CONVERSION OF TYROSINE TO CATECHOLAMINES BY RAT BRAIN SLICES

1963 ◽  
Vol 41 (7) ◽  
pp. 1565-1570 ◽  
Author(s):  
N. T. Iyer ◽  
P. L. McGeer ◽  
E. G. McGeer
Keyword(s):  
Rat Brain ◽  
Adrenal Medulla ◽  
Pyridoxal Phosphate ◽  
Brain Slices ◽  
Enzymatic Conversion

Evidence is presented for the enzymatic conversion of tyrosine to DOPA and the catecholamines by rat brain slices in vitro. Conversion is favored by ATP and TPNH and inhibited by pyridoxal phosphate. The conversion is very much less than that found under comparable conditions with rat adrenal medulla slices and also differs in that, in brain slices, there is a greater increase in DOPA than in dopamine or noradrenaline.

CONVERSION OF TYROSINE TO CATECHOLAMINES BY RAT BRAIN SLICES

1963 ◽  
Vol 41 (1) ◽  
pp. 1565-1570 ◽  
Author(s):  
N. T. Iyer ◽  
P. L. McGeer ◽  
E. G. McGeer
Keyword(s):  
Rat Brain ◽  
Adrenal Medulla ◽  
Pyridoxal Phosphate ◽  
Brain Slices ◽  
Enzymatic Conversion

Evidence is presented for the enzymatic conversion of tyrosine to DOPA and the catecholamines by rat brain slices in vitro. Conversion is favored by ATP and TPNH and inhibited by pyridoxal phosphate. The conversion is very much less than that found under comparable conditions with rat adrenal medulla slices and also differs in that, in brain slices, there is a greater increase in DOPA than in dopamine or noradrenaline.

Acute hypoxia induces elevation of ornithine decarboxylase activity in neonatal rat brain slices

1995 ◽  
Vol 7 (3) ◽  
pp. 385 ◽  
Author(s):  
LD Longo ◽  
S Packianathan
Keyword(s):  
Rat Brain ◽  
Ornithine Decarboxylase ◽  
Bovine Serum ◽  
Brain Slice ◽  
Brain Slices ◽  
Neonatal Rat ◽  
Newborn Rat ◽  
Rat Brain Slice

Recent studies in vivo have demonstrated that ornithine decarboxylase (ODC) activity in the fetal rat brain is elevated 4-5-fold by acute maternal hypoxia. This hypoxic-associated increase is seen in the rat brain in both the newborn and the adult. Because of the intimate involvement of ODC in transcription and translation, as well as in growth and development, it is imperative that the manner in which hypoxia affects the regulation of this enzyme be better understood. In order to achieve this, a brain preparation in vitro was required to eliminate the confounding effects of the dam on the fetal and newborn brain ODC activity in vivo. Therefore, brain slices from 3-4-day-old (P-3) newborn rats were utilized to test the hypothesis that ODC activity increases in response to hypoxia in vitro. Cerebral slices from the P-3 rat pups were allowed to equilibrate and recover in artificial cerebrospinal fluid (ACSF) continuously bubbled with a mixture of 95% O2 and 5% CO2 for 1 h before beginning hypoxic exposures. Higher basal ODC activities were obtained by treating the slices with 0.03% fetal bovine serum (FBS) and 0.003% bovine serum albumin (BSA), rather than with ACSF alone. Hypoxia was induced in the slices by replacing the gas with 40%, 21%, 10%, or 5% O2, all with 5% CO2 and balance N2. With FBS and BSA treatment, ODC activity was maintained at about 0.15-0.11 nM CO2 mg-1 protein h-1 throughout the experiment, which was 2-3-fold higher than that without FBS and BSA. ODC activity increased significantly and peaked between 1 h and 2 h after initiation of hypoxia. For instance, with 21% O2, ODC activity increased approximately 1.5-fold at 1 h and approximately 2-fold at 2 h. These studies demonstrate that: (1) the hypoxic-induced increases observed in vivo in the fetal and newborn rat brain ODC activity can be approximated in a newborn rat brain slice preparation in vitro; (2) newborn rat brain slice preparations may provide an alternative to methods in vivo or cell culture methods for studying the regulation of acute hypoxic-induced enzymes; and (3) high, stable baseline ODC activities in brain slices suggest that the cells in the slice are capable of active metabolism if FBS and BSA are available to mimic conditions in vivo.

scholarly journals Spindle-Like Thalamocortical Synchronization in a Rat Brain Slice Preparation

