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Review
. 2011 Apr;60(5):720-9.
doi: 10.1016/j.neuropharm.2010.12.016. Epub 2010 Dec 30.

Induction and expression rules of synaptic plasticity in hippocampal interneurons

Fernanda Laezza  1 , Raymond Dingledine
Affiliations
Review

Induction and expression rules of synaptic plasticity in hippocampal interneurons

Fernanda Laezza et al. Neuropharmacology. 2011 Apr.

Abstract

The knowledge that excitatory synapses on aspiny hippocampal interneurons can develop genuine forms of activity-dependent remodeling, independently from the surrounding network of principal cells, is a relatively new concept. Cumulative evidence has now unequivocally demonstrated that, despite the absence of specialized postsynaptic spines that serve as compartmentalized structure for intracellular signaling in principal cell plasticity, excitatory inputs onto interneurons can undergo forms of synaptic plasticity that are induced and expressed autonomously from principal cells. Yet, the rules for induction and expression of interneuron plasticity are much more heterogeneous than in principal neurons. Long-term plasticity in interneurons is not necessarily dependent upon postsynaptic activation of NMDA receptors nor relies on the same postsynaptic membrane potential requirements as principal cells. Plasticity in interneurons rather requires activation of Ca(2+)-permeable AMPA receptors and/or metabotropic glutamate receptors and is triggered by postsynaptic hyperpolarization. In this review we will outline these distinct features of interneuron plasticity and identify potential critical candidate molecules that might be important for sustaining long-lasting changes in synaptic strength at excitatory inputs onto interneurons. This article is part of a Special Issue entitled 'Synaptic Plasticity & Interneurons'.

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Figures

Fig. 1
Fig. 1
Two-photon images of Ca2+ transients mediated by CP-AMPA receptors in a cortical interneuron. (Aa) A horizontal dendrite filled with the Ca2+ dye Fluo-4. (Ab) Top, control line scan through dendrite in (Aa), average of three successes. Vertical scale, 400 ms. Bottom, ΔF/F image from line scan above. Vertical scale bar, 100 ms. (Ac) Images are presented as in (Ab), after addition of 1 mM CX-546, an inhibitor of AMPA receptor deactivation. Note how the microdomain spread to adjacent dendritic segment. Average of four successes. (Ba) ΔF/F versus dendritic space plot for calcium transient in (Ab). (Bb) Data plotted as in (Ba) for the transient in the presence of CX-546. Note that panels in (A)–(B) have the same x axis. (C) Top, calcium transients from bracketed regions of line scans in (A), before, black trace, and after, red, addition of CX-546. Bottom, EPSC time locked to the calcium transients above. Note how CX-546 dramatically prolonged the AMPA receptor-mediated currents. All the experiments were performed in the presence of the NMDA receptor blocker d-APV (2-amino-5-phosphonovaleric acid). Modified from Goldberg et al., Neuron 2003.
Fig. 2
Fig. 2
GluA2 induces dendritic spines in GABA-releasing interneurons. Hippocampal neurons at DIV14 were transfected with enhanced green fluorescent protein (EGFP) alone, or with EGFP plus a haemagglutinin (HA)-tagged GluA2 construct, and stained for GFP, glutamic acid decarboxylase (GAD) and HA at DIV22. Paired panels show GFP and GAD staining in the same neuron, as indicated. Interneurons (defined by typical dendritic morphology and GAD6 immunoreactivity in cell soma) have no dendritic spines when transfected with EGFP (top panel and middle panels, left images), but display protrusions with a clear head and neck when transfected with HA–GluA2 (top and middle panels, right images). Bottom panels show higher magnification of the dendrite (GFP image). Scale bar, 10 μm (low magnification) and 2.5 μm (high magnification). Modified from Passafaro et al. Nature 2003.
Fig. 3
Fig. 3
Working model of interneuron plasticity. At interneuron synapses containing CI-AMPA receptors (GluA2-rich), the mechanisms of induction and expression of synaptic plasticity might follow Hebbian rules and be more similar to principal cells. Conversely, at interneuron synapses containing CP-AMPA receptors (GluA2-deficient), the mechanisms of induction and expression of synaptic plasticity follows anti-Hebbian rules and might require different intracellular signaling cascades.
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References

    1. Alle H, Jonas P, Geiger JR. PTP and LTP at a hippocampal mossy fiber-interneuron synapse. Proc Natl Acad Sci USA. 2001;98:14708–14713. - PMC - PubMed
    1. Anwyl R. Metabotropic glutamate receptor-dependent long-term potentiation. Neuropharmacology. 2009;56:735–740. - PubMed
    1. Asrar S, Zhou Z, Ren W, Jia Z. Ca(2+) permeable AMPA receptor induced long-term potentiation requires PI3/MAP kinases but not Ca/CaM-dependent kinase II. PLoS One. 2009;4:e4339. - PMC - PubMed
    1. Bats C, Groc L, Choquet D. The interaction between Stargazin and PSD-95 regulates AMPA receptor surface trafficking. Neuron. 2007;53:719–734. - PubMed
    1. Bliss TV, Collingridge GL. A synaptic model of memory: long-term potentiation in the hippocampus. Nature. 1993;361:31–39. - PubMed

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