Neuro Intro Flashcards
Major Divisions of the NS
CNS (brain & SC)
PNS- further divided into Somatic (sensory/motor) Autonomic (fight/flight) and Enteric (gut)
Soma
Cell Body
Neuron
Major target of pharmecuticals- fundamental unit of the NS for transforming and relaying electrical signals.
Astrocyte
Provides biochemical support of endothelial cells that form BBB. Supplies nutrients to NT
Oligliodendrocyte
Mylenate
Vasculature
Supply O2 and nutrients
Dendrites
Receive signal
Axon Terminals (terminal boutons)
Make synaptic contact w/dendrites of the next neuron
Synaptic transmission typically occurs via
Axo-dendritic, Axo-somatic
Basic Elements of NT
AP Depolarization of axon terminal influx of CA2+ Fusion of vesicles to terminal Exocytosis Binding of NT to postsynaptic receptors Opening of ion gated channels Reup/Degredation of NT
EPSP
Depolarization, more positive
IPSP
Hyperpolarization, more negative
Cholchicine
Drug which can inhibit the transport of NT to terminals
Snare Cycle
Synaptobrevin interacts w/target proteins- syntaxin and SNAP-25
Form a tight complex, w/munc18 binding
CA influx triggers release of NT
NSF and SNAP bind causing dissocation (ATP)
NT Structures
Amines, Purines, Monamines, AA’s, Endocannabinoids,Peptides
+ AA NT’s
Glutamate & Aspartate- EPSP
- AA NT’s
GABA and Glycine- IPSP
Synethesis of GABA
Start w/Glutamate
L-Glutamic acid (GAD) GABA
GAD- glutamic acid decarboxylase
Catabolism of GABA
Breakdown by GABA-T
*transaminase
GABA Receptor subtypes
GABAA,GABAC (LG)
GABAB (GPCR)
Glycine MOA
Similar to GABA- increases Cl- Conductance
IN SC, not brain
GABA Reuptake
GAT1
gaba transporter into presynaptic neuron
Transport of GABA
GAT3- into glial cells
Conversion of GABA to Glutamine
GS- glutamine synthetase
Transport into GABAergic Neuron
SAT
Package of GABA into vescile
VGAT
Major excitatory transmitter of the brain
Glutamic acid, Glutamate
Receptor types of Glutamate
NMDA, AMPA, Kainate- Ligand gated ion channel receptors
mGluR 1-8 metabotropic- GPCR
Means of inactivation- Glutamate
REup’s GLT1
Transport into Glial cells- Glutamate
GLT/GLAST
Conversion to Glutamine- Glutamate
GS
Transport into GABAergic neuron- Glutamate
SAT
Package into vesciles- Glutamate
VGLUT
LTP
insertion of more AMPAR receptors (more glutamate)
receptor upregulation
LTD
fewer receptors on the surface.
Excitotoxicity
Due to too much calcium- can lead to:
Cell apoptosis, DNA damage, cytoskeletal damage
ACh Synthesis
Choline uptake; choline acetyltransferase (adds acetyl group onto choline)
Storage and release
in vesicle, CA2+ dependent exocytosis
Inactivation of Acetylcholine
Cholinesterase hydrolysis; yields choline and acetate
NO Reup of ACh
ACh Receptor Types
Nicotinic- LG
Muscarinic- GPCR M1-M5 Subtypes
Ach Degregation enzyme
AChE
Transport of ACh
CHT
Conversion to ACh
ChAT
Packing Ach into vesicles
VAChT
ACh Pathways
Cholinergic- Ch5-Ch8 brain stem nucli
Catecholamines are derived from
Tyrosine, taken up into neurons through active transport.
Catecholamine synthesis
Tyrosine hydroxylase, adds OH
AADC Remooves COOH, NH2
~Dopamine –> Add OH to get NE –> Add methyl to get Epi
Storage of Catecholamines
In vesicles, disrupted by reserpine
Inactivation of Catecholamines
Reuptake, degreation by MAO, Catechol-O-methyltransferase COMT
Reuptake of Catecholamines
DAT/NET
Packaging of Catecholamines
VMAT2
Cathecholamines pathways in CNS
Locus ceruleus
Dopamine pathways- 5 receptors, GPCRs
Norepinephrine pathways- 9
Seretonin
AA precursor- tryptophan Reup can be blocked by SSRI, TCA Metabolized by MAO, DAO Reup- SERT Packed- VMAT2
Seretonin Receptors
14 ID’d s far GPCR, LG
Endocannabinoids
Retrograde transmission- goes backwards