Cell-to-Cell Communication in Learning and Memory: From Neuro- and Glio-Transmission to Information Exchange Mediated by Extracellular Vesicles

Most aspects of nervous system development and function rely on the continuous crosstalk between neurons and the variegated universe of non-neuronal cells surrounding them. The most extraordinary property of this cellular community is its ability to undergo adaptive modifications in response to environmental cues originating from inside or outside the body. Such ability, known as neuronal plasticity, allows long-lasting modifications of the strength, composition and efficacy of the connections between neurons, which constitutes the biochemical base for learning and memory. Nerve cells communicate with each other through both wiring (synaptic) and volume transmission of signals. It is by now clear that glial cells, and in particular astrocytes, also play critical roles in both modes by releasing different kinds of molecules (e.g., D-serine secreted by astrocytes). On the other hand, neurons produce factors that can regulate the activity of glial cells, including their ability to release regulatory molecules. In the last fifteen years it has been demonstrated that both neurons and glial cells release extracellular vesicles (EVs) of different kinds, both in physiologic and pathological conditions. Here we discuss the possible involvement of EVs in the events underlying learning and memory, in both physiologic and pathological condition

Symposium on Frontiers of Molecular Neurobiology

Membrane structure, synaptic transmission, and fibrous proteins of neurons - conferenc

NEURONIC SYSTEM INSIDE NEURONS: MOLECULAR BIOLOGY AND BIOPHYSICS OF NEURONAL MICROTUBULES

Neurons are highly specialized cells that input, process, store and output information. Interneuronal communication is achieved in four basic ways: (i) Ca2+ evoked exocytosis with chemical neurotransmission, (ii) gap junction electrotonic coupling, (iii) secretion of neurosteroids, nitric oxide and derivatives of the arachidonic acid acting in paracrine manner, and (iv) cellular adhesive protein interactions with scaffold protein reorganization. Central structure integrating these anisomorphic signals is the neuronal cytoskeleton that is considered to be both sensitive to the local electromagnetic field and prone to intense biochemical modification. With the use of biophysical modeling we have shown that the local electromagnetic field interaction with neuronal microtubules could result in formation of dissipationless waves (solitons) of tubulin tail conformational states that propagate along the microtubule outer surface. Soliton collisions may subserve the function of elementary computational gates and the output of the computation performed by the microtubules may be achieved by the energase action of the tubulin tails that control microtubule-associated protein and motor protein attachment/detachment on the microtubule outer surface