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45 Cards in this Set

  • Front
  • Back
you are a NT if..
1. made in a neuron
-present in presyn terminal
2. released during depolarization
-AP depend, Ca depend, vessicles
3. act on rec and cause biological effect
4. have a mechanism for termination
Small MW NTs
1. Ach
2. AA- Glu, Gly, GABA
3. Biogenic Amines- DOPA, NE, Epi, Serotonin, His
4. Nucleotides- ATP, ADP
Principle NT of CNS

Principle NT of brainstem and SC
Glu and GABA

Gly
ATP


Adenosine
often found in vessicles that contain other NT- co-released

feeds back on presyn terminal
Caffeine
blockes adenosine feedback to presyn membrane
Neuropeptides
enkaphalins, endorphins
involved in pain
Unconventional Class of NT
not in vessicle
retrograde signaling (post->Pre)
might not be localized
Types of unconventional NTs
1. NO/CO- ie NO act gunaylate cyclase->inc cGMP-> vasodial
2. Endocanabinoids- from arach acid- retrograde- act back on presyn memb to enhance/depress
-lipid permeable, ~THC
Difference in synthesis
1. Neuropeptides
2. Small molecule
1. synth IN the cell body, put into vessicles and trans by FAST axonal transport
2. synth in presyn terminal, NZMs trans by SLOW axonal trans from cell body to terminal
-synth and packaging in terminal
Small Vessicles (FAST)

Dense-Core Vessicles
30-40nm in diameter

2xs the diameter- do NOT dock in the active zone. they are further back in terminal
what do Dense-core vessicles need differently?

what do they have to overcome?
prolonged Ca signal for vessicle fusion. fuse away from active zone
HIGHER AFFINITY ca sensor

*overcome high Ca buffering in terminal
Everyday working NT
Glu, Gly, GABA
Glu in the cortex
used in projection neurons
major excit NT in CNS
GABA
used in both Local and Projection neurons, but mostly in local circuit(interneurons)

major inhib NT
Gly
major inhib NT in brainstem/SC
basically like GABA
effector is Cl gated ion channel
Glu Shuttle
glu diffuses away from synapse, taken up by Astrocytes, coverted to Gln, resent to presyn terminal, resynth to Glu
GABA Synthesis
associated w/ Kreb's Cycle

glu-->GABA via Glutamic Acid Decarboxylase
GAD nzm
Ach
5% of neurons in brain
impt effects in brainstem
most motor nuclei use Ach
Ventral Horn alpha motor neurons
3 Main CNS areas with high density Ach
1. Septal Nuclei- to HC and Fornix. projects to limbic sys
2. Nucleus Basalis- alz disease
3. Striatum
General Importance of Ach
cognition and memory

septal nuclei input to HC critical
Norepinephrine
1% of neurons in brain
from Locus Ceruleus to everywhere in brain
some desending effects to SC
General Importance of NE


fast or slow?
attention, alertness, ciradian rhythms, memory, mood

Regulate vast areas, are SLOW
Serotonin (5-HT)
1% of neurons in brain: asc/desc

Ascending: DRN to all regions
Desc: caudal RN to SC
General importance of 5-HT
mood, sleep/wake, pain modulation

SSRIs affect mood
Which NT regulate circadian rhythms?
NE, Serotonin, Ach
Dopamine (3% of Neurons in brain)
SN->Striatum- mostly motor/mvmt
Ventral Teg to Amygdala/nucleus accumbens, prefrontal cortex
-largely motivation
Arcuate Nuc to median eminence of hypothalmus
-regulates GnRH
General Importance of Dopamine
mvmt, motivation, sex hormones

mainly from projections of substantia nigra and ventral tegmentum
Dominant role in motivation behavior
Ventral Tegmentum projectsion
-dopamine
Synthesis of Dopamine
Tyr->L-Dopa via Tyr Hydroxlyase
L-DOPA->Dopamine via Dopamine decarboxylase

Dopamine->NE DBH
Ritalin
acts in similar way to coccaine at dopamine reuptake site
MAOs
monamine oxidases

some drugs block reuptake of serotonin, etc
can also inhibit w/i cells
2 Types of NT receptors
Ionitropic (Ligand-Gated Rec)

Metabotropic Rec (GPCR)
Ionitropic Receptors

2 types
Ligand-gated receptors
bind NT, open channel

1. excitatory non-sel cations
2. Inhibitory- chloride
Metabotropic Rec
GCPRs, indirect
bound to heteromeric complexes
activation rel subunity which modulates an ion channel

alpha, beta, gamma subunits
Receptors use both ionitropic and metabotropic

just ionitropic

just metabotropic
Glu, Ach, GABA, Serotonin


Glycine

Dopamine, NE : much slower repsonse
agonist

gating

Antagonists
activates/opens rec when it binds
open/closing of the channel

competitive, non-comp, partial
competitive

noncomp

partial
blocks the binding site, overcome with high conc
acts at dfft site

mimic but dont produce full effect
2 Families of Ligang Gated Channels
1. Glutamate Family
-3memb spanning domains
-4 multimers
2. All others
-4memb spanning domains
-5 multimers
Benzodiazipines and barbituates
GABA is the site
Channelopathies
congenital myesthenia
affects open/closing of channel
GPCR


cytoplasmic domain
7 TMspanning domains, 0subunits
NOT heteromeric, single subunit?

interacts with Gprot

can work through 2nd messenger system, CASCADES
Cholera Toxin


Pertussis Toxin
stabilizes Galpha subunit. prolongs action

stabilizes interaction of rec and heterodimer. Inhibits action of G protein
Gprotein Splits
int Galpha and Gbeta/gamma

beta/gamma moves along membrane and interacts iwth other channels- ie Ca chan
Gating of Pain information
involves enkephalins and Gbeta/gamma proteins regulating calcium channels
Renshaw Cell
ventral horn of spinal cord

interneuron

uses glycine