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Biology subjects

Sarmiento, M.

Publications and source records attributed to Sarmiento, M..

2 recordsLinked to original sources

Priming of C-glycoside flavones in Colobanthus quitensis with salicylic acid, methyl jasmonate, pimelic acid, suberic acid, and azelaic acid elicits antifungal activity against Botrytis cinerea

Colobanthus quitensis, one of only two native angiosperms in Antarctica, produces C-glycosyl flavones with antifungal activity against Botrytis cinerea. In this study, the exogenous application of the elicitors salicylic acid (SA), methyl jasmonate (MeJA), pimelic acid (PA), suberic acid (SuA), and azelaic acid (AzA) was evaluated for their effect on the accumulation of bioactive metabolites in in vitro-cultivated plants. Exposure to these compounds significantly modulated the expression of key genes in the phenylpropanoid and flavonoid pathways, including pal, chs, chi, fnsII, as well as regulatory genes such as myb12, bhlh, and wrky33, enhancing PAL activity and the accumulation of schaftoside, neoschaftoside, saponarin, and swertiajaponin. This priming process improved the antifungal activity of the extracts, with MeJA and PA identified as the most effective treatments. The in vitro culture approach enabled the assessment of a protected and hard-to-access species without the need for wild harvesting. These results suggest that the exogenous application of elicitors constitutes an efficient strategy to modulate the biosynthesis of specialised metabolites, with implications for the development of biocontrol agents and the improvement of efficiency in sustainable agricultural systems. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=88 SRC="FIGDIR/small/646165v1_ufig1.gif" ALT="Figure 1"> View larger version (25K): org.highwire.dtl.DTLVardef@67f8corg.highwire.dtl.DTLVardef@9ff3a1org.highwire.dtl.DTLVardef@13403aaorg.highwire.dtl.DTLVardef@1dc95b2_HPS_FORMAT_FIGEXP M_FIG C_FIG

plant biology↗

High frequency DBS-like optogenetic stimulation of nucleus accumbens dopamine D2 receptor-containing neurons attenuates cocaine reinstatement in male rats

BackgroundPrevious work indicated that deep brain stimulation (DBS) of the nucleus accumbens shell in male rats attenuated reinstatement of cocaine seeking, an animal model of craving. However, the potential differential impact of DBS on specific populations of neurons to drive the suppression of cocaine seeking is unknown. Medium spiny neurons in the nucleus accumbens are differentiated by expression of dopamine D1 receptors (D1DRs) or D2DRs, activation of which promotes or inhibits cocaine-related behaviors, respectively. The advent of transgenic rat lines expressing Cre recombinase selectively in D1DR-containing or D2DR-containing neurons, when coupled with Cre-dependent virally mediated gene transfer of channelrhodopsin (ChR2), enabled mimicry of DBS in a selective subpopulation of neurons during complex tasks. HypothesisWe tested the hypothesis that high frequency DBS-like optogenetic stimulation of D1DR-containing neurons in the accumbens shell would potentiate, whereas stimulation of D2DR-containing neurons in the accumbens shell would attenuate, cocaine-primed reinstatement of cocaine seeking. ResultsResults indicated that high frequency, DBS-like optogenetic stimulation of D2DR-containing neurons attenuated reinstatement of cocaine seeking in male rats, whereas DBS-like optogenetic stimulation of D1DR-containing neurons did not alter cocaine-primed reinstatement. Surprisingly, DBS-like optogenetic stimulation did not alter reinstatement of cocaine seeking in female rats. In rats which only expressed eYFP, intra-accumbens optogenetic stimulation did not alter cocaine reinstatement relative to sham stimulation, indicating that the effect of DBS-like stimulation to attenuate cocaine reinstatement is mediated specifically by ChR2 rather than consequent to prolonged light delivery. ConclusionsThese results suggest that DBS of the accumbens attenuates cocaine-primed reinstatement in male rats through the selective manipulation of D2DR-containing neurons.

neuroscience↗