There are however also different specificities between these mechanisms. The synaptic changes reported here are surprisingly fast and predominantly observed during a critical period of development, unlike the receptor scaling effect and unlike the changes in spine density or properties reported following long-term, chronic blockade or genetic manipulation of NMDA or AMPA receptors. Additionally, unlike receptor scaling, spine growth triggered by interference with the excitation/inhibition balance is achieved by blockade of both AMPA and NMDA receptors, indicating that it is very sensitive to NMDA dependent mechanisms. The fast regulation of LY2584702 Tosylate synapse number reported here could thus maintain the level of excitatory activity required for ensuring plasticitymediated mechanisms. This could be particularly important at times where synapse turnover is high and selection of correct inputs is a central issue. This could also provide some clue regarding the physiopathological mechanisms possibly relating modulation or shifts of the excitatory/inhibitory balance to neuropsychiatric disorders such as proposed in Down or Rett syndromes as well as in autism spectrum disorders. There are two additional important aspects related to this homeostatic mechanism. First, the magnitude and rapidity of the effect produced probably account for some of the discrepancies reported in the literature concerning the development of spines during the first weeks of life. Recent studies using in vivo 2-photon imaging have reported mechanisms of spine pruning between the second, third and Ceftriaxone sodium salt fourth week of life in mice. This is however at variance with previous anatomical data obtained through classical staining and brain fixation methods that reported a continuous increase in spine density in many cortical regions during the same periods. Interestingly, in vivo imaging studies have been carried out in mice that had undergone a long anesthesia for the preparation of 2-photon imaging approach. This manipulation probably boosted spine density in these young mice and, as shown by our data, analyses in animals anesthetized around PND 15 then suggest a subsequent pruning of spines over the next 2 weeks, while analyses of mice that did not undergo anesthesia conversely indicate a progressive increase in spine density.