scholarly journals Effects of Supraphysiological Doses of Testosterone Cypionate and Stanozolol on Neuronal Density of Basolateral and Medial Amygdala and on the Anxious Behavior of Mice

2019 ◽  
Vol 36 (02) ◽  
pp. 115-121
Author(s):  
Melissa Ribeiro ◽  
Ariane Freitas ◽  
Bruno Damião ◽  
Wagner Costa Rossi ◽  
Flávia da Ré Guerra ◽  
...  
Keyword(s):  
Basolateral Amygdala ◽  
Chronic Administration ◽  
Nerve Tissue ◽  
Medial Amygdala ◽  
Behavioral Alterations ◽  
Neuronal Density ◽  
Behavior Response ◽  
Anxious Behavior ◽  
Androgenic Steroids ◽  
Staying Time

AbstractSupraphysiological doses of anabolic-androgenic steroids (AAS) have been associated to possible nerve tissue damage and behavioral effects. Considering the lack of knowledge of the neural aspects involved in these behavioral alterations, this work aimed to analyze the anxious behavior response or aggressiveness, besides quantifying the neuronal density of the basolateral amygdala (BLA) and of the ventral posterior nucleus (VPN) of the medial amygdala. The animals received doses of testosterone cypionate (CT Group) and stanozolol (ST Group) twice a week for 33 days. The effects of chronic administration of AAS related to anxious behavior (as determined by the elevated plus maze [EPM] test) in male animals are observed in a lower number of entries (< 45.25%), and a shorter staying time spent in the open arms (< 41.9%) was observed in the ST. In female animals, a longer staying time spent in the closed arms of the EPM test was observed in the CT (> 15%) as well as a shorter staying time spent in the open arms for CT (< 17.1%) also to ST (< 52.1%). Regarding the neuronal density in BLA, a significant reduction in neuronal density of male animals (17.55%) was observed only in CT, whereas for females, significant differences were found in CT (19.16%) and ST (18.36%). The reduction of neuronal density in VPN in male animals was 13.55% in CT and 17.68% in ST, whereas in group of females it was 13.53% and 14.32%, respectively for CT and ST. Therefore, the two steroids used in this experiment were able to significantly reduce neuronal density in two analyzed areas, regardless of sex, suggesting that indiscriminate use of these substances causes death of brain amygdala neurons.

scholarly journals Long-term consequences of alcohol use in early adolescent mice: focus on neuroadaptations in GR, CRF and BDNF

2021 ◽  
Author(s):  
Patricia Sampedro-Piquero ◽  
Roman Moreno-Fernandez ◽  
Azucena Begega ◽  
Matias Lopez ◽  
Luis J. Santin
Keyword(s):  
Test Performance ◽  
Emotional Regulation ◽  
Basolateral Amygdala ◽  
Immunohistochemical Analysis ◽  
Alcohol Exposure ◽  
Central Amygdala ◽  
Late Adolescent ◽  
Behavioral Alterations ◽  
Bdnf Expression

Our aim was to assess the cognitive and emotional state, as well as related-changes in Glucocorticoid Receptor (GR), Corticotropin-Releasing Factor (CRF) and Brain-Derived Neurotrophic Factor (BDNF) expression of adolescent C57BL/6J male mice after a 5-week two-bottle choice protocol (postnatal day (pd) 21 to pd52). Additionally, we wanted to analyze whether the behavioral and neurobiological effects observed in the late adolescence (pd62) lasted until the adulthood (pd84). Behavioral testing revealed that alcohol during early adolescence increased anxiety-like and compulsive-related behaviors and it was maintained in the adulthood. Concerning cognition, working memory was only altered in late adolescent mice, whereas object location test performance was impaired in both ages. In contrast, novel object recognition remained unaltered. Immunohistochemical analysis showed that alcohol during adolescence diminished BDNF+ cells in the cingulate cortex, the hippocampal CA1 layer and the central amygdala. Regarding hypothalamic-pituitary-adrenal axis (HPA) functioning, alcohol abuse increased the GR and CRF expression in the hypothalamic paraventricular nucleus and the central amygdala. Besides, GR density was also higher in the prelimbic cortex and the basolateral amygdala regardless of animals age. Our findings suggest that adolescent alcohol exposure led to long-term behavioral alterations along with changes in BDNF, GR and CRF expression in limbic brain areas involved in stress response, emotional regulation, and cognition.

