Lecture 1 Flashcards
4 requirements of a NT
- Synthesized in pre
- Present in terminal and released in amounts sufficient for response
- Exogenous application has same effect
- Mechanism to remove from cleft
Dale’s law
Each neuron releases only 1 NT
3 Amino acid NTs
Glutamate
GABA
Glycine
3 Catecholamine NTs
Dopamine
Norepinephrine
Epinephrine
2 Monoamine (not catecholamine NTs)
Serotonin
Histamine
2 NTs that do not fit into a category
Acetylcholine
ATP/Adenosine
Neuropeptides act through
Metabotropic receptors
Structure of ionotropic
Multiple subunits or variable numbers
Structure of metabotropic
Single protein w 7 transmembrane domains
2 ex of how allosteric modulators work
Affinity
Protein stability
Major forebrain NTs
Glutamate
GABA
6 Major brainstem NTs
Ach 5-HT Epi NE DA Histamine
Glutamate transporter
EAAT
Glutamate vesicular transporter
vGLUT
Allosteric antagonist of NMDA-R
PCP
How many Glu Rs
3 ionotropic
8 metabotropic
Who proved Glu was a NT and how
Curtis & Watkins
Analogue NMDA activated but is not a metabolite
Synthesis of GABA
Glutamate + Glutamic Acid Decarboxylase
GABA transporter
GAT
GABA vesicular transporter
vGAT
2 GABA receptors
GABA-A: ionotropic
GABA-B: metabotropic
GABA-B are primarily coupled to
Gi
Glycine vesicular transporter
vGAT
Glycine transporter
GLYT
GABA and Glycine share 2 things
vGAT vesicular transporter
Loaded into same vesicles
Glycine receptors are
Ionotropic
GABA ionotropic conduct
CL- in
Glycine receptors conduct
Cl- in
GlyR mutated subunits cause
startle disease
Ach synthesis steps
Acetyl-COA + Choline + Choline Acetyl-Transferase (ChAT)
Ach is cleared from synaptic cleft by
Acetylcholinesterase (no reuptake)
2 major loci of Ach
Nucleus Basalis
Pedunculopontine Nucleus
Sarin works by
Inhibiting Acetylecholinesterase = too much ACh = rigid paralysis
What is lost early in AD
Ach in Nucleus Basalis
2 Ach receptor types
Nicotinic: ionotropic
Muscarinic: metabotropic