Introduction of unsaturation into theN-n-alkyl chain of the nicotinic receptor antagonists, NONI and NDNI: Effect on affinity and selectivity

N-n-Octylnicotinium iodide (NONI) andN-n-decylnicotinium iodide (NDNI) are selective nicotinic receptor (nAChR) antagonists mediating nicotine-evoked striatal dopamine (DA) release, and inhibiting [3H]nicotine binding, respectively. This study evaluated effects of introducing unsaturation into theN-n-alkyl chains of NONI and NDNI on inhibition of [3H]nicotine and [3H]methyllycaconitine binding (α4β2* and α7* nAChRs, respectively),86Rb+ efflux and [3H]DA release (agonist or antagonist effects at α4β2* and α6β2*-containing nAChRs, respectively). In the NONI series, introduction of a C3-cis-(NONB3c), C3-trans-(NONB3t), C7-double-bond (NONB7e), or C3-triple-bond (NONB3y) afforded a 4-fold to 250-fold increased affinity for [3H]nicotine binding sites compared with NONI. NONB7e and NONB3y inhibited nicotine-evoked86Rb+ efflux, indicating α4β2* antagonism. NONI analogs exhibited a 3-fold to 8-fold greater potency inhibiting nicotine-evoked [3H]DA overflow compared with NONI (IC50=0.62 μM; Imax=89%), with no change in Imax, except for NONB3y (Imax=50%). In the NDNI series, introduction of a C4-cis-(NDNB4c), C4-trans-double-bond (NDNB4t), or C3-triple-bond (NDNB3y) afforded a 4-fold to 80-fold decreased affinity for [3H]nicotine binding sites compared with NDNI, whereas introduction of a C9-double-bond (NDNB9e) did not alter affinity. NDNB3y and NDNB4t inhibited nicotine-evoked86Rb+ efflux, indicating anatogonism at α4β2* nAChRs. Although NDNI had no effect, NDNB4t and NDNB9e potently inhibited nicotine-evoked [3H]DA overflow (IC50=0.02–0.14μM, Imax=90%), as did NDNB4c (IC50=0.08 μM; Imax=50%), whereas NDNB3y showed no inhibition. None of the analogs had significant affinity for α7* nAChRs. Thus, unsaturated NONI analogs had enhanced affinity at α4β2*-and α6β2*-containing nAChRs, however a general reduction of affinity at α4β2* and an uncovering of antagonist effects at α6β2*-containing nAChRs were observed with unsaturated NDNI analogs

The Legume–Rhizobia Symbiosis

The symbiotic nitrogen fixation (SNF) with legumes is the primary source of biologically fixed nitrogen for agricultural system. It is performed by a group of bacteria commonly called rhizobia. It is characterized by a host preference, and the differences among symbioses between rhizobial strains and legume genotypes are related to infection, nodule development and effectiveness in N2 fixation. The interaction between a rhizobia and the legume is mediated by a lipochitin oligosaccharide secreted by the rhizobia, and called “Nod factor”. It is recognized by transmembrane receptors on the root-hair cells of the legume. It can regulate the nodule organogenesis by inducing changes in the cytokinin balance of the root, during nodule initiation. N2 fixation in legume nodules is catalyzed by the nitrogenase enzyme depending upon the photosynthate supply, the O2 concentration, and the fixed-N export. Among environmental factors that influence the SNF, the temperature is essential for nodule formation; the salinity and drought decrease the nodule permeability to O2 and the photosynthate supply to the nodule, the phosphorus deficiency inhibits the nodule development and the total N2 fixation. Rhizobia strains differ in their efficiency in N2 fixation with host legume. There is evidence of genotypic variability for SNF at different levels of available P which show a possibility of selecting cultivars able to support biological N2 fixation under low P soils

Modulation of hippocampus-dependent learning and synaptic plasticity by nicotine

A long-standing relationship between nicotinic acetylcholine receptors (nAChRs) and cognition exists. Drugs that act at nAChRs can have cognitive-enhancing effects and diseases that disrupt cognition such as Alzheimer's disease and schizophrenia are associated with altered nAChR function. Specifically, hippocampus-dependent learning is particularly sensitive to the effects of nicotine. However, the effects of nicotine on hippocampus-dependent learning vary not only with the doses of nicotine used and whether nicotine is administered acutely, chronically, or withdrawn after chronic nicotine treatment but also vary across different hippocampus-dependent tasks such as the Morris water maze, the radial arm maze, and contextual fear conditioning. In addition, nicotine has variable effects across different types of hippocampal long-term potentiation (LTP). Because different types of hippocampus-dependent learning and LTP involve different neural and molecular substrates, comparing the effects of nicotine across these paradigms can yield insights into the mechanisms that may underlie the effects of nicotine on learning and memory and aid in understanding the variable effects of nicotine on cognitive processes. This review compares and contrasts the effects of nicotine on hippocampus-dependent learning and LTP and briefly discusses how the effects of nicotine on learning could contribute to nicotine addictio