RESUMO
Land use change in pastures is considered one of the leading drivers of tropical deforestation in the Ecuadorian Amazon Region (EAR). To halt and reverse this process, it is necessary to understand, among other factors, the local livelihoods, income from grazing area and the appropriate options to foster sustainable production, incorporating the land-sparing and land-sharing approach. This work was conducted using 167 household surveys along an altitudinal gradient within the buffer and transition zone of the Sumaco Biosphere Reserve (SBR) in the EAR. The results of a comparative analysis of the main capital variables (human, social, natural, financial, and physical), and the opportunity cost of grazing area assessment provides the following key findings: (a) the concepts of land sparing and land sharing should be considered as complementary local strategies, including household livelihoods and the opportunity cost of the grazing area; (b) we should encourage markets with differentiated restoration rights, based on households engaged in low grazing areas' opportunity costs, and making less impact on capitals' livelihood a key element of economic and conservation initiatives; and (c) sectoral policy implications, including moderate intensification and technological improvements to strengthen the pastureland-sparing and -sharing approach, are discussed.
RESUMO
Ryanodine receptors (RyR) amplify activity-dependent calcium influx via calcium-induced calcium release. Calcium signals trigger postsynaptic pathways in hippocampal neurons that underlie synaptic plasticity, learning, and memory. Recent evidence supports a role of the RyR2 and RyR3 isoforms in these processes. Along with calcium signals, brain-derived neurotrophic factor (BDNF) is a key signaling molecule for hippocampal synaptic plasticity and spatial memory. Upon binding to specific TrkB receptors, BDNF initiates complex signaling pathways that modify synaptic structure and function. Here, we show that BDNF-induced remodeling of hippocampal dendritic spines required functional RyR. Additionally, incubation with BDNF enhanced the expression of RyR2, RyR3, and PKMζ, an atypical protein kinase C isoform with key roles in hippocampal memory consolidation. Consistent with their increased RyR protein content, BDNF-treated neurons generated larger RyR-mediated calcium signals than controls. Selective inhibition of RyR-mediated calcium release with inhibitory ryanodine concentrations prevented the PKMζ, RyR2, and RyR3 protein content enhancement induced by BDNF. Intrahippocampal injection of BDNF or training rats in a spatial memory task enhanced PKMζ, RyR2, RyR3, and BDNF hippocampal protein content, while injection of ryanodine at concentrations that stimulate RyR-mediated calcium release improved spatial memory learning and enhanced memory consolidation. We propose that RyR-generated calcium signals are key features of the complex neuronal plasticity processes induced by BDNF, which include increased expression of RyR2, RyR3, and PKMζ and the spine remodeling required for spatial memory formation.
Assuntos
Fator Neurotrófico Derivado do Encéfalo/metabolismo , Hipocampo/citologia , Memória/fisiologia , Plasticidade Neuronal/fisiologia , Canal de Liberação de Cálcio do Receptor de Rianodina/metabolismo , Percepção Espacial/fisiologia , Sinapses/fisiologia , Análise de Variância , Animais , Cálcio/metabolismo , Hipocampo/metabolismo , Imuno-Histoquímica , Masculino , Aprendizagem em Labirinto/fisiologia , Ratos , Ratos Sprague-Dawley , Rianodina/administração & dosagem , Transdução de Sinais/fisiologiaRESUMO
Neuronal electrical activity increases intracellular Ca(2+) concentration and generates reactive oxygen species. Here, we show that high frequency field stimulation of primary hippocampal neurons generated Ca(2+) signals with an early and a late component, and promoted hydrogen peroxide generation via a neuronal NADPH oxidase. Hydrogen peroxide generation required both Ca(2+) entry through N-methyl-D-aspartate receptors and Ca(2+) release mediated by ryanodine receptors (RyR). Field stimulation also enhanced nuclear translocation of the NF-κB p65 protein and NF-κB -dependent transcription, and increased c-fos mRNA and type-2 RyR protein content. Preincubation with inhibitory ryanodine or with the antioxidant N-acetyl L-cysteine abolished the increase in hydrogen peroxide generation and the late Ca(2+) signal component induced by electrical stimulation. Primary cortical cells behaved similarly as primary hippocampal cells. Exogenous hydrogen peroxide also activated NF-κB-dependent transcription in hippocampal neurons; inhibitory ryanodine prevented this effect. Selective inhibition of the NADPH oxidase or N-acetyl L-cysteine also prevented the enhanced translocation of p65 in hippocampal cells, while N-acetyl L-cysteine abolished the increase in RyR2 protein content induced by high frequency stimulation. In conclusion, the present results show that electrical stimulation induced reciprocal activation of ryanodine receptor-mediated Ca(2+) signals and hydrogen peroxide generation, which stimulated jointly NF-κB activity.