After the birth of neuroblasts in the SVZ, they mutually interact and organize themselves into chains. Most common cells found in the RMS are migrating neuroblasts. human RMS are different, RMS in humans also contains migrating neuroblasts toward the olfactory tubercle, and the OB neurogenesis appears to persist in adulthood ( Bédard & Parent, 2004). Although the morphology and structure of rodent vs. In primates and humans, the RMS tube is very narrow and forms a sigmoidally curved path to laterally circumscribe the striatum ( Curtis et al., 2007). As the OB and ventricle begin to form, the developing RMS lies laterally from the olfactory ventricle. Generation of RMS precedes the bulge of the OB and formation of the olfactory ventricle which is an extension of anterior lateral ventricle. Initial formation of RMS occurs during the embryonic development on E15-17 in mouse ( Pencea & Luskin, 2003). The RMS tract terminates in the subependymal layer, the central region of OB granule cell layer ( Lois & Alvarez-Buylla, 1994 Lois et al., 1996). Rodent RMS arises from the SVZ of the lateral ventricle, proceeds to the rostrodorsal aspect of the striatum to the rostroventral aspect of the striatum and then extends rostrally into the olfactory tract ( Fig. RMS is organized as a tubular extension of the lateral ventricle reaching the OB. In this review, we will overview development and anatomy of RMS and regulatory signals for neuronal migration in the RMS. Furthermore, cell-cell adhesions and extracellular matrix proteins also significantly affect the mode, speed and direction of neuroblasts. The migration of neuronal precursors into the OB is regulated by the orchestrated activities of multiple secretory signals, such as repulsive factors in the septum, motogenic factors in the SVZa and the RMS, as well as chemoattractive factors derived from the OB or olfactory epithelium ( Coskun & Luskin, 2002 Whitman & Greer, 2009). In addition to migrating neuroblasts, RMS contains specialized surrounding glial cells, which form tube-like structure (glial tube), serving as a scaffold of migration neuroblasts. This is one of the longest migrations in CNS development, and the speed of chain migration (70~80 µm/hr) is considerably faster than other types of migration ( Nam et al., 2007). It is known that migrating neuroblasts form chain-like homophilic association, and they migrate tangentially without the aid of radial fibers ( Lois et al., 1996). This migration occurs throughout life in many species including rodents, primates, and humans ( Lois & Alvarez-Buylla, 1994 Kornack & Rakic, 2001 Curtis et al., 2007). Within the OB, neuroblasts finally locate in the granule cell layer and glomerular layer and differentiate into the granule and periglomerular cells, respectively. Upon genesis from neural stem cells, neuronal precursors then migrate tangentially to the OB through a distinct pathway called the rostral migratory stream (RMS). These changes in the properties of GABA(A) receptor binding following antipsychotic drug administration are not consistent with those observed in schizophrenia and suggest a 'reshuffling' in GABA(A) receptor subtypes over time.Interneurons in the olfactory bulb (OB) are produced from the lateral ganglionic eminences (LGE) during embryonic development and from the anterior subventricular zone (SVZa) in the lateral ventricles postnatally. In contrast there was a delayed increase in density of benzodiazepine-sensitive GABA(A) receptors in the PFC, suggesting that antipsychotic drugs have different effects on different GABA(A) receptor subtypes. Muscimol binding was enhanced in the prefrontal cortex after 7 days but no differences were observed after longer periods of drug administration. Sections of rat brain were then labelled with muscimol, which labels the total population of GABA(A) receptors, or the benzodiazepine site ligand flunitrazepam in separate saturation binding experiments using quantitative receptor autoradiography. Male SD rats received a sucrose solution containing either haloperidol (1.5 mg/kg), olanzapine (6.5 mg/kg) or no drug daily for either 7, 14 or 28 days. As antipsychotic drugs have delayed maximal therapeutic effects we also examined different drug treatment periods. To test this, we examined the effects of administering a typical (haloperidol) and an atypical (olanzapine) antipsychotic drug on the GABA(A) receptor agonist (orthosteric) and benzodiazepine (allosteric) binding sites in rat prefrontal cortex. However, long-term antipsychotic drug use in schizophrenia may underlie these changes. Changes in GABA(A) receptors are observed in schizophrenia, with benzodiazepine-sensitive GABA(A) receptor subtypes being affected differently to other subtypes.
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