Excitatory postsynaptic potentials (EPSP) were recorded from the superior cervical ganglion neurons (SCG) in the rats with experimental streptozotocininduced diabetes (ESD). EPSP was inducted by electrical stimulation of the cervical sympathetic trunk. It was founded that the average value of the EPSP time constant decay in the rats with ESD was 15% higher. At the same time, the amplitudes of EPSP of SCG neurons and the hexamethonium blocking effect in the rats with ESD on 30th day after streptozotocin injection didn’t differ significantly from those in control rats. This may indicate specific functional disorders associated as with steady-state elevated blood glucose level in rats as SCG neurons nicotinic cholinergic receptors.

Long-term potentiation is involved in the mechanisms of synaptic plasticity, provides such processes as memory and learning, and allows the nervous system of a living organism to adapt to changing environmental conditions. It is an increase in the efficiency of glutamatergic synapses, which lasts much longer than other types of potentiation in the nervous system. Despite the fact that long-term potentiation has been studied in detail, the physiological mechanisms of its formation, which lead to an increase of synaptic weight, remain incompletely understood. Well known that long-term potentiation is closely dependent on the processes of rapid axonal transport. However, how axonal transport is related to the mechanisms of long-term potentiation induction and expression, what substances are transported through axons, and how they affect the synaptic activity of postsynaptic neurons is currently unknown. We review here the main physiological mechanisms that occur in the neurons of the hippocampus and contribute to the formation of long-term potentiation. The works of recent years devoted to the study of the participation of synaptic tagging, retrograde signaling, morphological modifications and axonal transport in formation of the long-term potentiation are analyzed.