scholarly journals Adolescent forced swim stress increases social anxiety-like behaviors and alters the dynorphin/kappa opioid receptor system in the basolateral amygdala of males

2019 ◽  
Author(s):  
E.I. Varlinskaya ◽  
J.M. Johnson ◽  
T. Deak ◽  
M.R. Diaz
Keyword(s):  
Social Anxiety ◽  
Opioid Receptor ◽  
Basolateral Amygdala ◽  
Kappa Opioid Receptor ◽  
Adolescent Males ◽  
Adult Males ◽  
Behavioral Alterations ◽  
Kappa Opioid ◽  
Forced Swim Stress ◽  
Gaba Transmission

AbstractAdolescence is a developmental period marked by robust neural alterations and heightened vulnerability to stress, a factor that is highly associated with increased risk for emotional processing deficits, such as anxiety. Stress-induced upregulation of the dynorphin/kappa opioid receptor (DYN/KOR) system is thought to, in part, underlie the negative affect associated with stress. The basolateral amygdala (BLA) is a key structure involved in anxiety, and neuromodulatory systems, such as the DYN/KOR system, can 1) regulate BLA neural activity in an age-dependent manner in stress-naïve animals and 2) underlie stress-induced anxiety in adults. However, the role of the DYN/KOR system in modulating stress-induced anxiety in adolescents is unknown. To test this, we examined the impact of an acute, 2-day forced swim stress (FSS – 10 min each day) on adolescent (~postnatal day (P) 35) and adult Sprague-Dawley rats (~P70), followed by behavioral, molecular and electrophysiological assessment 24 hours following FSS. Adolescent males, but not adult males or females of either age, demonstrated social anxiety-like behavioral alterations indexed via significantly reduced social investigation and preference when tested 24 hours following FSS. Conversely, adult males exhibited increased social preference. While there were no FSS-induced changes in expression of genes related to the DYN/KOR system in the BLA, these behavioral alterations were associated with a robust switch in BLA KOR function. Specifically, while the KOR agonist, U69593, significantly increased GABA transmission in the BLA of non-stressed adolescent males, U69593 significantly inhibited BLA GABA transmission in stressed adolescent males, consistent with the observed anxiogenic phenotype in stressed adolescent males. This is the first study to demonstrate a KOR-dependent mechanism that may contribute to stress-induced social anxiety in adolescent males. Importantly, these findings provide evidence for potential KOR-dependent mechanisms that may contribute to pathophysiological interactions with subsequent stress challenges.

Interaction of high-intensity endurance exercise and nandrolone on cardiac remodeling: role of adipo-cardiac axis

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Manijeh Motevalian ◽  
Siyavash Joukar ◽  
Saeed Esmaeili-Mahani ◽  
Abdollah Karimi ◽  
Yaser Masoumi-Ardakani ◽  
...  
Keyword(s):  
Endurance Exercise ◽  
High Intensity ◽  
Chronic Administration ◽  
Left Ventricular ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Male Wistar Rats ◽  
Α Level ◽  
Androgenic Steroids

