nens220 lecture 4 interneuronal communication n.
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Nens220, Lecture 4 Interneuronal communication. John Huguenard. Synaptic Mechanisms. Ca 2+ dependent release of neurotransmitter Normally dependent on AP invasion of synaptic terminal Probabilistic. Short term plasticity. Dynamic changes in release probability Likely mechanisms

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synaptic mechanisms
Synaptic Mechanisms
  • Ca2+ dependent release of neurotransmitter
    • Normally dependent on AP invasion of synaptic terminal
  • Probabilistic
short term plasticity
Short term plasticity
  • Dynamic changes in release probability
    • Likely mechanisms
      • Ca2+ accumulation in synaptic terminals
      • Altered vesicle availability
    • To implement
      • update Prel upon occurrence of a spike
      • then continue to calculate state of Prel dependent on P0 (resting probability) and tP(rel)
longer term plasticity
Longer term plasticity
  • bidirectional
    • LTP
    • LTD
  • Both IE and synaptic strength may change
  • Implicated in learning and memory
slide6
LTP
  • Robust in hippocampus
    • Readily evoked and recorded with extracellular electrodes
    • Evoked by tract stimulation: simultaneous activation of many axons
  • More subtle (and interesting) versions of LTP
natural stimuli stdp
Natural stimuli & STDP

Further reading:

Coactivation and timing-dependent integration of synaptic potentiation and depression, Bi Lab, 2005

FROEMKE & DAN, 2002

back propagation aps and ltp
Back propagation APs and LTP

Ca dependent

- L channels

Na dependent

- back prop

Often NMDAR

dependent

Calcium spatio-temporal dynamics:

Calcineurin ~ LTD

CaMKII ~ LTP

Magee and Johnston, 1997

presynaptic receptor mediated alterations
Presynaptic receptor mediated alterations
  • Mainly metabotropic
        • An exception is nicotinic AchR
    • Homosynaptic “autoreceptors”
    • Heterosynaptic receptors
postsynaptic properties ionotropic receptors
Postsynaptic properties: ionotropic receptors
  • Ligand gated receptors
  • Directly gated by neurotransmitter – ion pores
  • Can be modeled analogously to voltage-gated channels
the probability of a ligand gated channel be open p s will depend on
The probability of a ligand gated channel be open (Ps) will depend on:
  • on and off rates for the channel
  • With the on rate dependent on neurotransmitter concentration
  • This can be approximated by a brief (e.g. 1ms) increase, followed by an instantaneous return to baseline
three major classes of ligand gated conductances
Three major classes of ligand gated conductances
  • GABAA
    • Fast IPSP signaling
    • trise < 1ms
    • tdecay : 1.. 200 ms !, modulable
    • Cl- dependent
    • EGABAA range: –45 .. –90 mV
    • Highly dependent on [Cl-]i
      • Which is in turn activity dependent
      • NEURON can track this
ampa glutamate
AMPA (glutamate)
  • Fast EPSP signaling
  • trise < 1ms
  • tdecay : 1..10 ms
  • Cation dependent
  • EAMPA 0 mV.
ca 2 permeability ampar
Ca2+ permeability: AMPAR
  • Depends on molecular composition
  • GluR2 containing receptors are Ca2+ impermeable
    • Unless unedited
  • Prominent in principle cell (e.g. cortical pyramidal neuron) synapses
  • GluR1,3,4 calcium permeable
    • Calcium permeable AMPA receptors more common in interneurons
ampar have significant desensitization
AMPAR have significant desensitization
  • Contributes to rapid EPSC decay at some synapses
nmda glutamate
NMDA (glutamate)
  • EPSP signaling, slower than with AMPA
    • trise : 2-50 ms
    • tdecay : 50-300 ms
  • cation dependent
  • ENMDA 0 mV
  • Significant Ca2+ permeability
  • NMDAR - necessary for many forms of long-term plasticity
ndmar blocked by physiological levels of mg 2 o
NDMAR Blocked by physiological levels of [Mg2+]o
  • Voltage and [Mg2+]o dependent
  • Depolarization relieves block
kainate receptors glutamate
Kainate receptors (glutamate)
  • Roles are less well defined than AMPA/NMDA
metabotropic receptors
Metabotropic receptors
  • Many classes
  • Conventional neurotransmitters, GABA, glutamate
  • Peptide neurotransmitters, e.g. NPY, opioids, SST
  • Often activate GIRKS
    • G-protein activated, inwardly-rectifying K+ channels
mreceptors
mReceptors
  • Inhibitory, hyperpolarizing responses.
  • Can be excitatory,
  • e.g. Substance P closes GIRKS
  • Slow time course
    • e.g. GABAB responses can peak in > 30 ms and last 100s of ms
  • Presynaptic & negatively coupled to GPCRs
electrotonic synapses
Electrotonic synapses
  • Transmembrane pores
  • Connect the intracellular compartments of adjacent neurons
  • Prominent in some inhibitory networks
perisynaptic considerations
Perisynaptic considerations
  • Neurotransmitter uptake by glia or neurons
  • Diffusion
  • heterosynaptic effects
  • extrasynaptic receptors
  • Hydrolysis