scholarly journals Sex Differences and Olfactory Bulb Alterations Contribute to Limbic Circuit Dysfunction and Behavioral Disturbances in Pilocarpine Model of Epilepsy

2021 ◽  
Author(s):  
Daniel Matovu ◽  
Esper A Cavalheiro
Keyword(s):  
Olfactory Bulb ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Female Rats ◽  
Behavioral Disturbances ◽  
Recurrent Seizure ◽  
Male And Female Rats ◽  
Isotropic Fractionator ◽  
Pilocarpine Model ◽  
Spontaneous Recurrent Seizures

Abstract The olfactory bulb at the sensory and circuit level transmits information to the limbic and cortical systems for behavioral outputs, and disruption of such circuits induces behavioral disturbances in rodents. Previously, data from our laboratory showed the occurrence of behavioral disturbances in Wistar rats submitted to the pilocarpine model of epilepsy (PME) and that these alterations were sex related. Here we deepen our findings that sex-linked differences are present in PME and that male epileptic rats exhibit profound recurrent seizure patterns, namely seizure duration, severity, and distribution along the light/dark cycle different from that observed in epileptic female rats. Further, using isotropic fractionator we observed significant alterations in the number of neuronal and non-neuronal cells of the olfactory bulb, amygdala, and hippocampus following 3 months of spontaneous recurrent seizures in epileptic male and female rats. Altogether, our study suggests that neuronal and non-neuronal cell death in olfactory bulb may interfere with sex-related differential recurrent seizure patterns, limbic circuit dysfunction, and behavioral disturbances in PME. Lastly, the pilocarpine epilepsy model provides an evidence-based tool to study mechanisms of behavioral disturbances in epileptogenesis that may provide future therapeutic insights in our quest to improve the life of people with epilepsy.

Scanning Electron Microscopy of neuronal cell bodies isolated from the adult mammalian central nervous system

1990 ◽  
Vol 48 (3) ◽  
pp. 426-427
Author(s):  
Wenshu Liu ◽  
J. Franklin Bailey ◽  
Visaka Limwongse ◽  
Mark DeSantis
Keyword(s):  
Electron Microscopy ◽  
Scanning Electron Microscopy ◽  
Motor Neuron ◽  
Motor Neurons ◽  
Neuronal Cell ◽  
Female Rats ◽  
Male And Female Rats ◽  
Neuronal Cell Bodies ◽  
Neuronal Soma ◽  
Scanning Electron

Action potentials generated in a motor neuron reflect the summation of synaptic inputs it receives from other neurons. Those synapses occur at points of contiguity between the presynaptic boutons and the surface of the motor neuron. Evidence that the density of axosomalic boutons on motor neurons varies directly with the size of the motor neuronal soma is indirect. Counts of the number of boutons per unit area at the surface of the motor neuron’s cell body using scanning electron microscopy (SEM) would allow an independent, direct assessment of that inference. We describe here procedures for consistently isolating the somas of CNS neurons, specifically those associated with the adult rat’s trigeminal nerve, so that axosomatic boutons can be seen by SEM (Figures 1 and 2).Adult male and female rats were anesthetized and then perfused with saline followed by 4% paraformaldehyde. The brain stem was removed and sectioned at 200 um thickness on a vibratome. Sections containing the trigeminal motor and mesencephalic nuclei were pinned to Sylgard-lined dishes containing phosphate buffer (0.1 M, pH 7.2).

Profound destructive effects of adolescent exposure to vincristine accompanied with some sex differences in motor and memory performance

2012 ◽  
Vol 90 (4) ◽  
pp. 379-386 ◽  
Author(s):  
Mohammad Shabani ◽  
Mohammad Hassan Larizadeh ◽  
Shahrnaz Parsania ◽  
Majid Asadi Shekaari ◽  
Nader Shahrokhi
Keyword(s):  
Motor Coordination ◽  
Cell Damage ◽  
Memory Performance ◽  
Neuronal Cell ◽  
Treated Group ◽  
Female Rats ◽  
Male Rats ◽  
Male And Female ◽  
Male And Female Rats ◽  
Probe Test

Vincristine, an anticancer drug, is known to induce neuronal cell damage. We have elucidated the alteration in performance of the hippocampus and cerebellum following chronic vincristine treatment (0.2 mg·(kg body mass)–1·week–1) in male and female rats. Intraperitoneal injection of vincristine in adolescent rats caused impairment of motor and cognitive behavior. In the probe test, the length of path traveled and percent swimming time for vincristine-treated rats in the correct quadrant was significantly less than for the saline-treated (control) groups. The path length and time latency at the 2nd and 3rd blocks of trials for the male vincristine-treated group was significantly higher than that for the female saline- and the vincristine-treated rats. In the rod test, vincristine exposure impaired the motor coordination in both male and female rats. Exposure to vincristine caused a significant decrease in hanging time in male rats, compared with the saline- and the vincristine-treated female rats, while there were no differences between the female vincristine-treated rats and the saline-treated rats of both sexes. The rearing frequency, total distance moved, and velocity for both male and female rats were dramatically affected by exposure to vincristine. We have observed that the hippocampal and cerebellar functions of male and female rats were profoundly affected by exposure to vincristine, especially the male rats, suggesting a sexual dimorphism in the developing central nervous system that is affected by chemicals such as anticancer drugs.

