Insulin-like growth factor-binding protein-2 (IGFBP-2) is a pleiotropic polypeptide that functions as autocrine and/or paracrine growth factors. IGFBP-2 is the most abundant of the IGFBPs in the cerebrospinal fluid (CSF), and developing brain showed the highest expression of IGFBP-2. IGFBP-2 expressed in the hippocampus, cortex, olfactory lobes, cerebellum, and amygdala. IGFBP-2 mRNA expression is seen in meninges, blood vessels, and in small cell-body neurons (interneurons) and astrocytes. The expression pattern of IGFBP-2 is often developmentally regulated and cell-specific. Biological activities of IGFBP-2 which are independent of their abilities to bind to insulin-like growth factors (IGFs) are mediated by the heparin binding domain (HBD). To execute IGF-independent functions, some IGFBPs have shown to bind with their putative receptors or to translocate inside the cells. Thus, IGFBP-2 functions can be mediated both via insulin-like growth factor receptor-1 (IGF-IR) and independent of IGF-Rs. In this review, I suggest that IGFBP-2 is not only involved in the growth, development of the brain but also with the regulation of neuronal plasticity to modulate high-level cognitive operations such as spatial learning and memory and information processing. Hence, IGFBP-2 serves as a neurotrophic factor which acts via metaplastic signaling from embryonic to adult stages.

Identifying the mechanisms underlying cognitive development in early life is a critical objective. The expression of insulin‐like growth factor binding protein 2 (IGFBP2) in the hippocampus increases during neonatal development and is associated with learning and memory, but a causal connection has not been established. Here, it is reported that neurons and astrocytes expressing IGFBP2 are distributed throughout the hippocampus. IGFBP2 enhances excitatory inputs onto CA1 pyramidal neurons, facilitating intrinsic excitability and spike transmission, and regulates plasticity at excitatory synapses in a cell‐type specific manner. It facilitates long‐term potentiation (LTP) by enhancing N‐methyl‐d‐aspartate (NMDA) receptor‐dependent excitatory postsynaptic current (EPSC), and enhances neurite proliferation and elongation. Knockout of igfbp2 reduces the numbers of pyramidal cells and interneurons, impairs LTP and cognitive performance, and reduces tonic excitation of pyramidal neurons that are all rescued by IGFBP2. The results provide insight into the requirement for IGFBP2 in cognition in early life.

The number of artificially ripened pineapples outnumbered the naturally ripened pineapples. However, there is a lack of understanding between artificially ripened and naturally ripened pineapples. Thus the inquiry was anticipated to explore the physicochemical changes and organoleptic acceptability of the naturally ripened and artificially ripened pineapples. Farmers used different chemicals such as calcium carbide, and ethylene, besides growth hormones to reduce production loss. Here we evaluated the content of moisture, ash, protein, fat, crude fiber, reducing sugar, total sugar, titratable acidity, sucrose, and vitamin C in both naturally ripened and artificially ripened pineapples. Artificially ripened pineapples showed a significantly lower vitamin C than naturally ripened ones, but arsenic content was nil in both samples. In the case of color and appearance, there was no significant difference between the two samples, but in the case of the other organoleptic properties, such as flavor, sweetness, and sourness, the natural one was more acceptable. Thus naturally ripened pineapples are more beneficial to consumers than artificially ripened ones.

In reward-based learning, synaptic eligibility traces are a well-defined theoretical solution for the conversion of initial co-activation of pre and postsynaptic neurons into long-term changes in synaptic strength by reward-linked neuromodulators. However, the types of neuromodulators involved in such a phenomenon in mouse visual cortex remain unknown. To characterize the Ex vivo condition, we used optogenetic stimulation of channelrhodopsin-(ChR2) expressing Cre/Ai32(ChR2-eYFP); Tph2-Cre/Ai32(ChR2-eYFP); Thi-Cre/Ai32(ChR2-eYFP) homozygous mice, which release acetylcholine, serotonin, and norepinephrine, respectively. With these mice it is possible to measure the transformation of eligibility traces into long-term changes by endogenous neuromodulators. Here we delineated that layer 2/3 neurons in the visual cortex showed no LTD after conditioning with paired-pulse low-frequency stimulation (ppLFS; 2Hz, 15 min). However, if conditioning was paired with acetylcholine, serotonin, or norepinephrine release upon 473 nm optical stimulation in brain slices, LTD occurs in every case. Thus, our data suggests a new pathway to connect the gap between stimulus and reward. Moreover, we found that stimulation by theta-glass or metal stimulators evoked IPSC traces with the same amplitudes but differences in decay kinetics, further questioning the appropriate use of stimulators in brain slices for evoking an event.

In reward-based learning, synaptic eligibility traces are a well-defined theoretical solution for the conversion of initial co-activation of pre and postsynaptic neurons into long-term changes in synaptic strength by reward-linked neuromodulators. However, the types of neuromodulators involved in such a phenomenon in mouse visual cortex remain unknown. To characterize the Ex vivo condition, we used optogenetic stimulation of channelrhodopsin-(ChR2) expressing Cre/Ai32(ChR2-eYFP); Tph2-Cre/Ai32(ChR2-eYFP); Thi-Cre/Ai32(ChR2-eYFP) homozygous mice, which release acetylcholine, serotonin, and norepinephrine, respectively. With these mice it is possible to measure the transformation of eligibility traces into long-term changes by endogenous neuromodulators. Here we delineated that layer 2/3 neurons in the visual cortex showed no LTD after conditioning with paired-pulse low-frequency stimulation (ppLFS; 2Hz, 15 min). However, if conditioning was paired with acetylcholine, serotonin, or norepinephrine release upon 473 nm optical stimulation in brain slices, LTD occurs in every case. Thus, our data suggests a new pathway to connect the gap between stimulus and reward. Moreover, we found that stimulation by theta-glass or metal stimulators evoked IPSC traces with the same amplitudes but differences in decay kinetics, further questioning the appropriate use of stimulators in brain slices for evoking an event.