B2W2 Flashcards
3 Types of neuronal signaling
Excitatory, Inhibitory, Modulatory
Excitatory Input
Inward flow of positive charge depolarization
Main Excitatory Neurotransmitter of the CNS
Glutamate
“Mates are exciting”
EPSP Reversal Potential
~0 mV
Main Inhibitory Neurotransmitter in the brain
GABA
“B” for brain
Main Inhibitory Neurotransmitter in the spine
Glycine
“s” sound for spine
IPSP Reversal Potential
~71 mV
Modulatory Neurotransmitters
Norepinephrine
Reversal Potential
Reversal potential is the point in which the flow flow of ions in and out of the cell is equal.
Factors Determining Membrane Threshold
Na+ Channels and K+ Channels concentration.
Low Na+ channels and High K+ channels mean higher threshold must be reached.
Types of neuronal signal summation
Spatial and Temporal
Spatial Summation
Many EPSPs from multiple dendrites onto one soma
Temporal Summation
EPSPs combined in rapid succession due to some channels always being open before the next signal.
Glutamate Receptors
Ionotropic
- AMPA
-NMDA
-Kainate
Metabotropic
AMPA Receptors
Fast acting excitatory channels that allow for the flow of Na+ into the cell resulting in a fast depolarization
1-10 ms
NMDA Receptor
Slow acting excitatory channel that allows for further depolarization from the flow of Ca2+ ions into the cell. Only occurs after the initial depolarization caused by the opening of AMPA receptors.
10-100 ms
Importance of Synaptic Plasticity
Important for working and long-term memory
Facilitation
Short term 10-100 ms increase in EPSP caused by the accumulation of Ca2+ ions in the nerve terminal.
Requires high frequency.
Increase in quantal content
Depression
Decrease in EPSPs caused by the depletion of usable vesicles. Happens at high and low frequency.
Decrease in quantal content
Quantal Size
Presynaptic: Transmitters per vesicle
Postsynaptic: Receptor availability
Quantal Content
Presynaptic: Number of vesicles released
NMJ Plasticity
Changes in EPP
NMJ Depression
Reduction in quantal content, Strong at high quantal content because it is caused by the depletion of releasable vesicles
NMJ Facillitation
Increase in quantal content. Strongest at low quantal content. Caused by high frequency activation and the accumulation of Ca2+ ions in the nerve terminal.
NMJ Blockade at postsynaptic AChrs
Threshold remains the same. Number of available ACh receptors decreases. Overall decrease in EPP amplitude.
Curare
Decreases EPP by blocking available AChrs
NMJ Blockade at presynaptic Ca2+ channels
Initial EPP is below threshold. High frequency of stimulation is needed to bring EPP above threshold. However, depression of the NMJ will be slower.
Other Excitatory Neurotransmitters besides Glutamate
Acetylcholine, Serotonin, and ATP
Ionotropic Receptors
Fast Transmission channels that can be excitatory or inhibitory
Metabotropic
Slow transmission GPCRs mainly used for modulatory effects
Putative Neurotransmitters
Molecules that act similar to Neurotransmitters but are not themselves Neurotransmitters
Nitric Oxide
Not released but produced by the influx of Ca2+ channels activating Nitric Oxide Synthase. As a lipophilic gas it is able to move through the cell membrane easily.
Endocannabinoids
Anandamide that mimics THC. Acts on GPCRs
Growth Factor
Plays important role in Signaling in adults
Autoinhibition
Molecules released into the synaptic cleft bind to the original neuron and inhibit it
Amino Acid Neurotransmitters
Glutamate, GABA, Glycine
Peptides
Long amino acid chains that are produced within the cell body and stored within large dense vesicles. May act far away from point of release
Bioamines
Norepinephrine, Serotonin, Dopamine
GABA Receptors
Pentameric ion channel with multiple binding sites for agonists, antagonists, and allosteric activators
GABA Allosteric Activators
Barbiturates and Benzodiazepines
Barbiturates
Increase the duration that GABA channels are open
Benzodiazepines
Increase frequency in which GABA binds to receptors
Sympathetic Nervous System
Fight or Flight
Think “its pathetic to run from a fight”
Parasympathetic Nervous System
Rest and Digest
Think “Para para the platypus, he is a chill platypus”
Sympathetic Nervous System Neuronal Structure
Cells exit from the Thoracic and Lumbar regions of the spinal cord. They start with a very short preganglionic neuron followed by a longer postganglionic neuron
Parasympathetic Nervous System Structure
Cells exit from the Cranial and Sacral regions of the Spinal Cord. They start with a long preganglionic neuron followed by an extremely short postganglionic neuron. Ganglion can even be within the target organ.
Peripheral Nervous System Pathways
Dorsal side receives sensory information
Ventral side sends signals
Muscarinic Cholinoceptor-Mediated effects
Activation by ACh receptors. Causes a myriad of effects mainly to do with rest.
Adrenergic Signaling
Activated by Norepinephrine
Adrenergic Receptor-Mediated effects
Alpha 1 Fight or flight contraction response
Alpha 2 Fight or flight inhibition response
Parasympathetic Postganglionic NT and Postsynaptic receptor
Acetylcholine -> Muscarinic
Parasympathetic relaxation of smooth muscle
ACh binds to GPCr (Muscarinic) or VIP receptor -> IP3 -> increase calcium -> Activates nitric oxide synthase -> nitric oxide relaxes smooth muscle
Sympathetic Stimulation of smooth muscle
ATP, Norepinephrine, and Neuropeptide Y release from synaptic vesicles
ATP binds to ion channels which allow for Ca2+ and Na+ to flow into the cell which depolarizes and opens another Ca2+ channel
Norepinephrine activates alpha 1 adrenergic g protein receptors and opens channel in the ER to release stored Ca2+
Neuropeptide Y bunds to Y1 receptors and move Ca2+ into the cell
Cholinergic Receptors
Muscarinic and Nicotinic
Adrenergic Receptors
Bind Norepinephrine
Alpha 1 and Alpha 2
Beta 1 and Beta 2
Postganglion Synapse Receptor of Sympathetic Nervous System
Adrenergic Receptors
