Synaptic Structure and Function Flashcards
Release of Neurotransmitters:
Influenced by rate of cell firing, transport of precursors and enzymes
Rate of Cell Firing
○ Action potentials follow an all or none principle, magnitude of action potentials are always the same
Quantity of neurotransmitters released is determined by frequency of firing
Transport of Precursors and Enzymes
Neurotransmitters are replenished quickly, neuropeptides take longer to replenished (precursors synthesized in the soma, takes a long time to reach synaptic terminal)
Heteroreceptors:
• Receptors are different than the neurotransmitter it releases (can’t act on itself)
Influencing different pre-synaptic neurons can increase or decrease firing of other pre-synaptic neurons, which influences the firing of the post-synaptic neuron
Autoreceptors:
• Pre-synaptic neuron has receptors for the same neurotransmitter that it is releasing, allows for negative feedback
• Usually metabotropic receptors
Located on terminal or dendrites/soma
Somatodendritic autoreceptors
§ Stimulated when the ligand binds, inhibits rate of firing by opening ion channels (K, Cl) that hyperpolarize the cell, prevents further action potentials
Inhibits rate of firing
Diagram
○ Terminal autoreceptors
§ Inhibits neurotransmitter release
Binding of ligand to autoreceptor reduces sensitivity to calcium channels, prevents vesicles from docking and releasing neurotransmitter
Diagram
Neurotransmitter Inactivation:
Enzymatic breakdown
Reuptake of amino acids and amines
Uptake
Enzymatic breakdown
○ Inactivates neurotransmitter
i.e. Acetylcholinesterase inactivates Ach, endocannabinoids are degraded, very lipid soluble, don’t want them diffusing out of the cell
Reuptake of amino acids and amines
○ Neurotransmitter binds to enzyme, either degraded or is removed from the synaptic cleft, taken back into the pre-synaptic terminal via ruptake transporters
○ Neurotransmitter degraded (recycled) or repackaged (so it isn’t degraded)
Many psychoactive drugs block reuptake mechanisms, allow neurotransmitter to stay in cleft longer
Uptake
○ Glial cells may participate in inactivating neurotransmitters (also has transporters) and degrades neurotransmitters once it is in the glial cell
Tyrosine Kinase Receptors:
• Not directly involved in neurotransmission
• Involved in neuronal growth during development and adulthood
• Activated by neurotrophic factors
○ Involved in maintenance of synapses, neuronal growth, survival, and development
• 3 tyrosine kinase receptors used by neurotrophic factors
○ trkA used by nerve growth factor (NGF)
○ trkB used by brain derived neurotrophic facto (BDNF) and NT-4
○ trkC for neurotrophin-3 (NT-3)
• Neurotrophic factor bind to receptor, 2 receptors come together in the cell membrane, 2 trk receptors are activated and phosphorylate each other on tyrosine residues located within the cytoplasm of each receptor, activates other protein kinases
Involved in long term changes in gene expression and neuronal functioning
Diagram
Ionotropic Receptors/Ligand Gated Channels:
• Operate quickly
• Involved in fast neuronal signaling
• Rapidly desensitized
○ Change in binding site of channel, channel can’t effectively open or closed
○ Results in loss of function after continued exposure
• Large proteins containing 4-5 subunits
○ Different subunits come together, creates lots of variety depending on how the subunits come together, leads to variations in function
• Contain one or more neurotransmitter binding sites
○ Orthosteric site- ion channel gated by the neurotransmitter (where the neurotransmitter binds)
○ Allosteric sites- binding sites for other molecules, helps modulate the function of the receptor
Effect of activation of the receptor depends on the ions that it is selective for (K, Ca…etc)
Nicotinic Ach Receptor:
• Na ion channel
○ Excitatory-depolarizes cell
• Consists of 5 subunits and a central pore
Found in periphery (neuromuscular junctions) and in the CNS
NMDA Receptor
• Ca ion channel
Ca enters cell, activates second messengers
