Lecture 4 - Synapse Structure and Function Flashcards
how does a neuron hand off the electrical signal of an AP to cause an effect in another cell
it generates a chemical signal at a structure called a synapse
chemical synapse - what happens at the axon terminus, primary NTs found in the PNS? CNS?
-the axon terminus synthesizes neurotransmitters and stores them in vesicles
-1 type of neuron usually makes 1 class or family of NT
-ACh and norepinephrine are the primary NTs found in PNS
-many different types of NTs in the CNS
what is a synapse
its a structure in the nervous system through which a neuron passes a chemical or electrical signal to another cell
what are the 4 major neurotransmitter families and examples
-amino acids (GABA, glycine, glutamate)
-acetylcholine (ACh)
-amines (seratonin, dopamine, epi, norepi)
-neuropeptides (oxytocin, vasopressin)
how are neurotransmitters released
when AP reaches axon terminus, voltage gated Ca channels open –> Ca enters cell –> stimulates a series of biochemical events that triggers exocytosis of NT vescicles, NT released into cleft
role isnt to change the membrane potential but rather let Ca in
after the neurotransmitter is released, how is the post synaptic cell stimulated? example
NT binds to different receptor proteins on post synaptic membrane
e.g. ACh binds to ACh receptors
types of NT receptors
-lignd gated ion channels (nicotinic AChR)
-receptors acting through G proteins (muscarinic AChR)
-several others, most of which lead to changes (+ve/-ve) in the RMP of the post synaptic membrane
what are the two important general signal transduction mechanisms for all cells that we need to know (think receptors)
-R is an ion channel
-R acts through G protein to activate enzyme/ion channel
what is ionotropic and metabotropic
ionotropic = ligand gated ion channels. direct gating
metabotropic = G protein coupled. indirect gating
do synapses always excite the post synaptic cell?
not always - it depends on the type of neuron and neurotransmitter
how do EXCITATORY synapses work, what is it called, examples?
the stimulation of post synaptic membrane leads to the opening of the ligand gated Na or Ca channels which promotes excitation of membrane (e.g. depolarization). charge becomes less negative and favours the formation of an AP. This is called an excitatory post synaptic potential (EPSP).
example - nicotinic AChR at neuromuscular junction
how do INHIBITORY synapses work, what is it called, examples
stimulation of post synaptic membrane opens K or Cl channels causing hyperpolarization (Charge becomes more negative) and may prevent the formation of an AP. This is called an inhibitory post-synaptic potential (IPSP)
example - GABA receptors in CNS - ligand-gated Cl channels
synapses: summation concept
EPSPs and IPSPs “add up” (summate) over space (spatial summation) and time (temporal summation) and influence the membrane potential on the neuron surface, particularily the axon hillock, a structure to which these charges migrate
what is the site where AP is produced
axon hillock
what does the summation of EPSPs and IPSPs determine?
determine membrane action potential at axon hillock
what limits the time over which temporal summation can occur?
hyperpolarization decreases as K+ leaks out slowly
8 steps in the synapse (summary)
- AP arrives at axon terminal
- Ca2+ channels open
- Ca2+ diffuses from ECF
- neurotransmitter releases by exocyosis
- Neurotransmitter diffuses across synpatic cleft
- Neurotransmitter-receptor complex opens specific ions channels
- Postsynaptic potential generated (Remember -this can be more positive OR more negative)
- Local currents spread in all directions along cell membrane
What happens to neurotransmitter molecules after synaptic transmission (e.g. AFTER they have generated a post synaptic response)
what do you have to consider for implications?
it depends on the NT and type of neuron - three most common outcomes are listed with examples below:
- ACh is broken down into acetic acid and choline by acetylcholinesterase. choline is taken up by presynaptic neuron and reused
- most amine neurotransmitters (NE, dopamine, seratonin) are taken up by the pre-synaptic neuron (re-uptake) and re-used, some is broken down by specific enzumes in axon terminus
- some diffuses away from synapse (GABA etc) to be metabolized by astrocytes
implications for toxins and drugs that interfere with this action (esterase inhibitors, re-uptake inhibitors, etc)
pharmacology: ion channels and synapses - examples of drugs and toxins act at synapses, mechanisms
many drugs and toxins act at synapses
-other examples: organophosphates, sarin, curare, atropine, strychnine, tensilon, neostygmine, etc
mechanisms:
-block release of NT (botulism, tetanus toxins)
-block re-uptake of NT (SSRI, SBARI)
-block receptor (atropine)
-block mechanism (sarin, organophosphate, tensilon)
electrical synapse - what are specialized, what happens when in contact, how does depolarization work, cardiac muscle and conduction pathways
-gap junction proteins in neighbouring cells are specialized
-when in contact, open to form water filled pore directly between 2 cells
-depolarizations sweep from cell to cell as if it were a single cell
-in cardiac muscle and conduction pathways, numerous cells connected by electrical synapses
