1. Neurotransmitter receptors
Domina Petric, MD

2. Ionotropic receptors I.

3. Nicotinic acetylcholine receptor
It is occupied and activated by nicotine in smokers.
Channel opening is gated by the binding of the neurotransmitter to its receptor.

4. Glutamate ionotropic receptors
AMPA
NMDA
Kainate

5. NMDA receptors
Both glutamate and glycine have to interact with the receptor to open the channel.
Magnesium ions can aggregate in the deep binding site of the NMDA receptor.
When the magnesium is bind there is no conductance.

6. GABA receptors There are places on the GABA receptors for: picrotoxin
benzodiazepines
barbiturates
steroids
Chloride ions pass through the channel from the inside to outside typically in mature neurons.

7.
Ionotropic receptor

8. Calcium is critical for mediating synaptic plasticity.

9. Metabotropic receptors
II.

10. G-protein coupled receptor
Receptor is a monomeric integral membrane protein.
It is associated with G proteins on its cytoplasmic surface.
When the neurotransmitter binds to the receptor, G proteins become activated.
G proteins interact with effector proteins.
Effector proteins produce variety of intercellular messengers and those messengers can gate some ion channels.

11. G-protein coupled receptor
Neurotransmitter binds
Intercellular
messengers
gate ion channel
Receptor
Effector
protein
produces
intercellular
messengers
G protein is activated and
interacts with effector protein.
Amplification of the signal

12. G-protein coupled receptor
There can be amplification of the signal as these metabolic steps are occuring.
G-protein coupled receptors can also interact with transcription factors that can modify gene expression.
CREB binding domene in our genes is the regulatory element which can be activated with G-protein cuopled receptors.
Transduction of photons into electrical energy requires the activation of G-protein coupled receptor system.

13. Synaptic integration
III.

14. Synapse
Action potential invades the end of an axon (presynaptic terminal).
Wave of depolarisation conveys positive charge along the length of presynaptic terminal.
When depolarisation reaches voltage gated calcium channels, channels open and there is influx of calcium.
Calcium is the key trigger that leads to the fusion of docked vesicles.
Neurotransmitter in docked and now fused vesicles passively diffuse out into the synaptic cleft.

15. Excitatory postsynaptic potential
The reversal potential of the active conductance is above the threshold for firing an action potential.

16. Inhibitory postsynaptic potential
For example if there is activation of GABA synapse, there will be hyperpolarisation due to chloride ions influx.

17. Excitatory activity of GABA in developing brain
In the immature neuron there is more chloride ions inside of the cell than in mature neuron because of:
Na+/K+/2 Cl- transporter (all ions go inside the cell) that will be replaced with K+/Cl- transporter (both ions go out of the cell) in mature neuron.
So in the immature neuron there is high concentration of chloride ions INSIDE the cell and low concentration of chloride ions in the extracellular space.
In immature neuron GABA is excitatory neurotransmitter.
In mature neuron GABA is inhibitory neurotransmitter.

18. Another book association (Domina Petric, MD)
Immature neuron
Mature neuron
When the child is born, ˝the book˝
opens and chloride ions escape
from the cell to the exctracellular
space because of the new
transporter that throws out
of the cell chloride ions.
Immature neuron is like closed
book with chloride ions inside
the book (inside the cell).
GABA is excitatory neurotransmitter GABA is inhibitory neurotransmitter.
When the channel opens, chloride ions When the channel opens there will be
go out of the cell and there is influx of chloride ions from extracellular space
depolarisation into the cell (hyperpolarisation).

19. Synapse integration
No one synapse is strong enough to result in the generation of an action potential in the postsynaptic neuron.
There must be many synapses, many excitatory inputs converging on the same neuron at the same time in order to depolarize that membrane sufficiently to reach treshold.

20. Literature
medical-neuroscience/lecture: Leonard E. White, PhD, Duke University