Excuses like 'All strokes are different, all stroke recoveries are different' ARE NOT ALLOWED.
http://journal.frontiersin.org/article/10.3389/fncel.2015.00140/full?
Carina Fernandes1,2, Nuno Barbosa F. Rocha3, Susana Rocha4, Andrea Herrera-Solís5, José Salas-Pacheco6, Fabio García-García7, Eric Murillo-Rodríguez8, Ti-Fei Yuan9, Sergio Machado10,11 and Oscar Arias-Carrión5*
- 1Faculty of Medicine, University of Porto, Porto, Portugal
- 2Laboratory of Neuropsychophysiology, Faculty of Psychology and Education Sciences, University of Porto, Porto, Portugal
- 3School of Health Technologies, Polytechnic Institute of Porto, Porto, Portugal
- 4School of Accounting and Administration of Porto, Polytechnic Institute of Porto, Porto, Portugal
- 5Unidad de Trastornos del Movimiento y Sueño, Hospital General Dr. Manuel Gea González/Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico
- 6Instituto de Investigación Científica, Universidad Juárez del Estado de Durango, Durango, Mexico
- 7Departamento de Biomedicina, Instituto de Ciencias de la Salud, Universidad Veracruzana, Xalapa, Mexico
- 8División Ciencias de la Salud, Laboratorio de Neurociencias Moleculares e Integrativas, Escuela de Medicina, Universidad Anáhuac Mayab, Mérida, México
- 9School of Psychology, Nanjing Normal University, Nanjing, China
- 10Panic and Respiration, Institute of Psychiatry of Federal University of Rio de Janeiro, Rio de Janeiro, Brazil
- 11Physical Activity Neuroscience, Physical Activity Sciences Postgraduate Program, Salgado de Oliveira University, Niterói, Brazil
Introduction
Thousands of new neurons are daily added to the adult brain of different species, including humans (Yuan et al., 2014), and this constant lifelong generation implies significant structural changes (Eriksson et al., 1998; Curtis et al., 2007).
Neurogenesis is involved in numerous brain processes but its
association with sleep deprivation was only recently addressed. Previous
research has focused on how generation and development of new neurons
are affected by sleep loss. Short periods of sleep deprivation do not
significantly alter the basal rate of cell proliferation, whereas long
periods result in a decrease of cell proliferation and survival in the
hippocampus (Mirescu et al., 2006).
In this review, we will discuss the possible effects of sleep
deprivation on the natural course of neurogenesis, and address the
potential connections between sleep and neurogenesis that may influence
other cognitive and neuropsychobiological functions, such as learning,
memory, and mood disorders.
Adult Neurogenesis
Neurogenesis includes the generation, proliferation,
fate specification and integration of new functional neurons in the
existing neural circuits from undifferentiated progenitor cells.
Traditionally, it was believed that neurogenesis mainly occurred during
the embryonic stages of the central nervous system (CNS), ending
permanently at puberty (Ming and Song, 2005; Meerlo et al., 2009).
New findings, based on techniques such as [3H]-thymidine autoradiography (Sidman et al., 1959) and 5-bromo-2′-deoxyuridine (BrdU; Nowakowski et al., 1989), which mark cells in S phase of mitosis, electronic microscopy (Kaplan, 1977, 1981, 1984, 1985) and combining retroviral-based lineage tracing with electrophysiological methods (Sanes et al., 1986; Price et al., 1987)
revealed the continuous adult neurogenesis and synaptic integration.
Newborn neurons were found in certain CNS regions of birds (Goldman and Nottebohm, 1983), rats (van Praag et al., 1999), monkeys (Kornack and Rakic, 1999), and humans (Eriksson et al., 1998; Curtis et al., 2007), throughout life.
Neurogenesis occurs in specific areas of the CNS, namely
in the subventricular zone (SVZ), lining the wall of the lateral
ventricles, and in the subgranular zone (SGZ) of the hippocampal dentate
gyrus (Alvarez-Buylla and Lim, 2004). The neurogenic behavior of these areas appears to be determined by signals of endothelial cells and astrocytes (Alvarez-Buylla and Lim, 2004).
Similarly, a cohort of glucogenic and neurogenic signals (Lim et al., 2000) regulates the underlying molecular mechanisms of neuronal differentiation, fate specification (Ming and Song, 2005; Arias-Carrión et al., 2007; Yuan and Arias-Carrion, 2011; Höglinger et al., 2014) and migration of new generated cells (Hu et al., 1996; Conover et al., 2000; Murase and Horwitz, 2002; Bolteus and Bordey, 2004). Newly formed neurons in the SVZ reach the olfactory bulb, by the rostral migratory stream (Saghatelyan et al., 2004), forming granule and periglomerular neurons. These neurons establish dendro-dendritic synapses with tufted cells (Abrous et al., 2005), beginning a maturation process by receiving GABAergic and glutamatergic synaptic inputs (Belluzzi et al., 2003). When maturate, the granule neurons secrete GABA, while periglomerular neurons secrete GABA and dopamine (Wang et al., 2000; Arias-Carrión et al., 2007). In the dentate gyrus, newborn neurons reach the anterior layer of the granule cells (Hastings and Gould, 1999), maintaining their neuronal maturation and synaptogenesis over several months (van Praag et al., 2002). It is believed that these neurons receive initially GABAergic and later glutamatergic inputs (Ming and Song, 2005). Once mature, most of these neurons secrete glutamate, while a small population releases GABA (Wang et al., 2000).
Adult neurogenesis is modulated by intrinsic and extrinsic factors (Table 1), being possible that several modulating factors remain unknown (Kempermann, 2002).
More at link.
No comments:
Post a Comment