Communication: Synapses & Receptors Flashcards
what are the three types of synpases which have chmical synapstic activity
- Axodendritic
axon to dendrite
- Axosomatic
axon to cell body
- Axoaxonal
axon to axon
What is the Chemical Synpase
waht is the presynaptic neuron
the ceft
the post sympatic neuron
Presynpatic Neuron
- knob shaped neuron end of the axon
- contains the NT within vesciles: docked and undocked
- Ca++ channels to allow th einflux to release vesicles
Cleft
- are for NT to flaot to PostSN
- 20-40 nm
Postsynamptic Neuron
- a thickening called the postsynpatic density a complex of receptors, proteins etc. for the proper binding fo the NT
how are NTs syntehsized in a neuron
NTs and their storage vesicles are sntheszied
- within the axon termial if its a small NT: but using enzymes which are shuttled down there from the body
- within the CB if its a big NT (neuropeptide) then trasnported down the axon to the terminal
what are some NTs
made of what components
excitatory v inhibitory
NTs: are chemically syntehsized within the neuron
- made of an amino acid, nucleic acid or peptide
Excitatory
- continue the signal down to spread the AP (+)
Inhibitory
- stop or hault the signal and spread of the AP (-)
common NTs
- GABA (-) in CNS and PNS
- glutamate (+) in CNS and PNS
- acetylcholine (+ in NMJ, but - in heart) in CNS and PNS and autonomic NS and NMJ
- Norepinephrine (+) in autonomic NS
Classes of NTs
Amino Acids
Monoamines
Cholenergics
Peptides
Purines
Gaseous
Small v Large
Amino Acids
- Glutamate
- GABA
Monoamines
- Serotonin
- Catecholamines (epi/norepi) & dopamine
Cholenergic
- achetylcholine
Peptides
- endorphins
- Substance P
Purines
- ATP
- adenosine
Gaseous Molecules
- Nitric oxide
Small
- amino acids (GABA, glut., glycine)
- monoamines: NE, epi, DA, SER, ATP
Large
- neuropeptides: Sub P, enkephalin, vasopressin
Neuotransmitters
how are they made (precursor pathways)
Amino Acids
- alpha ketogluterate + GABA-T => glutamate
- glutamine + Glutaminase => glutamate
- glutamate + GAD => GABA
Acetylcholine
- Acetyle CoA + choline = Ach
Serotonin
- tryptophan –> 5-hydroxtryptophan –> 5-hydroxytryptopatime
Catecholamines
- Tyrosine –> DOPA –> dopamine –> Norepi –> epi
what happens at the axon terminal whent esignal (AP) gets there
- the synapthic vesciles are filled wiht NT waiting docked or undocked
- voltage gated calcium channels open and calcium rushes in the presympatic neuron
- this triggers synapsin to release its hold on the vesicles to the cell wall (the glue is synapsin, and it breaks when calcium enters)
- the snare proteins are the ones which orignally made them dock and fuse to the wall when waiting
- they release, and then endocytosis to the cleft and release teh NT
triggers eith excitatory or inhibitory continuation of the signal
excitatory
- open more Na+ channels in next cell
- or decreased K+ and Cl- channels to avoid it from inhibiting
Inhibitory
- open K+ to outflow
- open Cl- to influx and hyperpolarize
Receptors
autoreceptors v heterreceptos
types
Receptors
- many subtypes for each NT
- some receptors can be present on a presynpatic neuron and the postsynpatic one
types
Autoreceptors: inhibits FURTHER secretion of the same NT
Heterreceptors: inhibits release of A DIFFERENT NT (like a competiting one)
Families
- Ligand-Gated Ion Channels (ionotropic)
- G-protein Coupled receptors (metabotropic)
receptors are clustered: in the postsynpatic cell the density of receptors in an area is dependent on specific proteins in teh cell
receptors can be desensitized with prolonged epsoure to the ligand (the NT)
how is the NT signal stopped
reuptake v deactivation
Reuptake
- some are reuptaken into the presyn. cell or taken up by astrocytes (glutamate)
Deactivaition
- some are brokedn down : like ACH via acetylcholenesterase
- these processes are sodium dependent and use specific trasnporters
- these processes help stop transmission and effect of a drug
- the vesicle is coated with clarhrin and taken up via endocytosis
Drug Mechanisms
agonis
antagonis
inverse agonists
allosteric modulation
agonist: potentiates (activates) a receptor
antagonists: block somehitng from activating that receptor
inverse agonist: blocks and has long term changes to the receptor
allosteric modulation: activates the receptor indirectly: from a neighboring site (can be +, - or neutral)
ACH to what receptors & where
ACH (cholenergic) binds to
- nicotinic receptors = (+) effect = inotropic= NMJ, para and sympa presynpatic neurons, CNS and adrenal medulla
- muscarinic receptors = (+ or -) effect = metabotropic = think peripheral NS (heart, lungs, upper GI, sweat) ; post-ganglionic, parasympa, CNS
GABA NT and receptors to where
GABA (-) always!!!
receptors = GABAa (ionotrpoci) or GABAb (metabotropic)
found literally everywhere bye
Glutamate NT and recetpros to where
Glutamate to NMDA receptors = (+) stimulus at inotropic/voltage receptors
- found in CNS and PNS
Glutamate to AMPA receptors = (+) stimulus at inotropic receptors
- found in CNS and PNS
Glutamate to kainate receptors (+ or -) stimulus at inontropic receptors
glutamate to mGLUr receptors (+, -) stimulus at metabotropic in CNS or PNS
Serotonins NT t receptors where
SER (+) to 5HT3 receptors (inotropic) = CNS
SER (+) to all other 5HTs receptors (metabotropic) CNS and #4 is gut
Dopamine NT to receptors where
Dopamine (+/-) to D1 receptors (metabotropic) = SN & VTA
DA(-) to D2 receptors (metabotropic) = SN & VTA
