RESUMO
In brief: Social insect queens display both extraordinary longevity and fertility. In this point of view, we describe their distinctive traits that make them useful models for reproductive longevity, holding implications for human health discoveries. Abstract: Social insects present an extraordinary opportunity as models for reproductive longevity because they challenge the conventional patterns of aging and reproduction seen in other model organisms. Their queens are simultaneously long-lived and highly fecund, and understanding how these traits co-occur may lead to discoveries with important implications for human health.
Assuntos
Envelhecimento , Fertilidade , Insetos , Longevidade , Reprodução , Animais , Longevidade/fisiologia , Reprodução/fisiologia , Insetos/fisiologia , Envelhecimento/fisiologia , Fertilidade/fisiologia , Humanos , Feminino , Comportamento SocialRESUMO
Mate choice is a critical decision with direct implications for fitness. Although it has been recognized for over 150 years, our understanding of its underlying mechanisms is still limited. Most studies on mate choice focus on the evolutionary causes of behavior, with less attention given to the physiological and molecular mechanisms involved. This is especially true for invertebrates, where research on mate choice has largely focused on male behavior. This review summarizes the current state of knowledge on the neural, molecular and neurohormonal mechanisms of female choice in invertebrates, including behaviors before, during, and after copulation. We identify areas of research that have not been extensively explored in invertebrates, suggesting potential directions for future investigation. We hope that this review will stimulate further research in this area.
Assuntos
Evolução Biológica , Invertebrados , Animais , Feminino , Masculino , ConhecimentoRESUMO
Systemic inflammation is a crucial factor for microglial activation and neuroinflammation in neurodegeneration. This work is aimed at assessing whether previous exposure to systemic inflammation potentiates neurotoxic damage by the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and how chronic systemic inflammation participates in the physiopathological mechanisms of Parkinson's disease. Two different models of systemic inflammation were employed to explore this hypothesis: a single administration of lipopolysaccharide (sLPS; 5 mg/kg) and chronic exposure to low doses (mLPS; 100 µg/kg twice a week for three months). After three months, both groups were challenged with MPTP. With the sLPS administration, Iba1 staining increased in the striatum and substantia nigra, and the cell viability lowered in the striatum of these mice. mLPS alone had more impact on the proinflammatory profile of the brain, steadily increasing TNFα levels, activating microglia, reducing BDNF, cell viability, and dopamine levels, leading to a damage profile similar to the MPTP model per se. Interestingly, mLPS increased MAO-B activity possibly conferring susceptibility to MPTP damage. mLPS, along with MPTP administration, exacerbated the neurotoxic effect. This effect seemed to be coordinated by microglia since minocycline administration prevented brain TNFα increase. Coadministration of sLPS with MPTP only facilitated damage induced by MPTP without significant change in the inflammatory profile. These results indicate that chronic systemic inflammation increased susceptibility to MPTP toxic effect and is an adequate model for studying the impact of systemic inflammation in Parkinson's disease.
Assuntos
1-Metil-4-Fenil-1,2,3,6-Tetra-Hidropiridina/metabolismo , Encéfalo/metabolismo , Inflamação/imunologia , Microglia/imunologia , Neurônios/fisiologia , Doença de Parkinson/imunologia , Animais , Fator Neurotrófico Derivado do Encéfalo/metabolismo , Proteínas de Ligação ao Cálcio/metabolismo , Morte Celular , Células Cultivadas , Modelos Animais de Doenças , Humanos , Lipopolissacarídeos/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos ICR , Proteínas dos Microfilamentos/metabolismo , RatosRESUMO
It has been long thought that the brain reorganizes itself in response to environmental needs. Sensory experiences coded in action potentials are the mean by which information on the surroundings is introduced into neuronal networks. The information approaching the brain in the form of electrochemical codes must then be translated in biochemical, epigenetic and genetic ones. Only until recently we have begun understanding the underpinning of such informational transformations and how this process is expressed as neuronal plastic responses. Central for our comprehension of this matter is the finding that signals transduction cascades can modify gene expression by remodeling the chromatin through epigenetic mechanisms. Hence, chromatin remodeling seems to be the process by which experiences are imprinted.