Abstract Objectives Given the cardiac pathological remodeling following to anabolic androgenic steroids (AASs) consumption, we examined the effect of chronic administration of nandrolone decanoate with high-intensity endurance exercise on the left ventricular hypertrophy index, levels of hydroxyproline, tumor necrosis factor-alpha (TNF-α), adiponectin (APN) and its receptors (AdipoR1 and AdipoR2) expression in rats’ hearts. Methods The male Wistar rats randomly divided to six groups included the control (CTL), exercise (Ex), nandrolone (Nan), vehicle (Arach), trained vehicle (Ex + Arach), and trained nandrolone (Ex + Nan) groups that were treated for eight weeks. Results Nandrolone consumption significantly enhanced the hypertrophy index (p<0.05) and exercise intensified this effect. It also increased the level of cardiac hydroxyproline (p<0.001), however exercise completely masked this effect. The values of TNF-α protein and AdipoR1 protein significantly increased in trained nandrolone-treated (Ex + Nan) group in comparison with CTL group (p<0.05), however, did not show significant alteration in Nan or Ex groups. High-intensity endurance exercise significantly enhanced the AdipoR2 protein (p<0.05), but, co-administration of nandrolone with exercise prevented this effect. The mRNA expression of AdipoR1 significantly reduced in the animals that received nandrolone for eight weeks and exercise recovered this effect (p<0.001). Conclusions Despite an additive effect of high-intensity endurance exercise plus nandrolone on TNF-α level, their effects on hydroxyproline and APN receptors expression is incompatible in heart of rat. It is suggests a part of beneficial regulatory role of endurance exercise against nandrolone induced heart remodeling may apply through modulation of APN system.

scholarly journals Centella asiaticaAttenuates D-Galactose-Induced Cognitive Impairment, Oxidative and Mitochondrial Dysfunction in Mice

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Anil Kumar ◽  
Atish Prakash ◽  
Samrita Dogra
Keyword(s):  
Cognitive Impairment ◽  
Oxidative Damage ◽  
Mitochondrial Dysfunction ◽  
Cognitive Task ◽  
Enzyme Level ◽  
Centella Asiatica ◽  
Chronic Administration ◽  
Behavioral Alterations ◽  
Gradual Loss ◽  
Protein Thiols

D-galactose induced neurotoxicity is well known model for studying aging and related oxidative damage and memory impairment. Aging is a biological process, characterized by the gradual loss of physiological functions by unknown mechanism.Centella asiatica, Indian pennywort has been documented in the treatment of various neurological disorders including aging. Therefore, present study has been conducted in order to explore the possible role of Centella asiatica against D-galactose induced cognitive impairment, oxidative and mitochondrial dysfunction in mice. Chronic administration of D-galactose (100 mg/kg s.c.) for a period of six weeks significantly impaired cognitive task (both in both Morris water maze and elevated plus maze) and oxidative defense (Increased lipid peroxidation, nitrite concentration and decreased activity of superoxide dismutase, catalase and non-protein thiols) and impaired mitochondrial complex (I, II and III) enzymes activities as compared to sham group. Six weeksCentella asiatica(150 and 300 mg/kg, p.o) treatment significantly improved behavioral alterations, oxidative damage and mitochondrial enzyme complex activities as compared to contro l (D-galactose).Centella asiaticaalso attenuated enhanced acetylcholine esterase enzyme level in D-galactose senescence mice. Present study highlights the protective effect ofCentella asiaticaagainst D-galactose induced behavioral, biochemical and mitochondrial dysfunction in mice.

Influence of chronic administration of anabolic androgenic steroids and taurine on haemostasis profile in rats

2013 ◽  
Vol 24 (3) ◽  
pp. 256-260 ◽  
Author(s):  
Adrian E. Roşca ◽  
Corin Badiu ◽  
Valentina Uscătescu ◽  
Irina Stoian ◽  
Radu Mirică ◽  
...  
Keyword(s):  
Chronic Administration ◽  
Anabolic Androgenic Steroids ◽  
Androgenic Steroids

scholarly journals Chronic Ethanol Differentially Modulates Glutamate Release from Dorsal and Ventral Prefrontal Cortical Inputs onto Rat Basolateral Amygdala Principal Neurons

