Cell : Astrocytes Put down the Broom and Pick up the Baton [N&V summary]
Some beautiful work [original article] by Oliet’s lab in a recent issue of Cell demonstrates the importance of glia in synaptic plasticity. The show a system where D-serine and not glycine controls the NMDA receptor in a coagonist role (or perhaps glutamate is really the coagonist…) and show how similar pairing protocols can have opposite effects (LTD vs. LTP) depending on D-serine modulation by astrocytes. Yet more hidden factors in plasticity are being revealed!
Here’s the key figure:
More details from the News & Views summary after the jump. Continue reading
Synaptic tuning : Nature Reviews Neuroscience
For those interested in neuromodulators:
Treatment of striatal neurons with a D1 receptor agonist led to an increase in the dendritic staining intensity of NMDA receptor NR2B subunits. There was also an increase in the association of NR2B subunits with PSD-95 — a scaffold protein required for the assembly of NMDA receptors — and in the surface localization of NR2B-containing receptors.
Original article in J. Neurosci. from Dunah and colleagues. An excerpt from the original aricle of a neat application of FRET continues after the jump.
Two Coincidence Detectors for Spike Timing-Dependent Plasticity in Somatosensory Cortex — Bender et al. 26 (16): 4166 — Journal of Neuroscience
Dan Feldman’s group at UCSD has found that different “sides” of STDP (ie. LTP vs. LTD) at cortical synapses might be mediated through distinct signalling pathways. The major finding was that LTD was induced independent of NMDA receptors. Rather, LTD required mGluRs and VGCCs.
There are many questions here. The most interesting to think about is, Are we going to find different STDP rules all over the brain? And, if so, what will be the commond ground between them?
Here’s the abstract:
Many cortical synapses exhibit spike timing-dependent plasticity (STDP) in which the precise timing of presynaptic and postsynaptic spikes induces synaptic strengthening [long-term potentiation (LTP)] or weakening [long-term depression (LTD)]. Standard models posit a single, postsynaptic, NMDA receptor-based coincidence detector for LTP and LTD components of STDP. We show instead that STDP at layer 4 to layer 2/3 synapses in somatosensory (S1) cortex involves separate calcium sources and coincidence detection mechanisms for LTP and LTD. LTP showed classical NMDA receptor dependence. LTD was independent of postsynaptic NMDA receptors and instead required group I metabotropic glutamate receptors and calcium from voltage-sensitive channels and IP3 receptor-gated stores. Downstream of postsynaptic calcium, LTD required retrograde endocannabinoid signaling, leading to presynaptic LTD expression, and also required activation of apparently presynaptic NMDA receptors. These LTP and LTD mechanisms detected firing coincidence on ~25 and ~125 ms time scales, respectively, and combined to implement the overall STDP rule. These findings indicate that STDP is not a unitary process and suggest that endocannabinoid-dependent LTD may be relevant to cortical map plasticity.
From this week’s Nature, the Poo lab shows how BDNF-induced plasticity in the optic tectum can lead to “back-propogated” changes in AMPA receptor density one synapse back in retinal ganglion cells. Click below for the full abstract
Mu-Ming Poo’s lab (which in 1998 found a very impressive result in hippocampal culture where excitatory synapses are potentiated when a Hebb-like protocol is used on the pre- and post-synaptic cell) has recently added two new Hebbian rules also found in hippocampal cell culture.
The first one applies to inhibitory hippocampal synapses (Neuron, Aug 2003) and the second one applies to spike trains in the mossy fiber pathway (Neuron, Feb 2004). The relative spike timing between the pre and post cells results in different amounts of potentiation/depression depending on the synapse type.
Some questions: Are there many different STDP rules? Or, are we missing the bigger picture (ie. a more general rule) of which these are all only specific examples? (Remember, this is just in hippocampus!)