| First Author | Nahmani M | Year | 2014 |
| Journal | J Neurosci | Volume | 34 |
| Issue | 7 | Pages | 2571-82 |
| PubMed ID | 24523547 | Mgi Jnum | J:206940 |
| Mgi Id | MGI:5553389 | Doi | 10.1523/JNEUROSCI.4600-13.2014 |
| Citation | Nahmani M, et al. (2014) Deprivation-induced strengthening of presynaptic and postsynaptic inhibitory transmission in layer 4 of visual cortex during the critical period. J Neurosci 34(7):2571-82 |
| abstractText | Inhibition from fast-spiking (FS) interneurons plays a crucial role in shaping cortical response properties and gating developmental periods of activity-dependent plasticity, yet the expression mechanisms underlying FS inhibitory plasticity remain largely unexplored. In layer 4 of visual cortex (V1), monocular deprivation (MD) induces either depression or potentiation of FS to star pyramidal neuron (FS-->SP) synapses, depending on the age of onset (Maffei et al., 2004, 2006). This reversal in the sign (- to +) of plasticity occurs on the cusp of the canonical critical period (CP). To investigate the expression locus behind this switch in sign of inhibitory plasticity, mice underwent MD during the pre-CP [eye-opening to postnatal day (p)17] or CP (p22-p25), and FS-->SP synaptic strength within layer 4 was assessed using confocal and immunoelectron microscopy, as well as optogenetic activation of FS cells to probe quantal amplitude at FS-->SP synapses. Brief MD before p17 or p25 did not alter the density of FS-->SP contacts. However, at the ultrastructural level, FS-->SP synapses in deprived hemispheres during the CP, but not the pre-CP or in GAD65 knock-out mice, had larger synapses and increased docked vesicle density compared with synapses from the nondeprived control hemispheres. Moreover, FS-->SP evoked miniature IPSCs increased in deprived hemispheres when MD was initiated during the CP, accompanied by an increase in the density of postsynaptic GABAA receptors at FS-->SP synapses. These coordinated changes in FS-->SP synaptic strength define an expression pathway modulating excitatory output during CP plasticity in visual cortex. |
