Describe the features of an Electrical Synapse. Where are they especially abundant?
- Electrical signal (current) flows between cells through gap junctions
- Can be uni- or bi- directional
- Allows very fast communication between cells
- Facilitate synchronization of neurons
- Esp. abundant in retina, cerebral cortex, cardiac & smooth muscle, escape mechanisms (esp. in invertebrates)
Describe the 3 major components of Chemical Synapses
- Presynaptic cell
- axon terminals
- synaptic vesicles (contain NT - usually synthesized in cell body, moves to axon terminals via fast axonal transport) - Synaptic cleft
- space btwn pre- and post- synaptic cells (~20nm wide) - Postsynaptic cell
- synapses usually involve dendrites, soma; sometimes axons, axon terminals
- receptors
Summarize the events of a Chemical Synapse
- Presynaptic cell
- AP depolarizes axon terminals
- voltage-gated Ca++ channels open; Ca++ enters axon terminal
- Ca++ stimulates exocytosis of synaptic vesicles
- NT molecules are released into cleft - Synaptic cleft
- NT molecules diffuse across cleft - Postsynaptic cell
- NT molecules bind to receptors
- Response is initiated
Each AP causes the same amount of NT release from a particular axon terminal. So, how can the amount of NT be adjusted?
Frequency modulation
Describe Frequency modulation
- Frequency of APs initiated at trigger zone varies w/ intensity/duration of stimulus
(stronger stimulus -> increase rate of APs) - Frequency of APs at axon terminals determines how much NT is released
(Increase rate of APs -> increase NT release)
–> Stronger stimulus -> increase NT release
What is GABA? Describe the difference between the 3 types of GABA receptors.
- Major inhibitory NT in CNS; 3 receptor types:
1. GABAb - metabotropic - G protein-coupled receptor; uses 2nd messenger-mediated signal-transduction pathway
2. GABAa, GABAc - ionotropic - ligand-gated Cl- channels
- At rest [Cl-]out > [Cl-]in (Ecl- = -80mV)
How are the effects of GABA potentiated?
- potentiated by alcohol, benzodiazepines (e.g. valium), barbiturates (e.g. pentobarbital)
- these substances allosterically modulate GABA ionotropic receptors and increase Cl- influx in response to GABA binding
What happens to GABA receptors in response to alcohol? Chronic alcohol?
GABA + EtOH -> Sensitization
Chronic alcohol -> Desensitization
What is Glutamate? Describe the 3 receptor types
- Major excitatory NT in CNS; 3 receptor types:
1. Metabotropic receptor - G protein-coupled receptor; uses 2nd messenger-mediated signal-transduction pathway
2. Ionotropic: AMPA receptor - Ligand-gated Na+/K+ channel
- Channel opens -> Na+ enters (& K+ exits) -> cell depolarizes
3. Ionotropic: NMDA receptor - Ligand-gated and voltage-dependent Na+/K+/Ca2+ channel
- At resting potential, Mg2+ blocks ligand-activated gat
- In order for ions to pass through channel, need: glutamate binding to open gate & depolarize to remove Mg2+
What leads to Long-term Potentiation? What is it?
- Glutamate signaling through AMPA and NMDA receptors can lead to L-TP
- Enhancement of the postsynaptic cells response to the presynaptic cell as a result of sustained synaptic activity
Describe the positive feedback mechanism involving NMDA receptors and glutamate
- Activation of NMDA receptors activates 2nd messenger pathways leading to:
1. Increased sensitivity to glutamate (postsynaptic cell)
2. Increased glutamate release (presynaptic cell)
Where are Acetylcholine (cholinergic receptors) found? Describe 2 receptor types
- CNS, autonomic nervous system, neuromuscular junctions
1. Muscarinic receptors - Metabotropic
2. Nicotinic Receptors - Ionotropic - Ligand-gated Na+/K+ channel
Name an agonist and 2 antagonists for Acetylcholine cholinergic receptors
- Agonist: Nicotine
- Antagonists: curare, alpha-bungarotoxin
Where are Epinephrin/norepinephrine (adrenergic receptors) found? Describe the 2 major receptor types (G protein-coupled receptors)
- CNS, autonomic nervous system
1. Alpha receptors - a1- receptors: (increase intracellular [Ca++]; increase contraction of smooth muscle)
- a2-receptors: (decrease intracellular [Ca++]; increase relaxation of smooth muscle; decrease exocrine secretion)
2. Beta receptors (use G protein coupled to adenylate cyclase -> increase [cAMP] in target cells - b1-receptors: (increase contraction of cardiac muscle)
- b2-receptors: (relaxation of smooth muscle)
- b3-receptors: (mostly in adipose tissue; increase lipolysis)
What is Divergence?
One presynaptic neuron can synapse onto many postsynaptic neurons
What is Convergence?
One postsynaptic neuron can receive input from many (thousands) presynaptic neurons
Describe Fast Synaptic Potentials
- Rapid onset, short duration (milliseconds)
- NT binds to, opens chemically gated ion channels -> alters ion flow into/out of postsynaptic cell
Describe Slow Synaptic Potentials
- Slower onset, long duration (seconds to minutes)
- NT binds to G protein-coupled receptors ->
- Activates signal-transduction pathway ->
- Alters membrane permeability &/or modifies existing proteins &/or alters protein synthesis
What is an EPSP?
Excitatory PostSynaptic Potential caused by depolarization
What is an IPSP?
Inhibitory PostSynaptic Potential caused by hyperpolarization
What is Spatial Summation?
Integration of simultaneous signals (graded potentials) from different synapses
What is Temporal Summation?
Integration of signals received from a signal synapse at slightly different times
What is Presynaptic Inhibition?
One neuron releases inhibitory NT onto or near (some of) the axon terminals of a second neuron, causing those axon terminals to release less NT
What is Presynaptic Facilitation?
One neuron releases excitatory NT onto or near (some of) the axon terminals of a second neuron, causing those axon terminals neuron to release more NT
