Deficits in synaptic plasticity have been identified in aged animals with cognitive impairment [17].
Structural variants and single base pair mutations in genes involved in synaptic function have been identified in neurodevelopmental disorders; nevertheless, their pathogenic role is often unclear and causative mutations are still not found in a large proportion of patients.
Several synaptic neurotransmitters have been identified in the dorsal column nuclei.
In particular, many genes involved in the synapse and synaptic complexity have been identified in ASD, for example, SHANK3, CNTNAP2, NLGN3, NLGN4, NRXN1, PCDH10, CDH8, CDH9 and CDH10 (Morrow et al, 2008; Pagnamenta et al, 2011a; Pinto et al, 2010; Wang et al, 2009).
Porifera does not possess neurons or recognizable synapses but homologs of neuronal post-synaptic genes have been identified in the sponge genome and have been shown to be expressed in the globular cells of the outer epithelial layer of sponge larvae [ 16, 23].
First, seasonal plasticity in synaptic appositions on GnRH terminals has been identified in sheep, probably reflecting retraction of ensheathing tanycyte end feet (Xiong et al., 1997).
GlyRs mediate rapid synaptic inhibition in spinal cord and brainstem and have been identified in higher brain areas, such as hippocampus, retina, or cochlea [ 1, 2].
Synaptic adhesion-like molecules (SALMs) are a newly discovered family of adhesion molecules: at least five members have been identified in the central nervous system.
One of the coding variants, M225I, was identified in the synaptic vesicle gene DOC2A and was predicted to alter protein function.
In this paradigm, the process of reconstruction is approached in the following way: tiny synaptic contacts are first located in neuropil using EM; pre-synaptic axons and post-synaptic dendrites are identified in EM images for each synaptic contact; axonal and dendritic projections are traced to their respective cell bodies using EM images over macroscopically large distances (e.g., see [16]).
