Adrenoceptor activators and blockers are widely used clinically for the treatment of cardiovascular and pulmonary disorders. More recently, adrenergic agents have also been used to treat neurodegenerative diseases. Recent studies indicate a location of sympathetic varicosities in close proximity to neuromuscular junctions. The pressing question is whether there could be any effects of endo- or exogenous catecholamines on cholinergic neuromuscular transmission. It was shown that the pharmacological stimulation of adrenoceptors, as well as sympathectomy, can affect both acetylcholine release from motor nerve terminals and the functioning of postsynaptic acetylcholine receptors. In this review, we discuss the recent data regarding the effects of adrenergic drugs on neurotransmission at the neuromuscular junction. The elucidation of the molecular mechanisms by which the clinically relevant adrenomimetics and adrenoblockers regulate quantal acetylcholine release from the presynaptic nerve terminals and postsynaptic sensitivity may help in the design of highly effective and well-tolerated sympathomimetics for treating a number of neurodegenerative diseases accompanied by synaptic defects.

Autophagy is a highly conserved process that degrades damaged macromolecules and organelles. Unlike animals, only scant information is available regarding nitric oxide (NO)-induced autophagy in plants. Such lack of information prompted us to study the roles of the NO donors’ nitrate, nitrite, and sodium nitroprusside in this catabolic process in wheat roots. Furthermore, spermine, a polyamine that is found in all eukaryotic cells, was also tested as a physiological NO donor. Here, we show that in wheat roots, NO donors and spermine can trigger autophagy, with NO and reactive oxygen species (ROS) playing signaling roles based on the visualization of autophagosomes, analyses of the levels of NO, ROS, mitochondrial activity, and the expression of autophagic (ATG) genes. Treatment with nitrite and nitroprusside causes an energy deficit, a typical prerequisite of autophagy, which is indicated by a fall in mitochondrial potential, and the activity of mitochondrial complexes. On the contrary, spermine sustains energy metabolism by upregulating the activity of appropriate genes, including those that encode glyceraldehyde 3-phosphate dehydrogenase GAPDH and SNF1-related protein kinase 1 SnRK1. Taken together, our data suggest that one of the key roles for NO in plants may be to trigger autophagy via diverse mechanisms, thus facilitating the removal of oxidized and damaged cellular constituencies.

Mitochondria play a key role in providing energy to cells. These organelles are constantly undergoing dynamic processes of fusion and fission that change in stressful conditions. The role of mitochondrial fusion in wheat root cells was studied using Mdivi-1, an inhibitor of the mitochondrial fragmentation protein Drp1. The effect of the inhibitor was studied on mitochondrial dynamics in the roots of wheat seedlings subjected to a wounding stress, simulated by excision. Treatment of the stressed roots with the inhibitor increased the size of the mitochondria, enhanced their functional activity, and elevated their membrane potentials. Mitochondrial fusion was accompanied by a decrease in ROS formation and associated cell damage. Exposure to Mdivi-1 also upregulated genes encoding the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and an energy sensor AMP-dependent protein sucrose non-fermenting-related kinase (SnRK1), suggesting that mitochondrial fusion is associated with a general activation of energy metabolism. Controlling mitochondrial fusion rates could change the physiology of wheat plants by altering the energy status of the cell and helping to mitigate the effects of stress.