WEEK 4 LECTURE + TUTORIAL Flashcards
neurotransmission and psychopharmacology (32 cards)
Synapses
-Junction between the terminal button of an axon and the membrane of another neuron
-Spaces between the terminal button of one neuron and the dendritic or somatic membrane of another
-Primary means of communication between neurons is synaptic transmission
-Info travels in one direction
Structure of a synapse
-presynaptic axon: terminal containing neurotransmitters, mitochondria and other organelles.
-Postsynaptic ending: receptor sites for neurotransmitters
-Synaptic cleft, contains extracellular fluid through which the neurotransmitter diffuses
-two prominent structures are located in the cytoplasm of the terminal button: mitochondria and synaptic vesicles, small, bubble-like structures made of membranes and filled with molecules
-The presence of mitochondria implies that the terminal button needs energy to perform its functions
-A chemical that attaches to a binding site is called a ligand
Synaptic Transmission Process:
Part 1
- Action potential arrives at axon terminal triggering CA2+ ions to move into the cell
1.Synaptic transmission is initiated when an action potential invades a nerve terminal, opening CA2+ at the active zone
1.CA2+ triggers synaptic vesicle exocytosis, thereby releasing the neurotransmitters contained in the vesicles and initiating synaptic transmission
Synaptic Transmission Process
Part 2/3
- CA2+ Ions cause the migration of vesicles (which contain NTs) to the pre-synaptic membrane
-The vesicles fuse to the pre synaptic membrane and break open, emptying their neurotransmitters into the synaptic cleft
Synaptic Transmission
Part 4/5/6
-Neurotransmitters diffuse across the synaptic cleft towards the post-synaptic membrane, move from an area of high concentration to disperse across the synapse due to the force of diffusion
-Neurotransmitters bind to receptor cites on the post synaptic membrane with the lock and key specificity - specific NT binds to the specific receptor
-The binding opens NT-dependent ion channels which change the excitability of the post-synaptic excitatory or inhibitory
Postsynaptic receptors
-Direct receptors (ionotropic)
-Binding site for a NT
-Ion channels open when NT molecule binds, ionotropic receptor
Indirect Receptor (metabotropic)
-Only a binding site for NT
-Activates enzyme
-Called this because it involves steps that require the cell to expend metabolic energy
Problems that could occur:
-Too much or not enough of one or more neurotransmitters
-The receptor on the receiver cell isn’t working properly
-The cell receptors aren’t taking up enough neurotransmitter due to inflammation and damage of the synaptic cleft
-NT’S are reabsorbed too quickly
-Enzymes limit the number of neurotransmitters from reaching their target cell
-Problems with other part of nerves
Diseases that can occur
-Not enough acetylcholine can lead to the loss of memory that’s seen in Alzheimer’s disease
-Too much serotonin is possibly associated with autism
-An increase in glutamate can cause seizures
-Too much dopamine and abnormal glutamate transmission contributes to mania
Endorphins/ Peptides
- Pain relievers and feel good feelings
-Released by hypothalamus and pituitary gland
-Inhibitors (opioid receptors)
-Low levels of endorphins may play a role in fibromyalgia and some types of headaches
Amino acids/ glutamate / GABA
-most common excitatory neurotransmitter
-used by brain to synthesise GABA
-most abundant NT in the brain
-Key role in cognitive functions like thinking, learning and memory
-Imbalances in glutamate levels associated with Alzheimer’s disease, dementia, Parkinson’s, Huntington’s, seizures
Gamma-aminobutryic acid (GABA)
-Synthesised from glutamate and vitamin B6
-The most common inhibitory neurotransmitter of the nervous system, particularly the brain
-Regulates brain activity to prevent problems in the areas of anxiety, irritability, concentration, sleep and depression
-Contributes to motor control, vision, regulation of anxiety, and many other cortical functions
-Drugs that increase GABA in the brain are used to treat epilepsy and calm trembling in Huntington’s disease
NT removal from synapse
- Reuptake: NT is quickly pumped back into nearby glia or the axon terminal that released it
- Deactivation: NT destroyed by enzymes near receptors, so its not recognised by receptor
- Removal: diffuses into surrounding area, blood
Enzymatic deactivation
-Enzymatic deactivation is accomplished by an enzyme that destroys molecules of the neurotransmitter
-E.g. Acetylcholinesterase (AChE) deactivates the neurotransmitter acetycholine (ACh) by breaking it into choline and acetate
Psychopharmacology definition
Study of the effects of drugs on the nervous system and behaviour
What are drugs
-Exogenous chemicals
-Unnecessary for normal functioning
-Alter molecular functions
-Effects are physiological or behavioural
-Natural VS Artificial
- Agonists VS 2. Antagonists
- Facilitate or mimics action of NT and facilitates postsynaptic effects
- Inhibit action of a NT and block postsynaptic effects
Mechanisms of drug actions
- Synthesis
- Storage
- Release
- Receptors
- Reuptake
- Destruction
- Synthesis
- Alter neurotransmitter synthesis in presynaptic neuron
-Modifies concentration in synaptic cleft
-NT produced from specific precursor molecules
-Enzymes required for change from precursor to NT
- Storage
- Alter neurotransmitter storage in presynaptic terminal
-Modifies concentration in synaptic cleft
-Transporter proteins in vesicle membranes move NT from cytoplasm into vesicles
-Antagonist inactive transporters
-Vesicles remain empty
Release
- Changes NT release from presynaptic cell
-Modifies concentration in synaptic cleft
- Receptors
-Act on neurotransmitter receptors
-Modify postsynaptic potentials
- Reuptake
-Modify removal of NT from synaptic cleft
-Changes NT concentrations in the cleft
-Agonists reduce or block reuptake
- Destruction
- Modify NT destruction in synaptic cleft
-Enzymes typically inactivates nt
-Acetylcholinesterase in post synaptic membrane deactivates ACH
Myasthenia Gravis
- A rare autoimmune neuromuscular junction disorder