PMID- 9336767
OWN - NLM
STAT- MEDLINE
DCOM- 19971126
LR  - 20191102
IS  - 1044-7393 (Print)
IS  - 1044-7393 (Linking)
VI  - 31
IP  - 3
DP  - 1997 Aug
TI  - Lesioning of the inferior olive using a ventral surgical approach. 
      Characterization of temporal and spatial astrocytic responses at the lesion site 
      and in cerebellum.
PG  - 245-64
AB  - Activated astrocytes, intrinsic components of both local and remote (axonal 
      target regions) central nervous system injury responses, are now recognized as 
      active metabolic and regulatory mediators in many neurological disorders. To 
      further define these responses, we devised a new ventral surgical approach to 
      unilaterally lesion the inferior olivary nuclear complex, which has a single 
      predominant remote target, the cerebellum. Activated astrocyte number, volume, 
      and density, as well as the total volume of brainstem involved in the astrocytic 
      response, all peaked at postlesion day (pld) 4, returning toward, but not to, 
      unoperated control values at pld 24 (p < 0.05). In contrast, the peak astrocyte 
      response in the cerebellum was delayed, being greatest at pld 6 (p < 0.05 
      compared to control or pld 2). These responses were associated with increases in 
      overexpression of S100 beta, an astrocyte-derived neurite growth factor, and with 
      an increase in cerebellar steady-state levels of a neuronal injury response 
      protein, the beta-amyloid precursor protein (beta-APP). This is similar to 
      correlated increases in these two proteins that are found in epilepsy and 
      Alzheimer disease. Our studies defining remote astrocytic and neuronal responses 
      may be important for understanding glial-neuronal mechanisms underlying the 
      spread of neuropathological changes in conditions such as Alzheimer disease.
FAU - Ito, K
AU  - Ito K
AD  - Department of Medicine, University of Arkansas for Medical Sciences, Little Rock, 
      USA.
FAU - Ishikawa, Y
AU  - Ishikawa Y
FAU - Skinner, R D
AU  - Skinner RD
FAU - Mrak, R E
AU  - Mrak RE
FAU - Morrison-Bogorad, M
AU  - Morrison-Bogorad M
FAU - Mukawa, J
AU  - Mukawa J
FAU - Griffin, W S
AU  - Griffin WS
LA  - eng
GR  - AG12411/AG/NIA NIH HHS/United States
GR  - HD14886/HD/NICHD NIH HHS/United States
GR  - NS27414/NS/NINDS NIH HHS/United States
GR  - etc.
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Mol Chem Neuropathol
JT  - Molecular and chemical neuropathology
JID - 8910358
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - 0 (S100 Proteins)
SB  - IM
MH  - Amyloid beta-Peptides/biosynthesis
MH  - Animals
MH  - Astrocytes/*physiology
MH  - Axons/physiology
MH  - Blotting, Western
MH  - Brain Mapping
MH  - Cerebellum/cytology/*physiology
MH  - Female
MH  - Glial Fibrillary Acidic Protein/biosynthesis
MH  - Male
MH  - Neural Pathways/cytology/physiology
MH  - Neurons, Afferent/physiology
MH  - Neurons, Efferent/physiology
MH  - Olivary Nucleus/*cytology/*physiology
MH  - Purkinje Cells/physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - S100 Proteins/biosynthesis
EDAT- 1997/08/01 00:00
MHDA- 1997/10/23 00:01
CRDT- 1997/08/01 00:00
PHST- 1997/08/01 00:00 [pubmed]
PHST- 1997/10/23 00:01 [medline]
PHST- 1997/08/01 00:00 [entrez]
AID - 10.1007/BF02815128 [doi]
PST - ppublish
SO  - Mol Chem Neuropathol. 1997 Aug;31(3):245-64. doi: 10.1007/BF02815128.