NT Systems Flashcards
Dopamine
Central Location - basa ganglia and VTA Functions - motor control, pleasure, consciousness Inonotropic R - none Metabotropic R - D1, D2, D3, D4, D5 Other - tyrosine derivative
Norepinephrine
Central Location - pons/brainstem (locus cerules)
Functions - wakefulness
Iontropic R - none
Metabotropic R - alpha and beta drenergics
Other - tyrosine derivatives
Epinephrine
Central Location - brainstem (adrenal medulla)
Functions - wakefulness
Iontropic R - none
Metabotropic R - alpha and beta adrenergics
Other - tyrosine derivative
Serotonin
Central Location - brainstem (raphe nucleus) Functions - mood, wakefulness Iontropic R - 5HT3 (vomiting) Metabotropic R - multiple 5HT6 - mood Other - tryptophan derivative
Histamine
Central Location - hypothalamus (tuberomammillary body) Functions - waking Iontropic R - none Metabotropic R - H1 and H2 Other - histidine derivative
Acetylcholine
Central Location - pons/midbrain Functions - consciousness, wakefulness, voluntary motion, REM sleep Ionotropic R - nicotonic (sodium) Metabotropic R - muscarinic Other - separate from ANS
GABA
Central Location - higher CNS (cerebellum, cortex, retina)
Functions - motor control, consciousness, major inhibitory NT in CNS
Ionotropic R - GABA-A
Metabotropic R - GABA-B
Other - extrasynaptic R (anesthetics)
Glycine
Central Location - spinal cord Functions - almost all inhibition Ionotropic R - glycine (Cl) Metabotropic R - none Other - none
Opioids
Central Location - hypothalamus/medulla, raphe nuclei
Functions - modulation of pain and production of pleasure
Ionotropic R - none
Metabotropic R - mu, kappa, delta
Other - endorphins, dynoprphins, enkephalins
Endocannibinoids
Central Location - multiple/Wid espread Functions - modulation of pain/Neuroprotection Ionotropic R - none Metabotropic R - CB1 and CB2 Other - anandaminde and 2-AG
synthesis of dopamine, NE, and Epi
tyr to L DOPA by tyrosine hydroxylase (rate limiting)
dopamine
conversion of dopamine to NE w/in vesicles
conversion of NE to Epi w/in cytoplasm
substantia nigra dopaminergic pathway
motor control
defect leads to Parkinson’s disease
mesolimbic dopaminergic pathway
core of pleasure/reward
defect leads to addiction
mesocortical dopaminergic pathway
attention and higher levels of consciousness
defect leads to schizophrenia
tuberoinfundibular dopaminergic pathway
suppression of prolactin release from ant. pituitary
Reserpine
limits the amount of monoamines packaged into vesicles and is used in treatment of hypertension
D1 and D5
Gs
voluntary motion control
D2-D4
Gi
inhibition of voluntary motion, pleasure/reward system
Removal from synaptic cleft - Dopamine, NE, Epi
MAO - central
COMT - periphery
Removal from synaptic cleft - Serotonin
MAO after uptake
H1 and H2 R
mediate neuronal effects
H3 R
presynaptic and decrease the release of histamine from presynaptic terminal
Removal from synaptic cleft - Histamine
diamine oxidase breaks down after uptake
Storage of ACH
clear vesicles
moved into vesicles by vAchT
Removal from synaptic cleft - ACH
acetylocholinesterase bound to postsynaptic cell membrane
Muscarinic R
blocked by atropine
smooth mm and glands
M1
neuronal
increased IP3/DAG leading to increased Ca influx
M2
cardiac
decreased cAMP leading to increased K efflux
M3
smooth mm of bronchi, vasculature, endothelial cells of vasculature
increased IP3/DAG leading to increased Ca influx
M4
glands
decreased cAMP leading to increased K efflux
M5
increased IP3/DAG leading to increased Ca influx
nicotinic R
located at: NMJ, autonomic ganglia
allow for Na and some Ca influx
Stiff Person Syndrome
due to autoimmunity to GAD which leads to increased GABA leading to mm rigidity and mm spasms
GABA A R
allow Cl into the cell causing hyperpolarization
activated by benzodiazepine
GABA B R
decreased adenylyl cyclase leads to K efflux
decreased IP3/DAG leaded to decreased Ca influx
both lead to hyperpolarization
Removal from synaptic cleft - GABA
Na/Cl cotransport then broken down by GAGA transaminase
Glycine R
allows Cl into the cell causing hyperpolarization
blocked by strychnine
Mu R
analgesia
respiratory depression
euphoria
increases K efflux leading to hyperpolarization
Kappa R
analgesia
decrease Ca influx leading to hyperpolarization
Delta R
analgesia
decrease Ca influx leading to hyperpolarization
Endocannaboinoids - hippocampus
memory formation
Endocannaboinoids - basal ganglia
affect/motor
Endocannaboinoids - spinal cord
modulation of nociception (pain perception)
Endocannaboinoids - neocortex
neuropcrotecive
CB - 1 R
axons presynaptic terminals
Gi
reduces NT
CB - 2 R
microglia
anti - inflammatory
macrophages to remove beta amyloid
