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Principles of network function (How much can we REALLY know about neural…
Principles of network function
How much can we REALLY know about neural networks?
Limitations of Selverston (1980) basic requirements for understanding
Main criteria of latency (Olsen & Wilson, 2008) for deriving synaptic organisation is not good enough (e.g. Mono- vs. Polysynaptic connections)
Each cell is unique (~143 genes for VG chanells); cell properties need to be specific for network classes
Identification of network neurons is tricky (ERR of
omission
&
commission
)
Approx. 200 substances act as transmitters; no two synapse environments are the same and again we need to classify synapses as being network specific
Network plasticity
is a basic neuronal property and will affect the functional states possible for any neural network (
adaptive
,
activity-dependent
,
neuromodulation
)
Considering there is
intrinsic plasticity
: Is plasticity a basic neuronal property or is it a basic neural network mechanism?
Glial cells
are functional --> synapses may comprise 3 players: presynaptic & postsynaptic cell, accompanying glial elements
Adipic acid (toxin for glial cells) breaks down the rhythmic activity a neural circuit
Stellwagen & Walenka (2006)
: Glial cells are the source of TNF-α which is essential for adaptive plasticity and adaptive plasticity in turn allows for optimal circuit output
Field effects
when neurons are active can influence behavior of nearby neurons
Mauthner cell
of goldfish
Variability
in cell properties, synaptic strength may be a functional signal and not just a result of random genetic variation (e.g. post-transcriptional splicing) or plasticity-induced changes
We can look for building blocks:
network motifs
(Koch, 2012)
Reciprocal inhibition
is an example of a motif that points limitations in using this approach to understand neural networks. We cannot differentiate between the following examples
Direct cross inhibition
Crossed excitation activating inhibitory interneurons
Strychnine (GlyR blocker) cannot differentiate b/w the 2 possibilities contrary to original thinking that it could
Kjaerulff & Kiehn:
Rat spinal cord experiment
showed it is
crossed excitation activating inhibitory interneurons
and not reciprocal inhibition as the original Brown's half-centres suggested
Applying GluR blockers i.e. blocking excitation, removes inhibition of motor neuron (3) activity
Even if reciprocal inhibition, doesn't mean it causes alternating activity:
Elton et al. (2002)
showed longer lasting inhibitory input causing
synchronous activity
and not alternating
A critical evaluation of 'characterised' networks
Lamprey
locomotion by Grillner
Apamin experiments to support cellular mechanism offer additional data which was ignored
Segmental network proposed under heavy criticism (e.g. Rovainen, 1983)
Fictive locomotive activity is not always matched with locomotive activity (e.g. Ayes et al., 1983)
Role of motor neuron feedback was not considered
Role of plasticity?
Aplysia
learning by Kandel
Hickie et al. (1997): Only 5% of postsynaptic potential of MNs is contributed by LE sensory neurons; is this monosynaptic connection a good choice to investigate this behaviour?
Glanzman: There are also cellular changes in MN; why did Kandel only show what goes on in SN?
Role of tool development
