5.1.3 Sz- Bio expl (NTs) Flashcards
Define ‘neurotransmitter’.
A chemical messenger that transfers an electrical impulse by diffusion at the synapse.
Briefly describe synaptic transmission, using 5 points.
1) The electrical impulse travels down the axon terminal and stimulates the vesicles full of neurotransmitters
2) The vesicles then move down the pre-synaptic neuron to fuse with the pre-synaptic membrane
3) The neurotransmitters are then released as chemical messengers and diffuse across the synaptic gap
4) They attach to the corresponding receptor on the dendrite of the post-synaptic neuron and will then be absorbed
5) Any neurotransmitters that are not absorbed will get reabsorbed by the pre-synaptic neuron in the process of reuptake through the transporters
What does the ‘dopamine hypothesis’ state about schizophrenia?
Chemical imbalance through excess dopamine in the brain causes schizophrenic symptoms.
What 3 ways can excess dopamine activity be explained?
1) Through excess release by the axon
2) Having too many dopamine (D2) receptors
3) Over-sensitivity of the receptors
Describe the dopamine hypothesis using the 3 explanations.
- Patients having more D2 receptors means more dopamine can bind to them which could lead to over-sensitivity that can occur through genetic inheritance
- Positive symptoms, such as paranoia, are therefore caused by over-activation of the D2 receptors
- The meso-limbic pathway is the reward and fear pathway that can contribute to positive symptoms when there is an excess of dopamine that causes intensified emotions
- The meso-cortical pathway is essential for normal cognitive function and so abnormalities here such as flooding of dopamine may lead to negative symptoms
How would drugs explain development of schizophrenia?
They change the neurochemicals within the brain and so may cause and imbalance.
How might amphetamines link to schizophrenia?
They give similar symptoms to those of excess dopamine through flooding the synapse with this neurotransmitter which can cause psychosis.
How might Parkinsons’s disease link to schizophrenia?
These people suffer from low levels of dopamine whereby they take drugs to increase activity that correlate to developing schizophrenic symptoms.
How might L-DOPA link to schizophrenia?
L-DOPA is a chemical that the brain uses to produce dopamine therefore taking drugs that use this chemical may cause an onset of schizophrenia.
What is ‘glutamate’?
An excitatory NT (stimulates neurons), controls mem, learning + regulates dopamine. Binds to glutamate (NMDA) receptors. Receptors for glutamate found everywhere in brain, key to keep glutamate lvls low by healthy glutamate uptake
Explain the glutamate hypothesis
-Began when Halberstadt 1995 & Krytsal et al 1994 proposed NMDA receptor antagonists can lead to positive + negative Sz symptoms
- PCP (Angel Dust) is an NMDA antagonist, soblocks glutamate recptors, leading to decr glutamate uptake and incr dopamine production.
- SO glutamate can’t turn off due to lack of uptake, so continues to stimulate dopamine production, but dopamine can’t experience uptake as NMDA receptors are blocked so can’t pass through to D2 receptors.
- Excess glutamate- can be uptaken by AMPA receptors in PFC. But incr lvls in PFC can lead to negative symptoms of Sz
EACH- Evidence
1.P- Falkai et al (1988) supports
E- Studied autopises + found that those w Sz have a larger than usual number of D2 receptors.
E- This is a strength as it provides evidence of dopamine and D2 receptors impacting the prevalence of developing Sz, if there are too many D2 receptors then there will be more dopamine uptake and cause sesnitivity which may cause the Sz positive symptoms such as hallucinations.
2. P - Lindstroem et al (1999) supports
E - He used PET scans to compare L-DOPA uptake of people with and without schizophrenia and found that those with schizophrenia took it up quicker
E - This therefore suggests that people with schizophrenia have more D2 receptors
EACH- Application
P- Yes
E- We can apply to the drug therapy treatment for Sz- antipsychotics- as they block Dopamine activity so decr dopamine stimulation and eliminate hallucinations and delusions.
E- This is a strength as it suggests dopamine is a contributing factor for Sz due to antipsychotics eliminating positive symptoms after inhibiting dopamine production. Can provide effective treatment for those w Sz
EACH- Criticisms
1.P-Reductionist
E- Attempts to explain causation of SZ - a complex illness- being tm dopamine, fails to consider the role of social factors such as psychosocial stressors and family influence.
2.P- Deterministic, Noll (2009)
E- Found in some cases, hallucinations and delusions occured in spite of normal dopamine lvls, so blocking D2 receptors has little/no effect on positive symptoms. So other NTs may be responsible for positive symptoms.
E- This is a weakness as it suggests the dopamine hypothesis is deterministic and doesn’t directly and solely cause Sz positive symptoms
EACH- How good?
1.P-Difficult to investigate
E-
E-
2.P- Cant astablish casue + effect
E- No research of dopamine hypothesis has been able to determine if Sz is the consequence or cause of incr dopamine activity.
E- This is a weakness as it’s difficult to establish whether high lvls of dopamine cause Sz or if Sz causes high lvls of dopamine, so it makes treatment difficult to apply.
