Psychiatric Disorders in Women
Michelle Tollefson, Nancy Eriksen, Neha Pathak in Improving Women's Health Across the Lifespan, 2021
Exercise may aid in preventing and treating psychiatric disorders through physiological mechanisms such as increased neurogenesis, angiogenesis, and synaptogenesis. Studies have shown that exercise is associated with increased neurogenesis, particularly in the hippocampus.47 Angiogenesis, or the growth in blood vessels in the brain, has also been found to be associated with exercise, which may be modulated through the increased production of vascular endothelial growth factor (VEGF).48 Angiogenesis in the brain may improve cognition by allowing for increased blood flow and cortical blood supply. Exercise is also associated with synaptogenesis, or the formation of new synapses between neurons. While the effects of exercise-induced synaptogenesis are not very well studied in humans, in mice, aerobic exercise in particular has been shown to increase the number of synaptic connections in the brain, and the associated enhancement in neural pathways has been shown to improve cognitive performance.49
EEG Maturation with Special Reference to Epileptogenic Effects of Hypoxia
Richard A. Jonas, Jane W. Newburger, Joseph J. Volpe, John W. Kirklin in Brain Injury and Pediatric Cardiac Surgery, 2019
The pattern of EEG activity changes most dramatically in the neonatal period and first year of life, a period of development characterized by multiple maturational events in the brain. In the human, neuronal proliferation and migration occur throughout gestation. At about 6 months conceptual age, there are rapid increases in axonal arborization, dendritic elaboration, and synaptogenesis. The peak of synaptogenesis actually occurs in the early postnatal period.1 Myelination occurs somewhat later, starting perinatally and continuing until the end of childhood.2,3 The prolonged development of myelinated fibers is likely to affect EEG activity. In fact, the frequency and amplitude of background activity progressively increases until mid to late childhood, at which point it stabilizes at the 9 Hz alpha activity that is seen in adults.4
Fetal Alcohol Syndrome
Merlin G. Butler, F. John Meaney in Genetics of Developmental Disabilities, 2019
Because of the cognitive and neurobehavioral abnormalities observed in patients with FAS, much research has been conducted as to the effects of alcohol on the developing brain in both animals and humans. In 2000, Ikonomidou et al. (15) demonstrated that alcohol can act as a trigger for neuronal apoptosis in rat brains through blockade of the N-methyl-D-aspartate (NMDA) glutamate receptors and activation of the GABAA receptors. In rats, the affected neurons appeared to be most sensitive to these effects during synaptogenesis, which is a period of time when the brain undergoes significant growth. In humans, synaptogenesis occurs primarily between the sixth month of gestation to several years after birth. Ikonomidou et al. (15) concluded that even transient alcohol exposure during critical times in brain development can lead to the death of millions of neurons through these two mechanisms. They suggested that this can explain the findings of reduced brain mass and neurobehavioral abnormalities described in patients with FAS (15). Their observations also provide evidence that there is no safe period of time during pregnancy for alcohol consumption.
Learnings in developmental and epileptic encephalopathies: what do we know?
Published in Expert Review of Neurotherapeutics, 2023
Martina Giorgia Perinelli, Antonella Riva, Elisabetta Amadori, Roberta Follo, Pasquale Striano
Through neurogenesis, neuronal cell migration, synapse formation, and structural and functional neuronal network specialization, learning and memory allow a child to acquire motor and non-motor developmental milestones and adapt to a constantly altering environment [1]. It is noteworthy that neurogenesis is more prominent in the early stages of normal foetal development. This process is followed by robust synaptogenesis between 27 weeks and two years after birth due to a cortex-specific maturation pattern during the first two years of life. During the first year of life, the subcortical and somatosensory areas develop, while connectivity to other brain regions increases after 12 months [2,3]. The development of the brain is somewhat parallel to the process of myelination, which sweeps up the brainstem and from posterior to anterior throughout the cerebral hemispheres. Learning occurs in the hippocampus and adjacent areas, which nearly doubles around three years of age, reaching adult size. The hippocampus undergoes substantial structural and functional changes from ages 3 to 7. From age 7 to 9 years, the language centres are fully myelinated, and language skills develop at the same rate [4]. In response to the evolution of connections and the emergence of specialization sites, functions lateralize [5]. By adolescence, the circuitry becomes far less complex due to the pruning away of what is not used or needed.
A perspective on C. elegans neurodevelopment: from early visionaries to a booming neuroscience research
Published in Journal of Neurogenetics, 2020
Upon navigation, neurites terminate their growth and form synapses to establish proper connectivity. Some Unc mutants from Brenner’s screens were shown to affect transcription factors that drive synaptic differentiation, sometimes in coordination with neurotransmitter signaling (Jin, 2005; Kratsios et al., 2015; Miller et al., 1992). Kinases, GTPases, and calcium mechanisms were also recognized early to regulate synaptogenesis (Crump, Zhen, Jin, & Bargmann, 2001; Rongo & Kaplan, 1999). Later studies dissected a rich array of synaptogenesis mechanisms including key signaling mechanisms. These include roles for gap junctions, insulins, and heparan sulfates (Grill et al., 2007; Hung et al., 2013; Lázaro-Peña, Díaz-Balzac, Bülow, & Emmons, 2018; Yeh et al., 2009) as well as adhesion and scaffolding complexes, some of which act hierarchically (Dai et al., 2006; Patel et al., 2006; Philbrook et al., 2018; Shen & Bargmann, 2003). On the postsynaptic end, dendrites are shown to differentiate functional spines, apposing presynaptic sites (Cuentas-Condori et al., 2019; Philbrook et al., 2018). Non-neuronal cells also influence synaptic connectivity; glia can affect postembryonic synapse localization (Colón-Ramos, Margeta, & Shen, 2007), and the epidermis acts to maintain peripheral synapses (Cherra, Goncharov, Boassa, Ellisman, & Jin, 2020; this edition). The full array of interactions driving synaptogenesis remains to be identified.
Effects of the application of general anesthesia with propofol during the early stage of pregnancy on brain development and function of SD rat offspring and the intervention of DHA
Published in Neurological Research, 2019
Xiangming Yu, Fei Ma, Xingnian Cao, Xiaodi Ma, Chenhu Hu
The use of propofol in pregnant rats can inhibit the exploratory activity and reduce the spatial learning ability of the offspring rats [23]. In our study, Morris water maze experiment showed that the application of general anesthesia with propofol during the early stage of pregnancy can significantly reduce the learning and memory ability. The hippocampus is mainly responsible for the development of learning and memory abilities [24]. Synaptogenesis is the process of the forming of connections between neurons, which is the key element of the exocytosis of synaptic vesicles [25]. The sequence of synaptogenesis in human fetal brain tissue and that many neurological developmental disorders of fetal life including brain malformations exhibit either delayed or precocious synaptogenesis because the programming of the timing of genetic expression is altered either by genetic mutations or by epigenetic events including exposure to toxic teratogens [26]. Synaptophysin is one of the principal glycoproteins forming synaptic vesicular membranes [26]. It has been shown that the decreased learning ability of the pups is related to the lower expression level of synaptophysin in the hippocampus, and the damage hippocampus structure can cause the abnormal expression of variety proteins [27]. In our study, abnormal expression of various proteins was observed after the application of propofol during the early stage of pregnancy.
Related Knowledge Centers
- Critical Period
- Motor Neuron
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- Neurotrophin
- Synapse
- Synaptic Pruning
- Muscle Cell
- Neuron
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