Chronic Testosterone Administration During Pregnancy Causes Autistic-like Traits in Rat Offspring: Possible Relationships with Cerebral Oxytocin, Dopamine, Serotonin and IGF-1 Levels.

2021 ◽  
Author(s):  
Evrim Senkal ◽  
Umut Eryigit ◽  
Mehmet Fatih Bozkurt ◽  
Volkan Solmaz ◽  
Oytun Erbas
Keyword(s):  
Neurodevelopmental Disorder ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Autism Spectrum ◽  
Female Rats ◽  
Behavioral Tests ◽  
Testosterone Undecanoate ◽  
Prenatal Testosterone ◽  
Group 2 ◽  
Group 1

Abstract Autism spectrum disorder (ASD) is a neurodevelopmental disorder that affects boys three times more frequently than girls. Previous studies have suggested that higher fetal testosterone exposure can cause autism-like behaviors in males. The mechanism of effect of fetal testosterone on autism development is not well known. In the present study, we investigated the relationship between prenatal testosterone exposure and ASD in an experimental study with the use of behavioral tests, histopathological examinations and biochemical measurements performed to compare offspring with and without exposure to testosterone. Female rats were randomly distributed into Group 1 (control, n = 6) and Group 2 (Testosterone undecanoate, n = 6). Female rats were caged with a fertile male (three female/one male) for 2–3 days during the oestrus period. Group 1 rats were given 1 ml/kg % 0.9 NaCl saline on the 10th day of pregnancy, while Group 2 rats were given 250 mg/kg testosterone undecanoate. The dams were allowed to raise their litters until weaning on postnatal day 21 (P21). On P21 , forty littermates (10 male control, ten female control, ten male Testosterone-exposed, and ten female Testosterone-exposed) were randomly separated and housed. These animals underwent behavioral testing in adulthood on P50. Subsequently, the rats were sacrificed. Biochemical analyses [Brain tissue 5-Hydroxyindoleacetic acid (5-HIAA), homovanillic acid (HVA), Insulin-like growth factor-1 (IGF-1), and oxytocin] and histopathological analyses were performed. Analysis of the behavioral tests (three-chamber social test, open field test) revealed significant differences among the groups, with the testosterone-exposed groups demonstrating autistic traits at a greater degree. Histologically, hippocampal CA1 and CA3 regions displayed significant alterations such as gliosis and neuronal cell death in the testosterone-exposed groups compared to controls. Brain levels of tissue 5-HIAA, HVA, IGF-1 increased while oxytocin level decreased in the testosterone-exposed groups. These results suggest a possible link between chronic prenatal testosterone exposure and neurodevelopmental disorders such as ASD. Testosterone exposure and autism-like traits can be linked to dopamine, serotonin, IGF-1 increase, and oxytocin decrease.

Monosodium glutamate administration early in life alters pineal melatonin nocturnal profile in adulthood

2021 ◽  
Vol 4 (1) ◽  
pp. 99-114
Author(s):  
Janaína B Garcia ◽  
Fernanda G Do Amaral ◽  
Daniela C Buonfiglio ◽  
Rafaela FA Vendrame ◽  
Patrícia L Alves ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Pineal Gland ◽  
Serum Insulin ◽  
Monosodium Glutamate ◽  
Female Rats ◽  
Pineal Melatonin ◽  
Melatonin Synthesis ◽  
Male And Female Rats ◽  
Melatonin Production

The pineal gland synthesizes melatonin exclusively at night, which gives melatonin the characteristic of a temporal synchronizer of the physiological systems. Melatonin is a regulator of insulin activities centrally and also peripherally and its synthesis is reduced in diabetes.  Since monosodium glutamate (MSG) is often used to induce the type 2 diabetic and metabolic syndrome in animal models, the purpose of this work is to evaluate the potential effects of MSG given to neonates on the pineal melatonin synthesis in different aged male and female rats. Wistar rats were subcutaneously injected with MSG (4mg/g/day) or saline solution (0.9%) from the second to eighth post-natal day. The circadian profiles both melatonin levels and AANAT activity were monitored at different ages. Body weight, naso-anal length, adipose tissues weight, GTT, ITT and serum insulin levels were also evaluated. Typical obesity with the neonatal MSG treatment was observed, indicated by a great increase in adipose depots without a concurrent increase in body weight. MSG treatment did not cause hyperglycemia or glucose intolerance, but induced insulin resistance. An increase of melatonin synthesis at ZT 15 with phase advance was observed in in some animals. The AANAT activity was positively parallel to the melatonin circadian profile. It seems that MSG causes hypothalamic obesity which may increase AANAT activity and melatonin production in pineal gland. These effects were not temporally correlated with insulin resistance and hyperinsulinemia indicating the hypothalamic lesions, particularly in arcuate nucleus induced by MSG in early age, as the principal cause of the increase in melatonin production.

