Glutamate & GABA: L16

Question 1

1. Glutamate & GABA both
2. most common
3. both act as

Answer 1

1. first to evolve & found in simple organisms
2. neurotransmitters in CNS
3. “true” neurotransmitters - directly affecting the likelihood of the post-synaptic neuron firing

Question 2

Glutamate

1. main
2. released by
3. how many brain synapses release glutamate

Answer 2

1. excitatory neurotransmitter in the brain (increases likelihood of postsynaptic nerve firing)
2. ALL excitatory neurons
3. over half

Question 3

Glutamate synthesis

1. glutamate =
2. it is a what?
3. But it does not pass

Answer 3

1. glutamic acid
2. amino acid that works as a neurotransmitter in its original form
3. the blood brain barrier so needs to be synthesised in the brain
4. synthesised from glutamine which is released by glial cells neighbouring the neurons

Question 4

Excitatory

1. connections are
2. what kind of functions

Answer 4

1. point to point

2. region-specific (e.g. connections along the visual pathways)

Question 5

Glutamate receptors

1. number of types & categories

Answer 5

1. 4 main

3 ion channels (ionotropic):

• NMDA
• AMPA
• Kainate

1 G-protein coupled
- metabotropic glutamate receptor

Question 6

Glutamate: NMDA

1. how many binding sites
2. it only works if (2)
3. the other binding cites modulate

Answer 6

1. at least 6 = lots of complex functions
2. (1) there is a glycine molecule attached
   (2) if magnesium is NOT bound to inside
3. receptor function

Question 7

NMDA receptors: Alcohol

1. NMDA what?
2. reduction in glutamate is believed to contribute to
3. alcohol + GABA

Answer 7

1. antagonist
2. sedative effects & memory effects of alcohol
3. GABA antagonist which leads to further brain inhibition

Question 8

NMDA receptors: PCP & ketamine

1. both are
2. cause

Answer 8

(- pcp = angel dust )
1. NMDA antagonists
2. dissociative hallucinations, risk of suicidal behaviour
= ketamine very safe on the body as it doesn’t impact cardio vascular system

Question 9

NMDA receptors: drugs

1. why is the exact mechanism of action not completely known?
2. NMDA receptors provide

Answer 9

1. because all 3 drugs ( ket, pcp, alcohol) effect some additional receptors
2. a great illustration of the complexities of psychopharmacology

Question 10

Glutamate and psychosis

1. stats
2. symptoms include

Answer 10

psychosis = symptom cluster not a diagnosis

1. schizophrenia 1%, psychosis 3%
2. • delusions, hallucinations, anxiety, depression, difficulty functioning, disorganised speech

Question 11

glutamate and psychosis link

1. controversial
2. symptoms suggest
3. structural differences

Answer 11

1. likely to involve other neurotransmitters like DA
2. widespread disruption and lack of coherent integration of sensory information
3. no major differences, illustrates the importance of chemical balance in healthy perception and cognition

Question 12

NDMA receptors and psychosis

1. NDMA receptor activity is
2. large genetic studies identify NDMA receptor genes as
3. these genetic studies point to

Answer 12

1. critical for learning, memory, perception and synaptic plasticity
2. likely being relevant in schizophrenia but also relevant to general function and IQ
3. a large number of genes that may each contribute a small amount of risk for psychosis. it may simply reflect altered synaptic activity

Question 13

GABA

1. it is
2. without what would happen?
3. structure
4. in a healthy brain
5. neurons are…
6. stimulus bar experiment

Answer 13

(gamma-amino butyric-acid)

1. primary inhibitory neurotransmitter
2. brain would be unstable causing neurons to fire uncontrollably > each excitatory neuron exciting the next > causing seizure
3. short local neurons form a dense web around excitatory neurons
4. GABA helps the coordination of neurons to signal very specific information
5. selective but not perfect. Inhibitory networks reduce the likelihood neurons fire for their non-preferred stimulus
6. GABA makes signals more accurate - reduction of noise = signals more precise

Question 14

GABA synthesis

1. produced from

Answer 14

1. glutamic acid (same as glutamate). Glutamate is converted into GABA & GABA can be converted back into glutamate

Question 15

2 types of GABA receptors

Answer 15

1. GABAa = ion channels

GABAb = G protein-coupled

Question 16

GABA & seizure disorders

1. how many in australia
2. define seizure
3. what is epilepsy?
4. Epilepsy is believed to be caused by

Answer 16

1. common, 400,000
2. sudden excessive activity of neurons (can cause muscle convulsions)
3. neurological disorder caused by seizures
4. abnormality of the GABA neurons and/or in the GABA receptors

Question 17

1. Generalised seizures

2. partial seizures (2)

Answer 17

1. widespread & involves most of the brain
2. definite focus and restricted to small part of the brain
   (1) simple: can cause changes in consciousness but not loss of consciousness
   (2) complex: loss of consciousness

Question 18

Febrile seizures (kids)

1. % of children under 5 have a seizure associated with?
2. vaccinations linked to epilepsy (gene)
3. vaccinations may therefore

Answer 18

1. 3%, high fevers
2. sam Berkovic & Ingrid Scheffer = discovered first genes linked to epilepsy. Those with the gene generally have first fit 2-3 years of age when they get a fever
3. trigger fever + seizure but without vaccinations seizure would have occurred anyway

Question 19

Seizures and genetics

1. genes identified control what channels
2. most seizures are not

Answer 19

1. ion channels (= control level of positive and negative charge that drive APs)
2. genetic and instead are due to abnormal brain tissue and require surgical treatments