Chronic neonatal nicotine exposure increases excitation in the young adult rat hippocampus in a sex-dependent manner

Background: The molecular pathogenesis of depression and psychopharmacology of antidepressants remain elusive. Recent hypotheses suggest that changes in neurogenesis and plasticity may underlie the aetiology of depression. The hippocampus is affected by depression and shows neuronal remodelling during adulthood.Objective: The present study on the adult rat hippocampus, was to evaluate the dose-related effects of chronic venlafaxine on the expression of brain-derived neurotrophic factor (BDNF) and phosphorylated cyclic-AMP response element binding protein (pCREB).Methods: Sprague-Dawley rats were exposed to a variety of chronic unpredictable stressors (CUSs) to establish a depression model. Rats were treated for either 14 or 28 days with venlafaxine (5 and 10 mg/kg, respectively). The hippocampal expression of pCREB and BDNF mRNA and protein was assessed by using immunohistochemistry, western blotting and reverse transcription polymerase chain reaction (RT-PCR).Results: Rats subjected to CUS procedure consumed less sucrose solution compared with non-stressed rats. The CUS influenced exploratory activity resulting in a reduction of the motility counts. Chronic low dose (5 mg/kg, 14 and 28 days), but not high dose (10 mg/kg, 14 and 28 days) of venlafaxine treatment increased the expression of pCREB and BDNF mRNA and protein in the CUS rat hippocampus.Conclusion: Neuronal plasticity-associated proteins such as pCREB and BDNF play an important role both in stress-related depression and in antidepressant effect.

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Liquid diets reduce cell proliferation but not neurogenesis in the adult rat hippocampus

Neuroscience ◽

10.1016/j.neuroscience.2013.09.024 ◽

2013 ◽

Vol 254 ◽

pp. 173-184 ◽

Cited By ~ 20

Author(s):

A.R. Patten ◽

D.J. Moller ◽

J. Graham ◽

J. Gil-Mohapel ◽

B.R. Christie

Keyword(s):

Cell Proliferation ◽

Rat Hippocampus ◽

Adult Rat ◽

Reduce Cell Proliferation

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Androgens and Postmeiotic Germ Cells Regulate Claudin-11 Expression in Rat Sertoli Cells

Endocrinology ◽

10.1210/en.2004-0834 ◽

2005 ◽

Vol 146 (3) ◽

pp. 1532-1540 ◽

Cited By ~ 62

Author(s):

Anne Florin ◽

Magali Maire ◽

Aline Bozec ◽

Ali Hellani ◽

Sonia Chater ◽

...

Keyword(s):

Germ Cells ◽

Sertoli Cells ◽

Inhibitory Effect ◽

Positive Control ◽

Maximum Effect ◽

Dependent Manner ◽

Adult Age ◽

Adult Rat ◽

Protein Levels ◽

Negative Effect

In the present study we investigated whether fetal exposure to flutamide affected messenger and protein levels of claudin-11, a key Sertoli cell factor in the establishment of the hemotesticular barrier, at the time of two key events of postnatal testis development: 1) before puberty (postnatal d 14) during the establishment of the hemotesticular barrier, and 2) at the adult age (postnatal d 90) at the time of full spermatogenesis. The data obtained show that claudin-11 expression was inhibited in prepubertal rat testes exposed in utero to 2 and 10 mg/kg·d flutamide. However, in adult testes, the inhibition was observed only with 2, and not with 10, mg/kg·d of the antiandrogen. It is shown here that these differences between prepubertal and adult testes could be related to dual and opposed regulation of claudin-11 expression resulting from positive control by androgens and an inhibitory effect of postmeiotic germ cells. Indeed, testosterone is shown to stimulate claudin-11 expression in cultured Sertoli cells in a dose- and time-dependent manner (maximum effect with 0.06 μm after 72 h of treatment). In contrast, postmeiotic germ cells potentially exert a negative effect on claudin-11 expression, because adult rat testes depleted in spermatids (after local irradiation) displayed increased claudin-11 expression, whereas in a model of cocultured Sertoli and germ cells, spermatids, but not spermatocytes, inhibited claudin-11 expression. The apparent absence of claudin-11 expression changes in adult rat testes exposed to 10 mg/kg·d flutamide therefore could result from the antagonistic effects of 1) the inhibitory action of the antiandrogen and 2) the stimulatory effect of the apoptotic germ cells on claudin-11 expression. Together, due to the key role of claudin-11 in the hemotesticular barrier, the present findings suggest that such regulatory mechanisms may potentially affect this barrier (re)modeling during spermatogenesis.

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