THE PITUITARY AND ADRENAL RESPONSES TO ADMINISTRATION OF OESTRIOL IN GONADECTOMIZED RATS

1961 ◽  
Vol 38 (1) ◽  
pp. 50-58 ◽  
Author(s):  
N. E. Borglin ◽  
L. Bjersing
Keyword(s):  
Pituitary Gland ◽  
Adrenal Cortex ◽  
Clinical Experience ◽  
Uterine Cervix ◽  
Morphological Changes ◽  
Physiological Significance ◽  
Female Rats ◽  
Experimental Conditions ◽  
Male And Female ◽  
Male And Female Rats

ABSTRACT Oestriol (oestra-1,3,5(10)-triene-3,16α,17β-triol) is a weakly oestrogenic substance which, however, in contrast to what was formerly believed, is of physiological significance. Its effect is localized largely to the uterine cervix and vagina. Clinical experience argues both for and against an effect on the pituitary gland. This investigation is concerned with the morphological changes in the pituitary gland and adrenal cortex of gonadectomized male and female rats after the injection of oestriol. It was found that oestriol has the same type of action on these glands as other oestrogens, but under the experimental conditions used, this effect proved much weaker than that produced by oestradiol (oestra-1,3,5(10)-triene-3,17β-diol).

INDUCTION OF GOITRE BY PTU OR KClO4 IN MALE AND FEMALE RATS. EFFECT OF GONADECTOMY

1973 ◽  
Vol 74 (1) ◽  
pp. 88-104 ◽  
Author(s):  
T. Jolín ◽  
M. J. Tarin ◽  
M. D. Garcia
Keyword(s):  
Iodine Content ◽  
High Plasma ◽  
Disc Electrophoresis ◽  
Female Rats ◽  
Male Rats ◽  
Adult Rats ◽  
Male And Female ◽  
Glucose Levels ◽  
Male And Female Rats ◽  
Tsh Levels

ABSTRACT Male and female rats of varying ages were placad on a low iodine diet (LID) plus KClO4 or 6-propyl-2-thiouracil (PTU) or on the same diet supplemented with I (control rats). Goitrogenesis was also induced with LID plus PTU in gonadectomized animals of both sexes. The weight of the control and goitrogen treated animals, and the weight and iodine content of their thyroids were determined, as well as the plasma PBI, TSH, insulin and glucose levels. The pituitary GH-like protein content was assessed by disc electrophoresis on polyacrylamide gels. If goitrogenesis was induced in young rats of both sexes starting with rats of the same age, body weight (B.W.) and pituitary growth hormone (GH) content, it was found that both the males and females developed goitres of the same size. On the contrary, when goitrogenesis was induced in adult animals, it was found that male rats, that had larger B.W. and pituitary GH content than age-paired females, developed larger goitres. However, both male and female rats were in a hypothyroid condition of comparable degree as judged by the thyroidal iodine content and the plasma PBI and TSH levels. When all the data on the PTU or KClO4-treated male and female rats of varying age and B.W. were considered together, it was observed that the weights of the thyroids increased proportionally to B.W. However, a difference in the slope of the regression of the thyroid weight over B.W. was found between male and female rats, due to the fact that adult male rats develop larger goitres than female animals. In addition, in the male rats treated with PTU, gonadectomy decreased the B.W., pituitary content of GH-like protein and, concomitantly, the size of the goitre decreased; an opposite effect was induced by ovariectomy on the female animals. However, when goitrogenesis was induced in weight-paired adult rats of both sexes, the male animals still developed larger goitres than the females. Among all the parameters studied here, the only ones which appeared to bear a consistent relationship with the size of the goitres in rats of different sexes, treated with a given goitrogen, were the rate of body growth and the amount of a pituitary GH-like protein found before the onset of the goitrogen treatment. Moreover, though the pituitary content of the GH-like protein decreased as a consequence of goitrogen treatment, it was still somewhat higher in male that in female animals. The present results suggest that GH may somehow be involved in the mechanism by which male and female rats on goitrogens develop goitres of different sizes, despite equally high plasma TSH levels.

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