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OBJECTIVES: Sexual orientation disparities in adolescent depressive symptoms are well established, but reasons for these disparities are less well understood. We modeled sexual orientation disparities in depressive symptoms from late adolescence into young adulthood and evaluated family satisfaction, peer support, cyberbullying victimization, and unmet medical needs as potential mediators. METHODS: Data were from waves 2 to 6 of the NEXT Generation Health Study (n = 2396), a population-based cohort of US adolescents. We used latent growth models to examine sexual orientation disparities in depressive symptoms in participants aged 17 to 21 years, conduct mediation analyses, and examine sex differences. RESULTS: Relative to heterosexual adolescents, sexual minority adolescents (those who are attracted to the same or both sexes or are questioning; 6.3% of the weighted sample) consistently reported higher depressive symptoms from 11th grade to 3 years after high school. Mediation analyses indicated that sexual minority adolescents reported lower family satisfaction, greater cyberbullying victimization, and increased likelihood of unmet medical needs, all of which were associated with higher depressive symptoms. The mediating role of cyberbullying victimization was more pronounced among male than female participants. CONCLUSIONS: Sexual minority adolescents reported higher depressive symptoms than heterosexual adolescents from late adolescence into young adulthood. Collectively, low family satisfaction, cyberbullying victimization, and unmet medical needs accounted for >45% of differences by sexual orientation. Future clinical research is needed to determine if interventions targeting these psychosocial and health care-related factors would reduce sexual orientation disparities in depressive symptoms and the optimal timing of such interventions. [ABSTRACT FROM AUTHOR]

More than 30 years have elapsed since the publication of the first reports of long-term potentiation by Bliss and Lomo (1973) and Bliss and Gardner-Medwin (1973). These two reports ushered in an exciting new era in which measurable persistent changes in synaptic strength were posited as substrates for learning and memory. Since that time, the study of long-term mechanisms of synaptic plasticity have arguably been one of the most intensely and perhaps the most rewarding fields of the neurosciences, casting important light on the nature of synaptic transmission and the events associated with the strengthening or weakening of synapses. Indeed, although once principally studied at excitatory glutamatergic synapses within the hippocampus and cortical formations, mechanisms of synaptic plasticity are observed at a myriad of synaptic connections throughout the mammalian central nervous system. Moreover, although many of these synapses share common mechanisms of plasticity, the last decade has seen an explosion in our understanding of plasticities peculiar to one synapse or another. This chapter does not attempt to cover all of these divergent mechanisms but instead focuses on those mechanisms of long-term potentiation (LTP) and depression (LTD) most commonly found within the hippocampal formation. A large portion of this review covers N-methyl-\fontsize77\selectfont D-aspartate-receptor-dependent LTP and LTD, the two most commonly studied forms of cortical plasticity; however, it also addresses plasticity mechanisms at other hippocampal synapses that have not enjoyed the same intensity of investigation but are worthy of attention. [ABSTRACT FROM AUTHOR]

The quest to understand the process of forming and storing memories has engaged scientists for hundreds of years. Recent advances in biology have led to the identification of some of the cellular and molecular mechanisms associated with these processes. Animal studies using both invertebrates and vertebrates have revealed that the mechanisms of learning and memory at the molecular level have been conserved throughout evolution, and that more complex forms of learning have been built on these evolutionarily conserved mechanisms. In this chapter, we discuss how behavioral training alters neuronal activity and neurotransmitter release leading to changes in intracellular kinase activity, protein phosphorylation, protein synthesis, and gene expression. We describe how the various phases of memory: working memory (lasting for seconds), short-term memory (lasting minutes), intermediate-term memory (lasting for hours), and long-term memory (lasting days to a lifetime) are established by the above intracellular changes. We present theories on how permanent memory storage occurs, how memories are recalled, and how they are extinguished. [ABSTRACT FROM AUTHOR]