The nervous system Flashcards
what does an archetypal neurone consist of
cell body, dendrite, axon hillock initial segment, axon, myelin sheath, nade of raniver, presynaptic terminals
how is the resting membrane potential generated
generated by the selective potassium permeability of the mebrane
absolute refractory period
during the time interval between the opening of the Na channel activation gate and the opening of the inactivation gate, a Na channel cannot be stimulated. this is the absolute refractory period,
relative refractory period
AP generated during the undershoot but it takes an initial stimulus that is much stronger than usual, this is the relative refractory period.
properties of action potentials
mediated by voltage gated channels, are all or none, can only signal stimulus strength in frequency and not amplitude, have a refractory period, are self propagating and therefore good at signalling over long distances, travel slowly-conduction velocity improved by big axons or mylenation.
how does myelination speed up AP transmission
APs are only ever evoked at the node of raniver, myelination increases membrane resistance and decreases membrane capacitance which produces saltatory conduction. velocity up to 120m/s
effect of myelination
travels further be ause less current is wasted leaking out of the membrane or charging upmthe capacitance
example of a de myelinating disease
multiple sclerosis
effect of demyelination
big local current decays wuicker and does not depolarise to next node to threshold and therefore conduction falls
difference between afferent and efferent
afferent is towards the CNS and efferent is away from the CNS they are both nerve pathways.
what is the peripheral nervous system divided into
somatic and autonomic
somatic nervous system
to the skeletal muscle (efferent)
from sense organs and skin (afferent)
under conscious control
behaviour and sensation
autonomic nervous system
nerve pathways whoch connect to internal organs a d glands. invoulantary processes such as respiration, digestion, blod circulTion. linked to hypothalamus/limbic system.
different outputs of ANS
parasympathetic output of craniosarcal origin
sympathetic output is of thoracolumbar in origin
energy requirements for sympathetic and parasympathetic
sympathetic-prep for activity using energy
parasympathetic%calming or regulating resoring or conserving energy
fight or flight response
sympathetic nervous system
noradrenaline neurotransmitter, increases beta2 concentration which will increase heart rate, perfusion of muscle, glucose and blood flow going to pulmonary circulation.
functions of sympathetic nervous system
promotes expenditure of energy in fight or flight reaction including
increase heart rate and blood sugar, dilation of blood vessels in skeletal muscle, bronchodilation, cessation of digestion,
function of parasympathetic nervous system
generation/conservation of energy e.g. increases activity of gastrointestinal tract, decreases heart rate, stimulation of glandular secretions
neurotransmitter is acetylcholine
differences between somatic and autonomic innervation
somatic-single neurone pathway to skeletal muscle, under voluntary, conscious control e.g. posture
autonomic- 2 neurones connected in series to smooth muscle, glands, heart
involuntary subconscious controls visceral function e.g. circulation, digestion
what do all preganglionic neurones exocytose
acetylcholine acting on post ganglionic nicotinic cholinergic receptors (ligand gated sodium channels)
neurotransmitter released by post ganglionic neurone depends on what
sympathetic- noradrenaline
parasympathetic-acetylcholine
post ganglionic receptors
sympathetic- adrenoreceptors alpha 1&2 and beta1,2&3
parasympathetic muscarinic acetylcholine receptors m1,2,3,4&5
m1-neuronal, m2-cardiac, m3-smooth muscke secretory
a1-increase contractility in smooth muscle
a2-smooth muscle, nerve endings, secretory cells inhibitory effect reduces secretion
beta facilitate relaxation in smooth muscle
cardiac and skeletal increase contractility
beta in liver associated with glucose
in what ways do neurones need to be able to conduct information
from one end of a neurone to the other (APs)
across the minute space separating one neurone from another(neurotransmitters)
potassium reduces excitability, sodium increases
how does diameter and stimulus effect APs
larger diameter- lots of insulation and signal will propagate very quickly
bigger stimulus-more APs
increased availability of neurotransmitters
what is the site of chemical interplay called
synapse
what is the site of transfuction
the conversion of an electrical signal into a chemical signal
how does synaptic transmission work
an AP reaches the axon terminal of the presynaptic cell and causes v gated ca channels to ops , ca rushes in, binds to regulatory proteins and inflated NT exocytosis, NTs diffuse across the synaptic cleft and then bind to receptors on the postsynaptic membrane and initiate some sort of response on the postsynaptic cell
what happens when anion/cation channels open
anion- graded hyper polarisation
cation- graded depolarisation
whatbhappens when there is a graded hyper polarisation/depolarisation
hyper- neuronal Vm father away from threshold and thus referred to as inhibitory postsynaptic potentials or IPSPs
depolarisation- neuronal Vm closer to threshold thus is often referred to as excitatory postsynaptic potentials EPSP
what is temporal summation
the same presynaptic neurone stimulates the postsynaptic neurone multiple times in a brief period. the depolarisation resulting from the combination of all the ESPS may be able to cause an AP
what is spatial summation
multiple neurones all stimulate a postsynaptic neurone resulting in a combination of ESPSs which may yield an AP
what happens upon transmitter release
formation of transmitter/receptor complex
change in postsynaptic membrane permeability
change in ionic flux across membrane
results in change in membrane potential
modifies activity of postsynaptic neurone
effects may be excitatory or inhibitory
examples of neurotransmitters
ACh NA dopamine glutamate 5-HT GABA
functions of acetylcholine
neuromuscular-excitatory-skeletal muscle contraction
para/sympathetic ganglia-excitatory-ganglionic neurotransmission
parasympathetic neuroeffector junction-excitatory/inhibitory- smooth/cardiac muscle &glands
CNS-excitatory/inhibitory-learning/short term memory
secreted by pre-ganglionic nerves to stimulate the post-ganglionic nerve
M2 receptor reduces cardiac contractility, secretion and contraction in the heart. increases contractility in smooth muscle by inhibiting pKa which actively causes relaxation
acetylcholine receptors
nicotinic (nAChR) and muscarinic (mAChR)
functions of nAChR
nAChR directly coupled to cation channels mediate fast excitatory synaptic transmission. differences occur between muscle and neuronal nAChR. Both occur presynaptically and post-synaptically & regulate transmitter release
functions of mAChR
mAChR are G-protein coupled receptors. effects mediated by: PLC, adenylate cyclase inhibition, potassium activation/calcium inhibition
mAChR effects on post ganglionic parasympathetic synapse
affects heart rate, smooth muscle and gland and contribute to ganglionic excitation.
