Long-term effects of postnatal undernutrition and maternal malnutrition on mouse cerebral cortex

1979 ◽  
Vol 37 (2) ◽  
pp. 299-308 ◽  
Author(s):  
G. Leuba ◽  
Th. Rabinowicz
Keyword(s):  
Cerebral Cortex ◽  
Long Term Effects ◽  
Maternal Malnutrition ◽  
Mouse Cerebral Cortex

Short- and long-term effects of low-dose prenatal X-irradiation in mouse cerebral cortex, with special reference to neuronal migration

1997 ◽  
Vol 93 (5) ◽  
pp. 443-449 ◽  
Author(s):  
S. Fushiki ◽  
Yasuko Hyodo-Taguchi ◽  
Chikako Kinoshita ◽  
Yuji Ishikawa ◽  
Tomohisa Hirobe
Keyword(s):  
Cerebral Cortex ◽  
Special Reference ◽  
Neuronal Migration ◽  
Low Dose ◽  
Long Term Effects ◽  
Mouse Cerebral Cortex ◽  
X Irradiation ◽  
Short And Long Term

scholarly journals Acute action of DSP-4 on central norepinephrine axons: biochemical and immunohistochemical evidence for differential effects.

1989 ◽  
Vol 37 (9) ◽  
pp. 1435-1442 ◽  
Author(s):  
R Grzanna ◽  
U Berger ◽  
J M Fritschy ◽  
M Geffard
Keyword(s):  
Cerebral Cortex ◽  
High Performance ◽  
Direct Evidence ◽  
Selective Vulnerability ◽  
Brain Regions ◽  
Acute Effects ◽  
Long Term Effects ◽  
Immunohistochemical Evidence ◽  
Immunohistochemical Studies

Previous immunohistochemical studies of the long-term effects of the noradrenergic neurotoxin DSP-4 have demonstrated a remarkably selective vulnerability of norepinephrine (NE) axons of the locus coeruleus (LC). NE axons originating in non-LC NE neurons appear to be largely resistant to the neurotoxic action of DSP-4. We conducted this study to evaluate the acute effects of DSP-4 on NE axons in four different brain regions: cerebral cortex, cerebellum, ventral forebrain, and hypothalamus. NE levels were determined by high-performance liquid chromatography (HPLC) 6 and 24 hr and 14 days after DSP-4 administration. NE axons in these brain regions were visualized in brain sections at 6 and 24 hr after drug treatment, using a specific antiserum to NE. HPLC assays revealed profound reductions of NE levels in cerebral cortex and cerebellum, but only minor decreases in ventral forebrain and hypothalamus. NE immunohistochemistry showed dramatic differences in the acute effects of DSP-4 on NE axon staining: nearly complete loss of staining in cortex and cerebellum, in contrast to an almost unchanged staining pattern in ventral forebrain and hypothalamus. This study demonstrates that NE immunohistochemistry is a valuable tool to assess the acute effects of DSP-4 on NE axons in different brain regions. The results provide the first direct evidence that NE axons are not uniformly acted on by DSP-4 and suggest that the acute effects of DSP-4 are restricted to LC axons.

Hyperthermia‐induced seizures produce long‐term effects on the functionality of adenosine A 1 receptor in rat cerebral cortex

2020 ◽  
Vol 80 (1) ◽  
pp. 1-12
Author(s):  
María Crespo ◽  
David Agustín León‐Navarro ◽  
María Ángeles Ruíz ◽  
Mairena Martín
Keyword(s):  
Cerebral Cortex ◽  
Rat Cerebral Cortex ◽  
Long Term Effects

scholarly journals Brief Alteration of NMDA or GABAAReceptor-mediated Neurotransmission Has Long Term Effects on the Developing Cerebral Cortex

2008 ◽  
Vol 7 (12) ◽  
pp. 2293-2310 ◽  
Author(s):  
Angela M. Kaindl ◽  
Andrea Koppelstaetter ◽  
Grit Nebrich ◽  
Janine Stuwe ◽  
Marco Sifringer ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Long Term Effects

Cortical cholinergic dysregulation as a long-term consequence of neonatal hypoglycemia

2015 ◽  
Vol 93 (1) ◽  
pp. 47-53 ◽  
Author(s):  
T.R. Anju ◽  
C.S. Paulose
Keyword(s):  
Cerebral Cortex ◽  
Life Stress ◽  
Energy Demand ◽  
High Energy ◽  
Acetylcholine Esterase ◽  
Long Term Effects ◽  
Neonatal Hypoglycemia ◽  
Acetylcholine Metabolism ◽  
Old Rats

Neonatal hypoglycemia limits the glucose supply to cells, affecting the function of brain due to its high energy demand. This can cause long-term consequences in brain function, leading to memory and cognitive deficits. The present study evaluated the cholinergic functional regulation in cerebral cortex of one month old rats exposed to neonatal hypoglycemia to understand the long-term effects of early life stress. Receptor binding and gene expression studies were done in the cerebral cortex to analyze the changes in total muscarinicreceptors, muscarinic M1, M2, M3 receptors, and the enzymes involved in acetylcholine metabolism, cholineacetyl transferase and acetylcholine esterase. Neonatal hypoglycemia decreased total muscarinic receptors (p < 0.001) with reduced muscarinic M1, M2, and M3 receptor genes (p < 0.001) in one month old rats. The reduction in acetylcholine metabolism is indicated by the downregulated cholineacetyl transferase, upregulated acetylcholine esterase, and decreased vesicular acetylcholine transporter expression. These alterations in cholinergic function in one month old rat brain indicates the longterm consequences of neonatal hypoglycemia in cortical function, which can contribute to the onset of many disease conditions in later stages of life.

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