scholarly journals Gonadal Hormones Modulate the Dendritic Spine Densities of Primary Cortical Pyramidal Neurons in Adult Female Rat

2009 ◽  
Vol 19 (11) ◽  
pp. 2719-2727 ◽  
Author(s):  
J.-R. Chen ◽  
Y.-T. Yan ◽  
T.-J. Wang ◽  
L.-J. Chen ◽  
Y.-J. Wang ◽  
...  
Keyword(s):  
Adult Female ◽  
Dendritic Spine ◽  
Pyramidal Neurons ◽  
Gonadal Hormones ◽  
Female Rat ◽  
Cortical Pyramidal Neurons

scholarly journals Reduced dendritic spine density on cerebral cortical pyramidal neurons in schizophrenia

1998 ◽  
Vol 65 (4) ◽  
pp. 446-453 ◽  
Author(s):  
L J Garey ◽  
W Y Ong ◽  
T S Patel ◽  
M Kanani ◽  
A Davis ◽  
...  
Keyword(s):  
Dendritic Spine ◽  
Pyramidal Neurons ◽  
Spine Density ◽  
Dendritic Spine Density ◽  
Cortical Pyramidal Neurons

The role of neonatal and pubertal gonadal hormones in regulating the sex dependence of the hepatic microsomal testosterone 5-reductase activity in the rat

1985 ◽  
Vol 106 (1) ◽  
pp. 71-79 ◽  
Author(s):  
R. C. K. Pak ◽  
K. W. K. Tsim ◽  
C. H. K. Cheng
Keyword(s):  
Enzyme Activity ◽  
Adult Female ◽  
Reductase Activity ◽  
Gonadal Hormones ◽  
Female Rats ◽  
Male Rats ◽  
Female Rat ◽  
Similar Treatment ◽  
Control Value ◽  
Level Of Activity

ABSTRACT Hepatic microsomal testosterone 5-reductase activity was approximately fourfold higher in adult female rats than in males. This discrepancy was only partly androgen-dependent since gonadectomy of male rats at 68 days of age resulted in only a partial increase of the enzyme activity. This increase was reversible by the administration of testosterone. Similar treatment, however, produced no effect in the female rat, indicating that there is a sex difference in testosterone responsivity. Castration of newborn male rats resulted in a marked increase in the basal enzyme activity. This increase was not affected by treating the adults with testosterone. Giving testosterone to male rats immediately after neonatal gonadectomy, or to newborn female rats, did not produce the male pattern of both the basal enzyme activity and the testosterone responsivity in adulthood. These results suggest that a brief exposure to neonatal androgen is not critical for the expression of the male type of enzyme activity, but that the continuous presence of the male gonads up to and including the pubertal period is essential. Exposure of pubescent female rats to testosterone during the period from 35 to 50 days of age resulted in a significant increase in testosterone sensitivity when tested at 90 days of age, suggesting that pubertal exposure to androgen is important for the expression of testosterone responsivity in adulthood. The sensitivity was potentiated when the animals were ovariectomized before puberty. Furthermore, the enzyme activity in prepubertally ovariectomized female rats was significantly lower than that in adult gonadectomized animals. The decreased level of activity returned to the control value when oestrogen was replaced during puberty, indicating that peripubertal oestrogen exposure is required for maintaining the high level of activity found in adult female rats. The present findings suggest that the pubertal period represents a sensitive phase during which sex hormones act to regulate the sexual differentiation of testosterone 5-reductase activity in the rat. J. Endocr. (1985) 106, 71–79

Ectopic HCN4 expression drives mTOR-dependent epilepsy in mice

2020 ◽  
Vol 12 (570) ◽  
pp. eabc1492
Author(s):  
Lawrence S. Hsieh ◽  
John H. Wen ◽  
Lena H. Nguyen ◽  
Longbo Zhang ◽  
Stephanie A. Getz ◽  
...  
Keyword(s):  
Mouse Model ◽  
Pyramidal Neurons ◽  
Focal Cortical Dysplasia ◽  
Repetitive Firing ◽  
Intracellular Camp ◽  
Main Role ◽  
Channel Activity ◽  
Mechanistic Target Of Rapamycin ◽  
Cortical Pyramidal Neurons ◽  
Causative Link

The causative link between focal cortical malformations (FCMs) and epilepsy is well accepted, especially among patients with focal cortical dysplasia type II (FCDII) and tuberous sclerosis complex (TSC). However, the mechanisms underlying seizures remain unclear. Using a mouse model of TSC- and FCDII-associated FCM, we showed that FCM neurons were responsible for seizure activity via their unexpected abnormal expression of the hyperpolarization-activated cyclic nucleotide–gated potassium channel isoform 4 (HCN4), which is normally not present in cortical pyramidal neurons after birth. Increasing intracellular cAMP concentrations, which preferentially affects HCN4 gating relative to the other isoforms, drove repetitive firing of FCM neurons but not control pyramidal neurons. Ectopic HCN4 expression was dependent on the mechanistic target of rapamycin (mTOR), preceded the onset of seizures, and was also found in diseased neurons in tissue resected from patients with TSC and FCDII. Last, blocking HCN4 channel activity in FCM neurons prevented epilepsy in the mouse model. These findings suggest that HCN4 play a main role in seizure and identify a cAMP-dependent seizure mechanism in TSC and FCDII. Furthermore, the unique expression of HCN4 exclusively in FCM neurons suggests that gene therapy targeting HCN4 might be effective in reducing seizures in FCDII or TSC.

scholarly journals Hormonal Modulation of Amino Acid Neurotransmitter Metabolism in the Arcuate Nucleus of the Adult Female Rat: A Novel Action of Estradiol

Endocrinology ◽  
2009 ◽  
Vol 150 (7) ◽  
pp. 3237-3244 ◽  
Author(s):  
Tamara Blutstein ◽  
Peter J. Baab ◽  
H. Ronald Zielke ◽  
Jessica A. Mong
Keyword(s):  
Amino Acid ◽  
Adult Female ◽  
Arcuate Nucleus ◽  
Female Rat ◽  
Hormonal Modulation ◽  
Neurotransmitter Metabolism
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