, 2011) In conclusion, we show that the interplay

betwee

, 2011). In conclusion, we show that the interplay

between different senses can occur by means of interareal synaptic inhibition. The elucidation of the synaptic basis of multimodal interactions in primary sensory areas could pave the way for further exploration of how a complete sensory deprivation of one modality during development affects interareal connectivity and the local microcircuitry (Bavelier and Neville, 2002). Intriguingly, such sensory deprivations cause anatomically detectable changes of the GABAergic system in the affected primary cortices (Sanchez-Vives et al., 2006). Four to six weeks C57BL/6J mice were used throughout all experiments adhering to the Italian Health Ministry Guidelines and Permissions. Mice were lightly anaesthetized under urethane (ca 0.9 g/kg i.p.) and anesthesia depth was monitored using CH5424802 supplier FPs and membrane potential spectra, together with physiological signs. Recordings in awake, head-fixed mice were done after implantation of a recording chamber and habituation to the setup. Craniotomies in V1, A1, and S1 were Quisinostat chemical structure guided by ISI through the thinned skull. Injections of muscimol (both normal and fluorescent) in A1 and in V1 were done

with a pressure-injection device (Picospritzer, General Valve, UK). Transections were done rostrocaudally based on ISI of V1 and A1 and were done with a 30 gauge blade: the depth and coronal height of the transection were verified postmortem in Nissl-counterstained sections. Cannulae for acute pharmacology were implanted in the center of V1 5–6 days before

experiments (done within 10–15 min from infusion of 0.7 μl of drugs). Single-, multiunit, and FP recordings were done using 1–3 MΩ borosilicate or tungsten electrodes for acute or chronic recordings in freely moving animals, respectively. In vivo whole-cell recordings were done in current clamp using an EPC 10 double-plus amplifier (HEKA, Germany) using 5–9 MΩ borosilicate pipettes. Series resistance, spike height and resting Vm were stable throughout recordings Chlormezanone (duration: 15–120 min). No holding currents were used unless for excitatory and inhibitory conductances estimates. At the end of the experiments, animals were perfused with fixative and biocytin-filled cells were revealed together with layering for cell recovery. For PSP measurements, sweeps have been averaged after spike removal, whereas for AP counts, 50 ms binning was applied. Unless otherwise stated, PSP amplitudes have been measured in the 0–300 ms poststimulus time window, whereas onset latencies were taken when the Vm was larger than 2 standard deviations above baseline. For conductance measurements and extracellular data analysis, see Supplemental Experimental Procedures.

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