neurology Flashcards
shapes of multipolar neurones
pyramidal
purkinje
golgi
oligodendrocyte vs schwann
myelin in CNS vs PNS
astrocyte
support + remove waste
microglia
macrophage of brain
ependyma
epithelial - line ventricles
what is an excitable cell
mp can change => sends electrical signals along pathways
saltatory conduction
cable transmission
action potential jumps between nodes of ranvier as myelin has high resistance and low capacitance
types of synaptic organisation
axodendritic
axoaxonic
axosomatic
NMJ
structure allowing unidirectional chemical communication between peripheral nerves + muscle
ACh at nicotinic receptors
end plate potential
voltages causing depolarisation of skeletal muscle fibres caused by neurotransmitters binding NMJ postsynaptic membrane
botulism
botulinum toxin = irreversible
disrupts ACh release from presynaptic membrane
myasthenia gravis
autoimmune abs against ACh-R on post synaptic membrane
causes fatiguable weakness (facial muscle weakness)
lambert eaton myasthenic syndrome
autoimmune antibodies against VGCCs
measuring MP
cell in saline
electrode inside
electrode outside (0 volt level)
electrochemical equilibrium
electrical forces balance diffusional
determines direction of flux
equilibrium potential
potential at which electrochemical equilibrium is reached
what are the nerst and goldman-hodgkins equations used to calculate
equilibrium potential
why is GH better than Nerst
takes permeability of membrane for each molecule into account
graded potential
small depolarisation due to weak stimulus
summate to determine if AP is initiated or prevented
AP = when GP reaches threshold
permeability and membrane potential
depolarisation: PNa > PK so MP increases towards eqbm potential of Na (+72mV)
repolarisation: PK > PNa as MP decreases towards eqbm potential of K (-90mV)
hyperpolarisation: some K+ still open => potential continues to decrease
absolute vs relative refractory period
absolute = sodium channels shut off by inactivation gate (peptide) so AP cannot be triggered
relative = some sodium channels unblocked so stronger stimulus is needed for AP triggering
factors slowing AP
cold, anoxia, compression, drugs, anaesthetics, decreased myelination, smaller diameter
pharmacology
study of how chemical agents (drugs) influence function of living systems by interacting with a specific target in a biological system to produce a physiological effect
effects + targets of heroin
analgesia (peri-aqueductal grey region)
euphoria (ventral tegmental area)
cough suppression (solitary nucleus)
receptor = opioid receptor
drug targets
receptors (e.g. Salbutamol)
enzymes (e.g. Atorvastatin)
transport proteins (e.g. Citalopram)
ion channels (e.g. Amlodipine)
why is selectivity more important in drugs than endogenous compounds
neurotransmitters are specifically delivered to their drug target (nerve → synapse → receptor)
drugs are transported via blood to relevant tissues - issue if drug can bind alternate targets
side effect vs adverse effect
side: secondary to the intended effect
advers = -ive side
safest drugs
large difference between dose required to induce desired effect and dose required to induce side effects/adverse effects
pramipexole
treat Parkinson’s disease
dopamine agonist
vesicle processing in presynaptic terminal
budding => docking => priming
vesicular proteins enable fusion + exocytosis
properties of synaptic transmission
rapid timescale
need diversity
need plasticity
role in learning + memory
NS poison target
vesicular proteins
alpha latrotoxin
activates VGCCs => ACh release until depletion
muscular paralysis as no new APs activated
botulinum toxin
Zn2+ dependant endopeptidases
inhibit transmitter release
disrupts stimulation induced ACh release from presynaptic terminal
all receptor types
slow response (sec-min) = G-protein couples
fast response (msec) = Ion channel receptor
IC excitatory = glutamate nt (Na+ influx)
IC inhibitory = GABA/glycine nt (Ca2+/Na+ influx)
fast excitatory = AMPA channel
slow excitatory = NMDA channel
excitatory channels
depolarisation
+ive influx
excitatory postsynaptic potential => mV made more +ive
inhibitory channels
hyperpolarisation
-ive influx
inhibitory postsynaptic potential => mV made more -ive
AMPA vs NMDA
AMPA: rapid onset, offset + depolarisation
NMDA: calcium second messenger
glutamate (synthesis, uptake, recycling)
S: TCA + transamination of glucose
U: excitatory aa transporters
R: glutamine synthase = glutamine
GABA (synthesis, uptake, recycling)
S: decarboxylation of glutamate via glutamic acid decarboxylase
U: GABA transporters
R: enz modified to succinic semialdehyde via GABA transaminase
electroencephalography
measures electrical activity in brain
SNARE
vesicular proteins = excytotic nt release
synapsin, synaptobrevin, SNAP25
tetanus on NS
inhibits GABA + glycine
2 mechanisms of nt inactivation
re-uptake into presynaptic terminal
enzymatic degradation