Topic 3 Flashcards
Parts of NT system
1) Metabolic enzyme that synthesis the NT
2) Vesicle transporter to package the NT
3) The receptor that they bind to
4) The transporter protein that is involved in their re-uptake
5) metabolic enzyme that degrades them
Glutamate
Excitaory - causes cation channels to open letting cations in
GABA
Inhibitory
Neuropharmacology
Drugs that alter the functions of the nervous system
Enhancer
doesn’t directly bind to receptor but enhances it’s affects
Antagonists
Binds directly to receptor and blocks it
Agonist
Mimics NT
Ionotropic receptor
embedded in the membrane
Let ions pass through
NT attaches to the outside which will either activate or deactivate it
generally fat
Ionotropic receptor structure
5 subunits of protein are put together to form a pentameric structure
Metabotropic receptor
uses G-proteins as a second messenger system to activate channel/ response
slower, but longer lasting
G-protein subunits
G-alpha
G-beta,gamma
Activation of G-protein
1) G-protein is freely floating around
2) NT binds to the Metabotropic receptor, then G-protein binds, then GDP turns into GTP
3) G -protein subunits split and do their own thing
4) GTP is phosphorylated back to GDP
5) Subunits reattach at messenger system stops
Push pull mechanism
push - message flows down system
pull - message stops and G-protein tells everybody else to stop
Signal amplification
When multiple G-proteins attach and amplify the signal
Convergence
One NT activates more than one receptor
Divergence
Different NT can act on the same receptor
Glutamate
Amino Acid NT
Inotropic and metabotropic
cognitive function, synaptic plasticity
Glutamate inoptropic receptors
AMPA
NDMA
Kainate
Glutamate Metabotropic receptors
mGluRs
AMPA and NMDA
often found together and working together, NDMA will often experience a magnesium block at -65mv
therefore AMPA has to do all the work
GABA
synthesised from glutamate
by GAD (GLUTAMIC ACID DECARBOXYLASE)
Action is terminated by takeup by GABA transporter and is then degraded
GABA receptors
Alpha - ionotropic
Beta - metabotropic - Ggamma binds to k+ channels - lowering membrane making it harder for an action potential to occur
Benzodiazapene (valium)
Anxiety Medication
increase the frequency of GABAalpha receptors opening
Barbituates
Act on GABAalpha receptors - keep gates open for longer
sedating affect
Glycine
only inotropic
inhibitory
caffeine is an antagonist for it
abundant in brainstem and spinal cord
Acetylcholine
Ach
neuromuscular junction
Activates muscle contraction
Excitatory
synthesized from Acetyl CoA and choline
degraded by acetylcholinesterase in synaptic cleft - reuptake of choline is the limiting reagent
ACh Receptors
Nicotinic
ionotropic
activation causes skeletal muscle to contract
Curare is antagonist for this
Muscaronic
Metabotropic
Found in the heart
Activates heart, GIT, bladder
Atropine is an antagonist
Acetylcholinesterase Inhibitor
Leaves ACh in the synaptic cleft for longer as it prevents it degradation
Reversible AChE inhibtiors
Neostigmine - treat Mystania Gravis and Alzheimers
Irreversible AChE Inhibitors
not clinically used
organophosphates, pesticides
Catecholamines
Dopamine, noradrenaline, adrenaline
movement, mood regulation, attention
all synthesised from tyrosine
hydroxylase converts tyrosine to dopamine
dopamine hydroxylase then onverts it to noradredaline
Catecholamine Receptors
All metabortropic
Termination of catecholamines
Dopamine is taken up by dopamine transport
noradrenaline - taken up by noradredaline transporter
both are then degraded in presynaptic terminal
Serotonin
Acts only on metabotropic receptors
AKA 5HT
comes from the amino acid tryptophan
tryptophan - hydroxylase- 5HT - decarboxylase to Serotonin
Mood, sleep, emotional behaviour
terminated by re-uptake of serotonin transporter
SSRI
Selective Serotonin reuptake inhibitor
stops the reuptake of serotonin so it stays in synaptic cleft for longer
used to treat depression
Endocannaboids
Retrograde messenger
go from post synaptic to pre synaptic
bind to their own cannaboid receptors but can affect GABA, glycine and glutamate receptors
Myasthina Gravis
Autoimmune disease
affects skeletal muscle
B-cells bind to nictonic recepetors, preventing ACh from binding
MG symtoms
Fatigue that worsens throughout the day or with exercise
droopy eyelids (affects extra occular muscle)
weaker doing repetitive movements
muscle weakness
tiredness that improves with rest
Types of MG
ocular MG - only affects the extraocular eye muscles
Generalised MG
MG Diagnosis
Tensilon test - given ultra short acting AChE to see if it stops the droopy eyes
Nerve conduction
Anitbody test
MG treatment and prognosis
AchE inhibtors
corticosteroids
plasmaphoresis
Hyperklexia
Exaggerated startle response
all muscles stiffen then the person faints but remains consciousness
drop seizures
caused by a gentic mutation in the glycine receptor
Hyperklexia Treatment
no cure
give benzodiazapene
Classifying Sezuires
1) generalised or focal
2) if patient still has awareness
3) Degree of motor involvment
Focal seziure
Only affects one portion of the brain
whatever portion is affect the symptoms will manifest accordingly
two types
focal aware
focal dyscognitive - loss of awareness
Genralised
When multiple areas of the brain are affected
Tonic - clonic
Tonic - all muscles contract and patient fall with teeth clenched and eyes open
clonic - convulsions
Absence Seizure
Short period of impaired conscouiness
zoned out
Atonic seizure
All muscles contract and the patient falls to the ground but they still fully aware
Myoclonic
Myo - muscle
clonic - contract
muscle contraction / jerks can be one muscle or multiple
patient is fully aware
Status Epilepticus
a series of seizure where there is no regain of consciousness
Epilepsy Diagnosis
EEG
Medical History
MRI
genetic testing
Treatment
Phenytoin - stops repetitive activation of sodium channels
Valproate - unclear mechanism of action
