What is the hallmark of Alzheimer’s Disease
- Massive neurodegeneration (memory loss)
- Amyloid Plaques are the hallmark of AD
- Amyloid means “starch” but it’s actually a protein
Explain Amyloid Precursor Proteins (where it’s found/relationship with Alzheimer’s)
- Found on chromosome 21 (same as Down’s syndrome)
- If you have 3 copies of APP, you will have 150% more Amyloid - more likely to get AD
- Genetic forms of AD have early onset and are usually mutations of the APP gene
