ABSTRACT
The aim was to describe current reports in the scientific literature on sleep in the intensive care environment and sleep deprivation associated with painful experiences in premature infant. A systematic search was conducted for studies on sleep, pain, premature birth and care of the newborn. Web of Knowledge, MEDLINE, LILACS, Cochrane Library, PubMed, EMBASE, Scopus, VHL and SciELO databases were consulted. The association between sleep deprivation and pain generates effects that are observed in the brain and the behavioral and physiological activity of preterm infants. Polysomnography in intensive care units and pain management in neonates allow comparison with the first year of life and term infants. We have found few references and evidence that neonatal care programs can influence sleep development and reduce the negative impact of the environment. This evidence is discussed from the perspective of how hospital intervention can improve the development of premature infants.
O objetivo foi descrever o estado atual na literatura científica sobre privação do sono associado a experiências dolorosas no prematuro e o papel na evolução do sono em ambiente de terapia intensiva. Realizou-se uma busca sistemática para estudos sobre sono, dor, prematuridade e programas de atenção ao neonato. Foram consultados as bases Web-of-Knowledge, MEDLINE, LILACS, Biblioteca Cochrane, PubMed, EMBASE, Scopus, BVS e SciELO. A associação entre privação do sono e dor gera efeitos que são observados na atividade cerebral, fisiológica e comportamental dos prematuros. A polissonografia nas unidades intensivas e o manejo da dor em neonatos permitem comparação no primeiro ano de vida com crianças nascidas a termo. Encontraram-se poucas evidências de que programas de cuidado neonatal podem influenciar o desenvolvimento do sono e diminuir o impacto negativo do ambiente. Estas evidências são discutidas na perspectiva de como a intervenção hospitalar pode melhorar o desenvolvimento do prematuro.
Subject(s)
Animals , Female , Pregnancy , Betamethasone/pharmacology , Brain/drug effects , Brain/embryology , Cytoskeleton/drug effects , Glucocorticoids/pharmacology , Presynaptic Terminals/drug effects , Body Weight , Brain Chemistry/drug effects , Cytoskeleton/chemistry , Microtubule-Associated Proteins/analysis , PapioABSTRACT
BACKGROUND: The hippocampal CA3 area contains large amounts of vesicular zinc in the mossy fiber terminals which is released during synaptic activity, depending on presynaptic calcium. Another characteristic of these synapses is the presynaptic localization of high concentrations of group II metabotropic glutamate receptors, specifically activated by DCG-IV. Previous work has shown that DCG-IV affects only mossy fiber-evoked responses but not the signals from associational-commissural afferents, blocking mossy fiber synaptic transmission. Since zinc is released from mossy fibers even for single stimuli and it is generally assumed to be co-released with glutamate, the aim of the work was to investigate the effect of DCG-IV on mossy fiber zinc signals. RESULTS: Studies were performed using the membrane-permeant fluorescent zinc probe TSQ, and indicate that DCG-IV almost completely abolishes mossy fiber zinc changes as it does with synaptic transmission. CONCLUSIONS: Zinc signaling is regulated by the activation of type II metabotropic receptors, as it has been previously shown for glutamate, further supporting the corelease of glutamate and zinc from mossy fibers.