Neuronal communication II Flashcards
receptors in postsynaptic neuron can be:
- ionotropic
- metabotropic
ionotropic receptors: features
- closed state until NT binds to receptor -> change shape
- allow passage of charged ions
- rapid opening of channel
- ligand dissociates from receptor and channel closes
- postsynaptic potential (PSP, graded potential lasts few ms)
metabotropic receptors: direct coupling
- G protein coupled receptors (GPCRs)
- membrane proteins coupled to ion channels through messenger molecules (G proteins)
- direct coupling: activated G protein subunit acts as ligand for ion channel
- slow acting (secs)
- longer lasting PSP
metabotropic receptors: indirect coupling
- G protein activates/ inhibits enzyme that causes changes in intracellular conc of secondary messenger molecule (ligand)
- 2ndary messenger binds to ion channels -> open/ close
- slower acting (secs)
- longer lasting PSP
postsynaptic potentials (PSPs):
- each presynaptic neuron generally releases only 1 type of NT
- depending, postsynaptic neuron membrane potential either polarised or depolarised
excitatory synapses: EPSPs - ionotropic
- fast response mediated by ionotropic receptors
- binding of NT causes nonspecific ion channels (Na, K) in membrane to open
- depolarised (Na flowing in more)
excitatory synapses: EPSPs - metabotropic
- slow response
- NT activates G protein -> activates membrane bound enzyme adenylate cyclase
- ATP -> cAMP (2ndary messenger)
- interior of postsynaptic cell depolarised (adds phosphate to K selective ion channels and closes)
inhibitory synapses: IPSPs - ionotropic K channels
- fast
- ligand/ NT binds to receptor
- K ion channels open
- K leaves cell
- hyperpolarised inside postsynaptic cell
inhibitory synapses: IPSPs - ionotropic Cl channels
- fast
- ligand binds to receptor (eg. GABA to GABA a)
- hyperpolarised
inhibitory synapses: IPSPs - metabotropic receptors
- slow
- ligand binds to metabotropic receptors
- activation of G protein causes enzymatic cascade= opening K channels
- hyperpolarisation (K leaves cell)
synaptic circuitry:
- neurons communicate w each other and effector organs
convergence:
- axon terminals converge/ synapse w single neuron
divergence:
- axon from single neuron branches out and synapses w many other neurons
multiple EPSPs required to generate depolarisation that reaches threshold needs:
- temporal summation
- spatial summation
collective potential of summation (both excitatory and inhibitory) at axon hillock
- grand postsynaptic potential (GPSP)
temporal summation:
one synapse through time
spatial summation:
- several synapses at same time
neuron receives types of synaptic input:
- axodendritic
- axosomatic
- axoaxonic
axodendritic and axosomatic synapses:
- postsynaptic facilitation or inhibition
- nonselective effect on postsynaptic neuron through generation of EPSPs or IPSPs
axoaxonic synapses:
- presynaptic facilitation or inhibition
- selective effect on NT release by presynaptic cell at 1 particular synapse
synaptic modulation/ plasticity:
- efficiency of synaptic transmission is dynamic (esp chemical synapses)
- synaptic strength can be modified over short/ long time scales
- strength altered by physiological, molecular and structural changes
- essential for strengthening functional circuits during development
- changes in synaptic strength -> basis of learning and memory
forms of synaptic plasticity:
- heterosynaptic (extrinsic) plasticity
- homosynaptic (intrinsic) plasticity
define extrinsic plasticity:
- changes in strength of synapse due to activity in other pathways:
- presynaptic facilitation/ inhibition
define intrinsic plasticity:
- changes in strength of synapse due to its own activity:
- synaptic facilitation (short/long term effects)
- synaptic depression (short/long term effects)
heterosynaptic plasticity: axoaxonic synapses function as
- modulatory synapses
- presynaptic facilitation/ inhibition
heterosynaptic plasticity: presynaptic facilitation
- activating modulatory neuron causes greater release of NT from normal excitatory neuron is active
heterosynaptic plasticity: presynaptic inhibition
- activating modulatory neuron causes reduction of NT released when normal excitatory neuron is active
homosynaptic plasticity: short term enchancement
- postsynaptic potentials get larger w subsequent action potentials
- paired pulse facilitation (PPS) ms
- augmentation (secs) and post tetanic potentiation (PTP) mins
homosynaptic plasticity: short term depression
- postsynaptic potentials get smaller w subsequent APs
- paired pulse depression (secs)
- post tetanic depression (mins)
homosynaptic plasticity: long term plasticity
- long term potentiation (LTP) long lasting increase in synaptic strength following repeated stimulation
- long term depression (LTD) long lasting decrease in strength
short term enhancement: paired pulse facilitation
- increased amplitude of postsynaptic potential induced by AP that arrives within few ms of previous identical AP
- residual Ca accumulated in cell following first AP increases no. of NT filled vesicles released by presynaptic terminal -> synaptic cleft
- larger PSP
- last ms
short term enhancement: augmentation and post tetanic potentiation
- repetitive high frequency (>1 Hz) and long lasting stimulation of presynaptic neuron
- raised Ca conc activates enzymes -> increase no. and size of NT vesicles
- larger PSP in post synaptic cell
- last several secs (augmentation) or minutes (PTP)
short term depression: paired pulse depression
- decreased amplitude of PSP induced by AP that arrives within few ms of previous identical AP
- first AP depolarises cell
- cause Ca influx
- subsequent AP will depolarise cell but no. of vesicles readily available for release into synapse are reduced
- less NT released
- smaller PSP in postsynaptic cell
short term depression: post tetanic depression
- reduction of amplitude of PSP during and after repeated stimulation
- inactivation of presynaptic voltage gated Ca channels from repeated stimulation
- reduced influx of Ca during depolarisation
- less NT released
- smaller PSPs
autoreceptors:
- feedback mechanism to modulate release of NT
- receptors on axon terminals of presynaptic neuron that bind ligands (NTs) released by same presynaptic cell (autocrine signalling)
- eg. dopaminergic neurons use NT dopamine
dopamine autoreceptors:
- dopamine release stimulates postsynaptic cell but also metabotropic dopamine autoreceptors on presynaptic axon terminal
dopamine autoreceptors: short term effects
- G protein mediate increase K+ and decrease Ca reduce ability of terminal to depolarise in response to further AP
- increased uptake of dopamine from synaptic cleft = reduced stimulation of postsynaptic cell
dopamine autoreceptors: long term effects
- decreased synthesis/ packaging of dopamine into vesicles cause reduction in release of dopamine in response to AP and reduced stimulation of postsynaptic cell
- negative feedback to reduce dopamine release
