Despite the disorganization of the ischemic tissue, we observed recipient axons (GFP-negative, a in Fig. 6A-C), possibly pyramidal neurons in the CA1 layer of the hippocampus, making synaptic contacts with the GFP-labeled processes (d in Fig. 6A-C).
Indeed i) the molecular layer of the cerebellar cortex, which contains the glutamatergic varicosities making synaptic contacts between granule cells (highly susceptible to ET), and the dendritic tree of Purkinje cells appears almost unlabelled by ET; ii) no co-staining was observed between ET and synaptic markers such as synaptotagmin, synaptophysin and PSD-95 in the granular layer.
However, these altered presynaptic elements were making synaptic contacts with morphologically normal dendrites or dendritic spines with postsynaptic density (see Fig. 6a d).
Dendrites and thorny excrescences protruded into MFTs, making synaptic contacts, and mitochondria aligned along the inside border of the plasma membrane of the axon terminal.
Ultrastructural investigation demonstrated that vesiculated efferent nerve endings make synaptic contact with the outer hair cells in the organ of Corti and with type II hair cells in the vestibular end-organs.
Besides growth factor effects on functional maturation it is likely that precursor cells are driven towards differentiation by the neurons that make synaptic contact with them.
These include thin unmyelinated C-fibers and myelinated Aδ-fibers, whose central terminals make synaptic contact with second order neurons that are at the origin of pain-related pathways [25].
The integration of glomeruli expressing different receptors occurs within each subdomain only and no study has reported, to our knowledge, evidence that any AOB neuron -projection or interneuron- would make synaptic contact with terminals from both subpopulations.
Because A-type horizontal cells make synaptic contact exclusively with cones, these observations indicate that the circadian clock in the mammalian retina substantially increases rod input to A-type horizontal cells at night by enhancing rod-cone coupling.
On the other hand, according to the same model, blockade of presynaptic A2AR localized in the cortico-striatal glutamatergic terminals that make synaptic contact with the direct MSN should decrease motor activity (by inhibiting glutamate release).
