As sessile organisms, plants cannot escape from adverse conditions and, therefore, they have developed complex responses to the changing environment. Plant responses to abiotic cues involve changes in metabolism, photosynthesis, gene expression, ion levels, etc., and must be perfectly coordinated by phytohormones. The abscisic acid (ABA) is the main phytohormone involved in abiotic stress responses although it is nowadays clear that its signaling pathways are not isolated but interconnected with other hormone signals in complex networks. This article revises molecular mechanisms involved in the crosstalks of ABA with other phytohormones in response to different physiological processes. Moreover, ABA is not a molecule exclusive from plants but it can be found in many other organisms including bacteria, algae, fungi, animals, etc. Interestingly, it can be synthesized and secreted by a variety of human cells. These aspects that confer to the ABA a range of ubiquitous molecule will be also revised in this article.

The beneficial effects of insulin and insulin-like growth factor I on cognition have been documented in humans and animal models. Conversely, obesity, hyperinsulinemia, and diabetes increase the risk for neurodegenerative disorders including Alzheimer's disease (AD). However, the mechanisms by which insulin regulates synaptic plasticity are not well understood. Here, we report that complete disruption of insulin receptor substrate 2 (Irs2) in mice impairs long-term potentiation (LTP) of synaptic transmission in the hippocampus. Basal synaptic transmission and paired-pulse facilitation were similar between the 2 groups of mice. Induction of LTP by high-frequency conditioning tetanus did not activate postsynaptic N-methyl-D-aspartate (NMDA) receptors in hippocampus slices from Irs2^−/− mice, although the expression of NR2A, NR2B, and PSD95 was equivalent to wild-type controls. Activation of Fyn, AKT, and MAPK in response to tetanus stimulation was defective in Irs2^−/− mice. Interestingly, IRS2 was phosphorylated during induction of LTP in control mice, revealing a potential new component of the signaling machinery which modulates synaptic plasticity. Given that IRS2 expression is diminished in Type 2 diabetics as well as in AD patients, these data may reveal an explanation for the prevalence of cognitive decline in humans with metabolic disorders by providing a mechanistic link between insulin resistance and impaired synaptic transmission.