1 / 15

A Calcium dependent model of synaptic plasticity (CaDp) Describe various induction protocols

A Calcium dependent model of synaptic plasticity (CaDp) Describe various induction protocols. Can a single model, based on a limited set of assumptions, account for the various induction protocols?

livana
Télécharger la présentation

A Calcium dependent model of synaptic plasticity (CaDp) Describe various induction protocols

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. A Calcium dependent model of synaptic plasticity (CaDp) Describe various induction protocols

  2. Can a single model, based on a limited set of assumptions, account for the various induction protocols? Approach: Find a minimal set of assumptions that can qualitatively account for the various forms of induction.

  3. θd θp LTP Ca I. A Unified theory of NMDA Receptor-Dependent synaptic plasticity Assumption 1: The calcium control hypothesis. The idea that calcium levels control the sign and magnitude of synaptic plasticity has been around for a while (Lisman, 1989; Bear et. al., 1987; Artola et. al. 1990) Ω function ΔW LTD

  4. 1 1 0.8 h 0.75 0.6 W -1 sec q q 0.5 0.4 p d 0.25 0.2 0 0 0.2 0.4 0.6 0.8 1 0.2 0.4 0.6 0.8 1 m m Ca ( M) Ca ( M) The calcium control hypothesis, is a generalization of this equation. * Where and has the form the rate function is: *This equation can be derived from a lower level biophysical formulation.(Castellani et. al. 2001, Shouval et. al. 2002)

  5. Assumption 2: NMDA receptors are the primary source of calcium influx to spines during synaptic plasticity (Sabatini et. al 2002). Standard assumptions • Voltage dependence of NMDAR (Jahr and Stevens, 1990) Fraction of open NMDAR ICa

  6. Ligand binding kinetics – sum of two exponentials with different time constants (Carmignoto and Vicini, 1992) • Calcium Dynamics- first order ODE NMDA receptor kinetics- sum of two exponents 0.7 0.5 0.0 NR2A+NR2B In these examples

  7. Pairing Induced Plasticity Voltage clamping postsynaptic neuron while stimulating presynapticaly at 1 Hz. Examples LTP/LTD curve W W

  8. Spike time dependent plasticity (STDP) STDP Curve Bi and Poo, 1998

  9. For the calcium control hypothesis to account • for STDP it is necessary that: • For (post-pre) the calcium influx is • higher than at baseline () • For ( pre-post) the calcium influx is • higher than at ()

  10. Back propagating action potentials Neuron – cell body | || | || | Action potentials Axon: output | | || | | | | | Synapse Dendrite: input

  11. Back spike – assume width 3ms Assume a narrow spike (Width 3ms) • Problems: • No difference between • baseline and post-pre • Only a small elevation • in Ca for pre-post

  12. An example of a BPAP recorded by C. Colbert from a hippocampal dendrite (slice, from 180 gm Sprague Dawley rat at 31o C , 150µM from soma) Assumption 3: The Back Spike has a slow component (long tail). narrow spike (3ms) spike with long tail (width 25 ms)

  13. Back Spike with long tail (tail width 25ms) • Problems solved • Ca level in post-pre larger than at baseline. • Larger elevation of Ca in pre-post condition.

  14. BPAP with wide tail Similar results: Karmarkar and Bunomano, 2002; Abarbanel et. al. 2003; Kitijima and Hara, 2000 (ms)

  15. Nishiyama et. al. Nature, 2000 Bi and Poo J. Neurosci. 1998 Wittenberg and Wang, J. Neurosci 2006 Froemke and Dan, Nature 2006 Does the second LTD Window exist?

More Related