2000 ◽  
Vol 84 (2) ◽  
pp. 1093-1097 ◽  
Author(s):  
Virginia Tancredi ◽  
Giuseppe Biagini ◽  
Margherita D'Antuono ◽  
Jacques Louvel ◽  
René Pumain ◽  
...  
Keyword(s):  
Rat Brain ◽  
Kynurenic Acid ◽  
Brain Slice ◽  
Excitatory Amino Acid ◽  
Brain Slices ◽  
Reticular Nucleus ◽  
Antidromic Responses ◽  
Rat Brain Slice

We obtained rat brain slices (550–650 μm) that contained part of the frontoparietal cortex along with a portion of the thalamic ventrobasal complex (VB) and of the reticular nucleus (RTN). Maintained reciprocal thalamocortical connectivity was demonstrated by VB stimulation, which elicited orthodromic and antidromic responses in the cortex, along with re-entry of thalamocortical firing originating in VB neurons excited by cortical output activity. In addition, orthodromic responses were recorded in VB and RTN following stimuli delivered in the cortex. Spontaneous and stimulus-induced coherent rhythmic oscillations (duration = 0.4–3.5 s; frequency = 9–16 Hz) occurred in cortex, VB, and RTN during application of medium containing low concentrations of the K+ channel blocker 4-aminopyridine (0.5–1 μM). This activity, which resembled electroencephalograph (EEG) spindles recorded in vivo, disappeared in both cortex and thalamus during application of the excitatory amino acid receptor antagonist kynurenic acid in VB ( n = 6). By contrast, cortical application of kynurenic acid ( n = 4) abolished spindle-like oscillations at this site, but not those recorded in VB, where their frequency was higher than under control conditions. Our findings demonstrate the preservation of reciprocally interconnected cortical and thalamic neuron networks that generate thalamocortical spindle-like oscillations in an in vitro rat brain slice. As shown in intact animals, these oscillations originate in the thalamus where they are presumably caused by interactions between RTN and VB neurons. We propose that this preparation may help to analyze thalamocortical synchronization and to understand the physiopathogenesis of absence attacks.

4-Aminopyridine differentially affects the spontaneous release of radiolabelled transmitters from rat brain slices in vitro

1995 ◽  
Vol 686 (2) ◽  
pp. 233-238 ◽  
Author(s):  
Dirk H.G. Versteeg ◽  
Frank M.J. Heemskerk ◽  
Henk A. Spierenburg ◽  
Pierre N.E. de Graan ◽  
Loes H. Schrama
Keyword(s):  
Rat Brain ◽  
Brain Slices ◽  
Spontaneous Release

scholarly journals Effect of hyperphenylalaninaemia on lipid synthesis from ketone bodies by rat brain

1976 ◽  
Vol 154 (2) ◽  
pp. 319-325 ◽  
Author(s):  
M S. Patel ◽  
O E. Owen
Keyword(s):  
Rat Brain ◽  
Ketone Bodies ◽  
Brain Slices ◽  
Lipid Synthesis ◽  
Coa Transferase ◽  
Old Rats ◽  
And Function ◽  
Developing Rat

The effect of hyperphenylalaninaemia on the metabolism of ketone bodies in vivo and in vitro by developing rat brain was investigated. The incorporation in vivo of [14C]acetoacetate into cerebral lipids was decreased by both chronic (for 3 days) and acute (for 6h) hyperphenylalaninaemia induced by injecting phenylalanine into 1-week-old rats. In studies in vitro it was observed that the incorporation of the radioactivity from [14C]acetoacetate and 3-hydroxy[14C]butyrate into cerebral lipids was inhibited by phenyl-pyruvate, but not by phenylalanine. Phenylpyruvate also inhibited the incorporation of 3H from 3H2O into lipids by brain slices metabolizing either 3-hydroxybutyrate or acetoacetate in the presence of glucose. These findings suggest that the decrease in the incorporation in vivo of [14C]acetoacetate into cerebral lipids in hyperphenylalaninaemic rats is most likely caused by phenylpyruvate and not by phenylalanine. Phenylpyruvate as well as phenylalanine had no inhibitory effects on ketone-body-catabolizing enzymes, namely 3-hydroxybutyrate dehydrogenase, 3-oxo acid CoA-transferase and acetoacetyl-CoA thiolase, in rat brain. Phenylpyruvate but not phenylalanine inhibited the activity of the 2-oxoglutarate dehydrogenase complex from rat and human brain. These findings suggest that the metabolism of ketone bodies is impaired in brains of untreated phenylketonuric patients, and in turn may contribute to the diminution of mental development and function associated with phenylketonuria.

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