Lecture 4 (Revised) Flashcards
Types of Synapses?
-Electrical Synapse
-Chemical Synapse
Electrical Synapse communication via?
Direct electrical coupling of 2 cells through gap junctions
Chemical Synapse communication through?
Release and binding of neurotransmitters
Electrical Synapsis - Gap Junctions?
-Several connexions make up 1 connexon
-2 connexons combine to make a gap junction
-Pro: rapid signal transmission
-Con: postsynaptic signal = presynaptic signal
Chemical Synapsis - Neurotransmitters?
Types:
1) Acetylcholine
2) Amino Acids
3) Purines
4) Biogenic Amines
5) Gases (NO, CO)
6) Peptides (much larger)
-Pro: postsynaptic signal differs from presynaptic signal
-Con: slow signal transmission
(Amino Acid Neurotransmitters) Inhibitory?
1) GABA
2) Glycine
-Primarily responsible for IPSP’s (influx of Cl- ions and/or efflux of K+ ions)
(Become more negative)
(Amino Acid Neurotransmitters) Excitatory?
1) Glutamate
2) Acetylcholine
3) Catecholamines (Epi, NE, Dopamine)
4) Serotonin
5) Histamine
6) Aspartate
-Primarily responsible for EPSP’s (influx of Ca2+)
(Become more positive)
Biogenic Amines?
-Tyrosine (derived from phenylalanine) is precursor for dopamine, epinephrine, and NE
-Histidine is precursor for Histamine
-Tryptophan is precursor for Serotonin
Peptide Neurotransmitters?
-Brain-gut peptides
-Opioid peptides
-Pituitary peptides
-Hypothalamic-releasing peptides
-Miscellaneous peptides
Life Cycle of Neurotransmitter?
1) Synthesis
2) Packaging/Transport
3) Docking (Priming)
4) Fusion and Release (Exocytosis)
5) Budding (Endocytosis)
6) Binding
7) Inactivation (Removal)
(1) Synthesis (and)
2) Packaging/Transport)
Small-Molecule Transmitters?
1) Enzymes synthesized in cell body and transported to presynaptic
2) Transmitters synthesized at presynaptic
3) Transmitters stored in endosomes, bud off CLEAR CORE vesicles
(1) Synthesis (and)
2) Packaging/Transport)
Peptide Transmitters?
1) Large pro-peptide transmitters + enzymes are synthesized in cell body
2) Transmitter + enzymes are packaged in DENSE CORE vesicles which bud off Golgi apparatus
3) Dense core vesicles are transported down axon via microtubules
4) Enzymes process large pro-peptide at presynaptic terminal
3) Docking (Priming)?
(Docking is a vesicle so close to pre-synaptic membrane that once AP fires it is ready)
-v-SNAREs (Synaptobrevin) on vesicle membrane
-t-SNAREs (Syntaxin) on target membrane
-Soluble NSF Attachment Protein (SNAP) fuses v-SNARE and t-SNARE
4) Fusion and Release (Exocytosis)?
1) AP triggers influx of Ca2+ via voltage-gated Ca2+ channels
2) Synaptotagmin senses and binds Ca2+
3) Ca2+ + Synaptotagmin induces vesicular fusion via interaction with SNAP-25
5) Budding (Endocytosis)?
-Clathrin: coats membrane and begins process of endocytosis (lifts it up and bring it back into presynaptic terminal and cleave it off)
-Dynamin: “molecular scissor” which pinches vesicle off membrane
6) Binding?
Neurotransmitter binds to postsynaptic receptor and alters postsynaptic membrane potential
7) Inactivation?
-Methods:
1) Diffusion of transmitter from synaptic space
2) Cleaving transmitter into inactive constituents
3) Reuptake of transmitter back into presynaptic neuron via transporters
Neuromuscular Junction?
1) Voluntary neuronal stimulus form CNS
2) AP leads to alpha-motor neuron stimulation
3) ACh released at postsynaptic membrane in NMJ
Nicotinic Acetylcholine Receptor (NAChR)?
1) 2 ACh molecules bind to a single NAChR (pentamer)
2) Receptor opens an ion channel that is equally permeable to Na+ and K+
3) Diffusion of Na+ and K+ across receptor causes depolarization (End Plate Potential)
4) EPP opens voltage-gated Na+ channels, which allows for firing of EPs and muscular contraction
Myasthenia Gravis?
-Autoimmune diseaes, where auto-antibodies target nAChR on postsynaptic membrane (make it have nothing to bind to)
-Symptoms:
1) Muscle Weakness
2) Drooping eyelids
3) Fatigue
-Treatment:
1) ACh inhibitors
