Lactation Alters γ-Aminobutyric Acid Neuronal Activity in the Hypothalamus and Cerebral Cortex in the Rat

2001 ◽  
Vol 73 (3) ◽  
pp. 175-184 ◽  
Author(s):  
Joseph J. Kornblatt ◽  
David R. Grattan
1984 ◽  
Vol 62 (6) ◽  
pp. 715-719 ◽  
Author(s):  
H. M. Geller ◽  
S. A. Springfield ◽  
A. R. Tiberio

This paper reviews data which illustrate that histamine has prominent actions on the electrophysiology of mammalian central neurons. Extracellular recordings reveal that this amine can either excite or depress neuronal activity in different regions of the brain. The excitations are associated with activation of H1 histamine receptors, whereas depressions are associated with occupancy of H2 receptors. Intracellular experiments have revealed multiple actions of histamine on membrane potential and conductance as well as on amplitude and frequency of postsynaptic potentials. In addition, we present preliminary data from rat cerebral cortex and hippocampal slices which suggest a modulatory role for histamine on γ-aminobutyric acid mediated neurotransmission in the areas of the brain.


2002 ◽  
Vol 30 (04) ◽  
pp. 507-519
Author(s):  
Sue Yu ◽  
Yee-Yung Ng ◽  
Zhi-Hong Jian ◽  
Chien-Chih Chen ◽  
Mei-Shiun Lu ◽  
...  

Levels of monoamines and metabolites, excitatory amino acids, and γ-aminobutyric acid (GABA) were investigated in discrete brain areas of chronic Jiawey Siwu (JS)-treated rats. Male Sprague-Dawley rats were dosed orally for 3 months with normal saline or JS at 0.21, 1.05 or 4.2 g/kg/day. Body weights of these four groups were similar over 3 months. Most effects of JS revealed a dose dependency with levels of neurotransmitters. Levels of norepinephrine (NE) and epinephrine (EPI) in cerebral cortex; EPI, vanillylmandelic acid (VMA), dopamine (DA) and 5-hydroxytryptamine (5-HT) in medulla oblongata; DA in midbrain; NE and 5-HT in amygdala; and 5-HT in hypothalamus had decreased in JS-treated rats. 3-Methoxytyramine (3-MT) in cerebral cortex; 5-hydroxyindole-3-acetic acid (5-HIAA) in medulla oblongata; NE, 3-MT and homovanillic acid (HVA) in pons; EPI and 3-MT in midbrain; 3-MT and HVA in amygdala; 3-MT, 3,4-dihydroxyphenylacetic acid (DOPAC), HVA and 5-HIAA in cerebellum; HVA in hypothalamus; and DOPAC and HVA in hippocampus had all increased in JS-treated rats. In pons, 5-HT increased with low and decreased with high JS doses. Ratios of DA/3-MT in pons and midbrain; DA/HVA in pons and cerebellum; and 5-HT/5-HIAA in medulla oblongata, cerebellum and hypothalamus had decreased. Furthermore, aspartate (ASP) and glutamate (GLU) levels had decreased in cerebral cortex, midbrain, hypothalamus and hippocampus or amygdala, and increased in pons. GABA levels were reduced in cerebral cortex, and higher in medulla oblongata, pons, amygdala, cerebellum, hippocampus and striatum of JS-treated rats. These results indicate that the synthesis and (or) metabolism of NE, DA, EPI and 5-HT, and the levels of ASP, GLU and GABA in rat brains were differentially regionally altered by JS, which may contribute to the central manifestations of JS treatment.


1961 ◽  
Vol 200 (1) ◽  
pp. 34-38 ◽  
Author(s):  
Guy M. McKhann ◽  
Olaf Mickelsen ◽  
Donald B. Tower

Pyridoxine deficiency was produced in weanling kittens by dietary means. Clinically, the deficient animals showed failure to gain weight, ataxia, and, if left on the diet, seizures and death. In vitro study of isolated cerebral cortex slices from the deficient animals showed decreased formation of γ-aminobutyric acid and decreased oxygen uptake when glucose was the substrate. Addition of pyridoxal phosphate to the incubation media corrected both of these defects toward the levels found in normal littermate controls. The decreased oxygen uptake was also corrected by the addition of γ-aminobutyric acid to the media. It is suggested that in pyridoxine deficiency, cerebral oxidative metabolism is impaired by blockage of the γ-aminobutyric acid ‘shunt’ pathway at the glutamic decarboxylase step. The role of this shunt pathway in normal neuronal metabolism is discussed.


2015 ◽  
Vol 72 (8) ◽  
pp. 747 ◽  
Author(s):  
Sohei Kimoto ◽  
Mark M. Zaki ◽  
H. Holly Bazmi ◽  
David A. Lewis

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