TY - JOUR
T1 - Alcohol exposure during adulthood induces neuronal and astroglial alterations in the hippocampal CA-1 area
AU - Tagliaferro, Patricia
AU - Vega, Maite Duhalde
AU - Evrard, Sergio Gustavo
AU - Ramos, Alberto Javier
AU - Brusco, Alicia
PY - 2002
Y1 - 2002
N2 - Ethanol (ETOH) exposure can result in neuronal damage. Astrocytes are morphologic and functionally related to neurons, and astrocyte-neuron interactions provide strategic sites for the actions of many chemical compounds. The aim of the present work was to study the morphologic alterations of glial cells and neurons on the hippocampus after long-term ETOH exposure using GFAP and S-100β protein, neurofilaments of 200 kDa (Nf200), MAP2, and serotonin transporter (5HT-T) immunocytochemical staining. Adult Wistar male rats (200-250 g) were orally exposed to ETOH (6.6% v/v ad libitum) for 6 weeks. Control rats received water ad libitum. Brain sections from control and exposed rats were processed by immunocytochemistry. After ETOH exposure we observed in the CA1 area of the hippocampus: (1) an important astroglial reaction evidenced by the presence of GFAP+ reactive astrocytes; (2) an increase in S-100β immunostaining in astroglial cells; and (3) a decrease in Nf200, 5HT-T, and MAP2 immunoreactivity. The current study provides evidence that long-term ETOH exposure induces alterations in the neuronal cytoskeleton and an astroglial reaction, which is a common response to brain injury and may promote functional recovery of the nervous system, as by the release of glial-derived trophic factors (such as S-100β) that promote cell survival and neurite growth.
AB - Ethanol (ETOH) exposure can result in neuronal damage. Astrocytes are morphologic and functionally related to neurons, and astrocyte-neuron interactions provide strategic sites for the actions of many chemical compounds. The aim of the present work was to study the morphologic alterations of glial cells and neurons on the hippocampus after long-term ETOH exposure using GFAP and S-100β protein, neurofilaments of 200 kDa (Nf200), MAP2, and serotonin transporter (5HT-T) immunocytochemical staining. Adult Wistar male rats (200-250 g) were orally exposed to ETOH (6.6% v/v ad libitum) for 6 weeks. Control rats received water ad libitum. Brain sections from control and exposed rats were processed by immunocytochemistry. After ETOH exposure we observed in the CA1 area of the hippocampus: (1) an important astroglial reaction evidenced by the presence of GFAP+ reactive astrocytes; (2) an increase in S-100β immunostaining in astroglial cells; and (3) a decrease in Nf200, 5HT-T, and MAP2 immunoreactivity. The current study provides evidence that long-term ETOH exposure induces alterations in the neuronal cytoskeleton and an astroglial reaction, which is a common response to brain injury and may promote functional recovery of the nervous system, as by the release of glial-derived trophic factors (such as S-100β) that promote cell survival and neurite growth.
KW - Astrocytes
KW - Ethanol
KW - GFAP
KW - MAP2
KW - Neurofilaments
KW - S100β
KW - Serotonin transporter
UR - http://www.scopus.com/inward/record.url?scp=0036291548&partnerID=8YFLogxK
U2 - 10.1111/j.1749-6632.2002.tb04175.x
DO - 10.1111/j.1749-6632.2002.tb04175.x
M3 - Article
C2 - 12105109
AN - SCOPUS:0036291548
SN - 0077-8923
VL - 965
SP - 334
EP - 342
JO - Annals of the New York Academy of Sciences
JF - Annals of the New York Academy of Sciences
ER -