Amiloride-sensitive sodium transport of the rat distal colon during early postnatal development

1987 ◽  
Vol 409 (1-2) ◽  
pp. 194-199 ◽  
Author(s):  
J. Pácha ◽  
M. Popp ◽  
K. Čapek
Keyword(s):  
Postnatal Development ◽  
Sodium Transport ◽  
Distal Colon ◽  
Early Postnatal Development ◽  
Rat Distal Colon

Sodium transport by lamb proximal colon measured during early postnatal development

1982 ◽  
Vol 98 (1) ◽  
pp. 155-159 ◽  
Author(s):  
M. W. Smith ◽  
P. S. James
Keyword(s):  
Postnatal Development ◽  
Sodium Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Proximal Colon ◽  
Early Postnatal Development ◽  
The Third ◽  
Electrolyte Absorption ◽  
Chloride Absorption

SUMMARYProximal colons taken from lambs up to 3 weeks after birth were shown to transport both sodium and chloride from lumen to blood when incubated in vitro.Sodium transport fell into three phases during postnatal development. The first covered the period from birth to 3 days of age when sodium transport was high and equal to that calculated from measurement of short-circuit current. The second was seen in 5- and 7-day-old lambs where the short-circuit current was low and the net transport of sodium was negligible. The third was seen in 2-3-week-old lambs where sodium transport was high, but the short-circuit current was low.Chloride absorption by colons taken from 1-day-old lambs appeared to be in exchange for an anion, possibly bicarbonate. Chloride absorption by colons taken from 3-week-old lambs appeared to be electrogenie or coupled directly to the transport of sodium.A possible explanation for the failure of electrolyte absorption by colons taken from 5- and 7-day-old lambs is discussed.

Effect of aldosterone and dexamethasone pretreatment on sodium transport in rat distal colon in vitro

1984 ◽  
Vol 400 (3) ◽  
pp. 257-261 ◽  
Author(s):  
R. D. Perrone ◽  
E. A. Alexander ◽  
H. H. Bengele ◽  
J. H. Schwartz
Keyword(s):  
Sodium Transport ◽  
Distal Colon ◽  
Rat Distal Colon

Adenosine A3 receptor expression in peplidergic neural circuits of the rat distal colon

2001 ◽  
Vol 120 (5) ◽  
pp. A177-A177
Author(s):  
S SHARP ◽  
J YU ◽  
J GUZMAN ◽  
J XUE ◽  
H COOKE ◽  
...  
Keyword(s):  
Neural Circuits ◽  
Distal Colon ◽  
Receptor Expression ◽  
Adenosine A3 Receptor ◽  
Rat Distal Colon

scholarly journals Impact of repeated co-treatment with escitalopram and aripiprazole on the schizophrenia-like behaviors and BDNF mRNA expression in the adult Sprague–Dawley rats exposed to glutathione deficit during early postnatal development of the brain

2021 ◽  
Author(s):  
Marta A. Lech ◽  
Kinga Kamińska ◽  
Monika Leśkiewicz ◽  
Elżbieta Lorenc-Koci ◽  
Zofia Rogóż
Keyword(s):  
Mrna Expression ◽  
Postnatal Development ◽  
Repeated Treatment ◽  
Sprague Dawley ◽  
Biochemical Tests ◽  
Bdnf Mrna ◽  
Adult Rats ◽  
Behavioral Deficits ◽  
Glutathione Synthesis ◽  
Early Postnatal Development

Abstract Background Preclinical and clinical studies have indicated that impaired endogenous synthesis of glutathione during early postnatal development plays a significant role in the pathophysiology of schizophrenia. Moreover, some studies have suggested that antidepressants are able to increase the activity of atypical antipsychotics which may efficiently improve the treatment of negative and cognitive symptoms of schizophrenia. Methods In the present study, we investigated the influence of repeated co-treatment with escitalopram and aripiprazole on the schizophrenia-like behavior and BDNF mRNA expression in adult rats exposed to glutathione deficit during early postnatal development. Male pups between the postnatal days p5–p16 were treated with the inhibitor of glutathione synthesis, BSO (L-buthionine-(S,R)-sulfoximine) and the dopamine uptake inhibitor, GBR 12,909 alone or in combination. Escitalopram and aripiprazole were given repeatedly for 21 days before the tests. On p90–92 rats were evaluated in the behavioral and biochemical tests. Results BSO given alone and together with GBR 12,909 induced deficits in the studied behavioral tests and decreased the expression of BDNF mRNA. Repeated aripiprazole administration at a higher dose reversed these behavioral deficits. Co-treatment with aripiprazole and an ineffective dose of escitalopram also abolished the behavioral deficits in the studied tests. Conclusion The obtained data indicated that the inhibition of glutathione synthesis in early postnatal development induced long-term deficits corresponding to schizophrenia-like behavior and decreased the BDNF mRNA expression in adult rats, and these behavioral deficits were reversed by repeated treatment with a higher dose of aripiprazole and also by co-treatment with aripiprazole and ineffective dose of escitalopram.

scholarly journals Glutathione Deficiency during Early Postnatal Development Causes Schizophrenia-Like Symptoms and a Reduction in BDNF Levels in the Cortex and Hippocampus of Adult Sprague–Dawley Rats

2021 ◽  
Vol 22 (12) ◽  
pp. 6171
Author(s):  
Marta Anna Lech ◽  
Monika Leśkiewicz ◽  
Kinga Kamińska ◽  
Zofia Rogóż ◽  
Elżbieta Lorenc-Koci
Keyword(s):  
Postnatal Development ◽  
Time Course ◽  
Postnatal Life ◽  
Positive Symptoms ◽  
Gbr 12909 ◽  
Sprague Dawley ◽  
Bdnf Mrna ◽  
Synthesis Inhibitor ◽  
Early Postnatal Development ◽  
Middle Adolescence

Growing body of evidence points to dysregulation of redox status in the brain as an important factor in the pathogenesis of schizophrenia. The aim of our study was to evaluate the effects of l-buthionine-(S,R)-sulfoximine (BSO), a glutathione (GSH) synthesis inhibitor, and 1-[2-Bis(4-fluorophenyl)methoxy]ethyl]-4-(3-phenylpropyl)piperazine dihydrochloride (GBR 12909), a dopamine reuptake inhibitor, given alone or in combination, to Sprague–Dawley pups during early postnatal development (p5–p16), on the time course of the onset of schizophrenia-like behaviors, and on the expression of brain-derived neurotrophic factor (BDNF) mRNA and its protein in the prefrontal cortex (PFC) and hippocampus (HIP) during adulthood. BSO administered alone decreased the levels of BDNF mRNA and its protein both in the PFC and HIP. Treatment with the combination of BSO + GBR 12909 also decreased BDNF mRNA and its protein in the PFC, but in the HIP, only the level of BDNF protein was decreased. Schizophrenia-like behaviors in rats were assessed at three time points of adolescence (p30, p42–p44, p60–p62) and in early adulthood (p90–p92) using the social interaction test, novel object recognition test, and open field test. Social and cognitive deficits first appeared in the middle adolescence stage and continued to occur into adulthood, both in rats treated with BSO alone or with the BSO + GBR 12909 combination. Behavior corresponding to positive symptoms in humans occurred in the middle adolescence period, only in rats treated with BSO + GBR 12909. Only in the latter group, amphetamine exacerbated the existing positive symptoms in adulthood. Our data show that rats receiving the BSO + GBR 12909 combination in the early postnatal life reproduced virtually all symptoms observed in patients with schizophrenia and, therefore, can be considered a valuable neurodevelopmental model of this disease.

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