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ref: -2013 tags: larkum calcium spikes dendrites association cortex binding date: 02-23-2021 19:52 gmt revision:3 [2] [1] [0] [head]

PMID-23273272 A cellular mechanism for cortical associations: and organizing principle for the cerebral cortex

  • Distal tuft dendrites have a second spike-initiation zone, where depolarization can induce a calcium plateau of up to 50ms long.  This depolarization can cause multiple spikes in the soma, and can be more effective at inducing spikes than depolarization through the basal dendrites.  Such spikes are frequently bursts of 2-4 at 200hz. 
  • Bursts of spikes can also be triggered by backpropagation activated calcium (BAC), which can half the current threshold for a dendritic spike. That is, there is enough signal propagation for information to propagate both down the dendritic arbor and up, and the two interact non-linearly.  
  • This nonlinear calcium-dependent association pairing can be blocked by inhibition to the dendrites (presumably apical?). 
    • Larkum argues that the different timelines of GABA inhibition offer 'exquisite control' of the dendrites; but these sorts of arguments as to computational power always seem lame compared to stating what their actual role might be. 
  • Quote: "Dendritic calcium spikes have been recorded in vivo [57, 84, 85] that correlate to behavior [78, 86].  The recordings are population-level, though, and do not seem to measure individual dendrites (?). 

See also:

PMID-25174710 Sensory-evoked LTP driven by dendritic plateau potentials in vivo

  • We demonstrate that rhythmic sensory whisker stimulation efficiently induces synaptic LTP in layer 2/3 (L2/3) pyramidal cells in the absence of somatic spikes.
  • It instead depends on NMDA-dependent dendritic spikes.
  • And this is dependent on afferents from the POm thalamus.

And: The binding solution?, a blog post covering Bittner 2015 that looks at rapid dendritic plasticity in the hippocampus as a means of binding stimuli to place fields.