M1- neuronal, slow excitation via increase in IP3&DAG
M2- cardiac, decrease in cAMP and calcium, increase in potassium conductance
M3- glandular, smooth muscle contraction, vascular relaxation.
cholinergic transmission
nAChR increase permeability to Na, K and Ca
influx of Na causes depolarisation
neuromuscular junction known as endplate potential
in muscle fibre, localised epp spreads. if reach threshold action potential initiated and contraction
at synapse, fast excitatory postsynaptic potential (fast epp)
depolarises axon, if epsp large causes action potential
acetylcholine sysnthesis
choline required (enters via carrier-mediated transport) acetylation via cytosolic enzyme choline acetyl-transferase using acetyl-coenzyme A rate limiting step=choline transport vesicle accumulation around 100mM. vesicular transporter results in accumulation of H. H actively pumped into vesicle. uses “energy” of H gradient (low in cytosol, high in vesicle) in H-Ach exchanger. packaged Ach released through exocytosis
acetylcholine desensitisation
caused by persistent exposure to nAChR agonist. conformational (shape) change of receptor. agonist bound but not opening ion channel. e.g. persistent exposure to ACh results in block of depolarising effect but may also occur due to loss of electrical excitability. voltage gated sodium channels inactivated during sustained depolarisation.
types of adrenergic receptors
alpha adreno-receptor (noradrenaline>adrenaline>isoprenaline)
beta adreno-receptor (isoprenaline>adrenaline>noradrenaline)
subtypes;
alpha 1&2
beta 1,2&3
all are G-protein coupled receptors but differ in 2nd messenger pathways
noradrenaline site/action/effect
sympathetic neuro-effector junction- excitatory/inhibitory- increased hesrt rate, vasoconstriction
CNS- mainly inhibitory but some excitatory- blood pressure regulation
noradrenaline synthesis
metabolic precursor is L-tyrosine (AA in body fluids taken up by adrenergic neurones)
tyrosine hydroxylase is cytosolic enzyme found only in catecholamine containing cells
catalyses conversion of tyrosine to dopa
primary control of NA synthesis (TH is rate limiting step but can be inhibited by NA)
dopa carboxylase is a cytosolic enzyme found only in catecholamine synthesising cells. catalyses the conversion of dopa to dopamine
dopa carboxylase is non specific and catalyses decarboxylation of other AA such as L histidine (histamine) and tryptophan (seratonin)
dopamine-beta-hydroxylase catalyses conversion of dopamine to NA. small amounts released with NA
phenylalanine N methyltransferase (PNMT) catalyses methylation of NA to adrenaline
PNMT located in adrenal medulla
ATP also released along with NA (responsible for rapid excitatory synaptic potential and rapid excitatory synaptic potential and rapid contractile response in smooth muscle)
regulation of NA release
release affected by presynaptic receptor activation:represents important control mechanism
noradrenaline regulates its own release (and co-released ATP) affect is inhibitory
known as auto-inhibitory feedback mechanism.
noradrenaline uptake
action terminated upon reuptake primarily by nor adrenergic nerve terminals
circulating noradrenaline and adrenaline degraded very slowly (contrast with ACh)
2 main metabolising enzymes found both intra and extracellular
y
re-uptake important for efficient metabolism to take place
2uptake mechanisms; differ in location, kinetic properties and inhibition
uptake 1-neuronal transporter. has high affinity(able to transport very low
concentration) is relatively selective for NA, uptake rate is low
uptake 2- extra(non)-neuronal transporter. has low affinity (only able to transport when concentration is high) transports adrenaline and isoprenaline as well. uptake rate is high.
noradrenaline metabolism
MAO (monoamine oxidase) is abundant in nor adrenergic nerves but also present in liver and intestinal epithelium. converts NA to corresponding aldehyde. in sympathetic nervous system, MAO controls NA and dopamine content. releasable store of either increase in MAO inhibited
COMT (catechol-O-methyl-transferase) is a ubiquitous enzyme (gut, liver, kidney, brain)
acts either on NA itself or products of MAO. final metabolite is VMA(3-methoxy-4-hydroxymandelic acid)
VMA excreted in the urine.
release of adrenaline from chromaffin cells in the adrenal medulla can be increased ip to 5-fold in response to fear, pain, and physical exercise.
what cells contain adrenaline
chromaffin cells
ways to remember sympathetic and parasympathetic systems
sympathetic- fight or flight. changes that occur during “e situations” embarrassment emergency and excitement
parasympathetic- rest and digest
SLUDD- salivation, lacrimation, urination, digestion and defaecation
