Differentiation of radial glia from radial precursor cells and transformation into astrocytes in the developing rat spinal cord

Glia ◽  
2005 ◽  
Vol 50 (3) ◽  
pp. 187-197 ◽  
Author(s):  
Denis Barry ◽  
Kieran McDermott
Author(s):  
V. Kriho ◽  
H.-Y. Yang ◽  
C.-M. Lue ◽  
N. Lieska ◽  
G. D. Pappas

Radial glia have been classically defined as those early glial cells that radially span their thin processes from the ventricular to the pial surfaces in the developing central nervous system. These radial glia constitute a transient cell population, disappearing, for the most part, by the end of the period of neuronal migration. Traditionally, it has been difficult to definitively identify these cells because the principal criteria available were morphologic only.Using immunofluorescence microscopy, we have previously defined a phenotype for radial glia in rat spinal cord based upon the sequential expression of vimentin, glial fibrillary acidic protein and an intermediate filament-associated protein, IFAP-70/280kD. We report here the application of another intermediate filament-associated protein, IFAP-300kD, originally identified in BHK-21 cells, to the immunofluorescence study of radial glia in the developing rat spinal cord.Results showed that IFAP-300kD appeared very early in rat spinal cord development. In fact by embryonic day 13, IFAP-300kD immunoreactivity was already at its peak and was observed in most of the radial glia which span the spinal cord from the ventricular to the subpial surfaces (Fig. 1). Interestingly, from this time, IFAP-300kD immunoreactivity diminished rapidly in a dorsal to ventral manner, so that by embryonic day 16 it was detectable only in the maturing macroglial cells in the marginal zone of the spinal cord and the dorsal median septum (Fig. 2). By birth, the spinal cord was essentially immuno-negative for this IFAP. Thus, IFAP-300kD appears to be another differentiation marker available for future studies of gliogenesis, especially for the early stages of radial glia differentiation.


2002 ◽  
Vol 454 (3) ◽  
pp. 263-271 ◽  
Author(s):  
Siobhan S. McMahon ◽  
Kieran W. McDermott

2006 ◽  
Vol 55 (3) ◽  
pp. 209-222 ◽  
Author(s):  
Iris Kulbatski ◽  
Andrea J. Mothe ◽  
Armand Keating ◽  
Yoji Hakamata ◽  
Eiji Kobayashi ◽  
...  

Neuroreport ◽  
1992 ◽  
Vol 3 (5) ◽  
pp. 401-404 ◽  
Author(s):  
Elisa Marti ◽  
Stefano Biffo ◽  
Aldo Fasolol

2001 ◽  
Vol 86 (3) ◽  
pp. 1202-1210 ◽  
Author(s):  
Murat Oz ◽  
Miloslav Kolaj ◽  
Leo P. Renaud

Prominent arginine-vasopressin (AVP) binding and AVP V1 type receptors are expressed early in the developing rat spinal cord. We sought to characterize their influence on neural excitability by using patch-clamp techniques to record AVP-induced responses from a population of motoneurons and interneurons in neonatal (5–18 days) rat spinal cord slices. Data were obtained from 58 thoracolumbar (T7–L5) motoneurons and 166 local interneurons. A majority (>90%) of neurons responded to bath applied AVP (10 nM to 3 μM) and (Phe2, Orn8)-vasotocin, a V1receptor agonist, but not V2 or oxytocin receptor agonists. In voltage-clamp, postsynaptic responses in motoneurons were characterized by slowly rising, prolonged (7–10 min) and tetrodotoxin-resistant inward currents associated with a 25% reduction in a membrane potassium conductance that reversed near −100 mV. In interneurons, net AVP-induced inward currents displayed three patterns: decreasing membrane conductance with reversal near −100 mV, i.e., similar to that in motoneurons (24 cells); increasing conductance with reversal near −40 mV (21 cells); small reduction in conductance with no reversal within the current range tested (41 cells). A presynaptic component recorded in most neurons was evident as an increase in the frequency but not amplitude (in motoneurons) of inhibitory and excitatory postsynaptic currents (IPSCs and EPSCs), in large part due to AVP-induced firing in inhibitory (mainly glycinergic) and excitatory (glutamatergic) neurons synapsing on the recorded cells. An increase in frequency but not amplitude of miniature IPSCs and EPSCs also indicated an AVP enhancement of neurotransmitter release from axon terminals of inhibitory and excitatory interneurons. These observations provide support for a broad presynaptic and postsynaptic distribution of AVP V1 type receptors and indicate that their activation can enhance the excitability of a majority of neurons in neonatal ventral spinal cord.


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