Amino-acid neurotransmission Flashcards
1
Q
What are the non-essential amino-acids?
(11)
A
- Don’t need though diet, create ourselves
- Alanine
- Asparagine
- Aspartate
- Cysteine
- Gultamate>GABA
- Glutamine
- Glycine
- Proline
- Serine
- Tyrosine>L>DOPA>Dopa>Nora>Adre
- Arginine
2
Q
What are the essential AA?
(9)
A
- Need to take in through diet
- Histidine - histamine
- Isoleucine
- Leucine
- Lysine
- Methionine
- Phenylalanine
- Threonine
- Tryptophn - 5-HT - Melatonin
- Valine
3
Q
What can deficiencies of essential AA lead to?
A
- Histidine - Eczema
- Isoleucine - Similar to hypoglycaemia
- Leucine - Lethargy, weight loss
- Lysine - Loss of app, poor growth
- Methionine - Liver damage
- Phenylalanine - “, apathy, stunted growth
- Threonine - Hypo again
- Tryptophan - Aggro
- Valine - Impaired mental func
4
Q
What are Ketogenics?
A
- AA that yield acetyl CoA or acetoacetyl CoA
- Lycine and Leucine
- Don’t produce metabolites that can be conv to glucose
5
Q
What are glucogenics?
A
- AA whose catabolism yields to the formation of pyruvate or krebs metabolites
- Metabolites CAN be converted into Glucose through gluconeogenesis
- Alanine, Glutamate, Glycine, serine and like 10 more
6
Q
What are glucogenic and ketogenic AA?
A
- AA that yield some products that can become glucose and others that yield acetyl CoA or Acetoacetyl CoA
- Isoleucine, Phenylalanine, Tryptophan, Tyrosine, Threonine
7
Q
What is Glutamate?
A
- Glutamte –> Glutamine
- Present in high concs
8
Q
Explain glutamate metabolism?
A
- Glutamate can become:
1. Cysteine
2. Glutathione
3. GABA
4. Glutamine
9
Q
What is stereospecifity?
A
- Non stereo-specific effects of glutamate and aspartate.
- NMDA was more potent than L-form
10
Q
What are potent compounds?
A
- L-homocysteate
- ODAP
- Kainic acid
- Quisqualic acid
- AMPA
11
Q
What are Multiple receptor sites?
A
- Identification of multiple receptor types preceded definitive establishment of a role in glutamate in syn function
12
Q
What are the effects of Mg2+?
A
- Found to inhibit synaptic activity/reduce synaptic release of NT
13
Q
What are renshaw cells?
A
- Added glutamate to Renshaw cells – known to respond to ACh – glutamate also excited them – he thought glutamate was having a non-specific effect so withdrew his statement even though he was right (but he thought he was wrong)
14
Q
Explain renshaw cells?
A
- The presynaptic terminal from afferent sensory information is glutamatergic, which excites the postsynaptic terminal to produce the efferent output (muscle contraction) – myotatic reflex
- Some cells in the spinal cord have a recurrent collateral – which comes off the main axon and feeds back – which releases ACh – the ACh impinges upon the Renshaw cell, which releases glycine onto the same postsynaptic membrane as glutamate – glycine is an inhibitor –
- Essentially a negative feedback loop – prevents uncontrolled excitation and limits the firing frequency
15
Q
What is Mg2+?
A
- Mg2+ binds to NMDA receptor and prev glutamate from having an effect Mg2+ abolishes NMDA response
- Kaginate + quisqualate unaffected
- L-gutamate inhibited to an intermediate degree
- Suggests kainate and NMDA bound to dif receptors
17
Q
Explain renshaw antagonists?
A
- can stimulate the afferent and record the efferent, or stimulate the cell in the middle and measure the effect
- Was found that individual Renshaw cells are excited by ACh and glutamate
- Renshaw cells excited by both ventral and dorsal stimulation
- D⍺AA blocked glutamate and dorsal stimulation but did not block ACh or ventral stimulation
- DHβE blocked ACh and ventral stimulation but did not block glutamate or dorsal stimulation
18
Q
What are Glutamate receptor sub-types?
A