2019 ◽  
Author(s):  
Molly M. McGinnis ◽  
Brian C. Parrish ◽  
Ann M. Chappell ◽  
Brian A. McCool
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Basolateral Amygdala ◽  
Glutamate Release ◽  
Ethanol Exposure ◽  
Chronic Ethanol ◽  
Sprague Dawley ◽  
Behavioral Alterations ◽  
Release Probability ◽  
Chronic Ethanol Exposure

AbstractThe medial prefrontal cortex (mPFC) and the basolateral amygdala (BLA) have strong reciprocal connectivity. Projections from the BLA to the mPFC can bidirectionally modulate anxiety-related behaviors but it is unclear if the same is true for mPFC to BLA projections. Our laboratory is specifically interested in withdrawal-related anxiety-like behavior and the underlying synaptic plasticity. Here, we use optogenetics and chemogenetics to characterize the neurophysiological and behavioral alterations produced by chronic ethanol exposure and withdrawal on dorsal mPFC/prelimbic (dmPFC/PL) and ventral mPFC (vmPFC/IL) terminals in the BLA. We exposed adult male Sprague-Dawley rats to chronic intermittent ethanol (CIE) using vapor chambers, measured anxiety-like behavior on the elevated zero maze (EZM), and used electrophysiology to record glutamatergic and GABAergic responses in BLA principal neurons. We found that 24-hour withdrawal following a 7-day CIE exposure significantly increased the glutamate release probability from PL/dmPFC terminals, but significantly decreases the glutamate release probability from IL/vmPFC terminals. Chemogenetic inhibition of PL/dmPFC terminals in the BLA attenuated the increased withdrawal-dependent, anxiety-like behavior. These data demonstrate that chronic ethanol exposure and withdrawal strengthens the PL/dmPFC – BLA pathway but weakens the IL/vmPFC – BLA pathway. Moreover, we provide novel evidence that the PL/dmPFC – BLA pathway can modulate anxiety-like behavior. These findings suggest that mPFC-BLA circuits known to regulate the acquisition of aversive behaviors are up-regulated by chronic ethanol while those involved with the extinction of these behaviors are down-regulated.Significance StatementAccumulating evidence suggests that the medial prefrontal cortex and its projections to the basolateral amygdala bidirectionally modulate fear-related behaviors. Since the neuronal circuits for fear and anxiety are thought to overlap, we sought to examine the role of prelimbic and infralimbic subdivisions of the medial prefrontal cortex and their inputs to the basolateral amygdala in regulating anxiety. Specifically, we focused on alcohol withdrawal-induced anxiety-like behavior, which is a commonly reported cause of relapse in human alcoholics. In our study, we used optogenetics and chemogenetics to demonstrate, for the first time, that withdrawal from chronic ethanol exposure strengthens prelimbic synapses, but weakens infralimbic synapses in the basolateral amygdala and that inhibiting glutamate release from prelimbic terminal in the basolateral amygdala reduces anxiety-like behavior.

Embryonic Exposure to Ethanol Increases Anxiety-Like Behavior in Fry Zebrafish

2020 ◽  
Vol 55 (6) ◽  
pp. 581-590
Author(s):  
Jaquelinne Pinheiro-da-Silva ◽  
Thais Agues-Barbosa ◽  
Ana Carolina Luchiari
Keyword(s):  
Inhibitory Avoidance ◽  
Ethanol Exposure ◽  
Initial Growth ◽  
Behavioral Alterations ◽  
Fetal Alcohol ◽  
Embryonic Exposure ◽  
Behavioral Abnormalities ◽  
Fast Development ◽  
Anxious Behavior ◽  
Fetal Alcohol Spectrum

Abstract Aims Fetal alcohol spectrum disorder (FASD) is an umbrella term to describe the effects of ethanol (Eth) exposure during embryonic development, including several conditions from malformation to cognitive deficits. Zebrafish (Danio rerio) are a translational model popularly applied in brain disorders and drug screening studies due to its genetic and physiology homology to humans added to its transparent eggs and fast development. In this study, we investigated how early ethanol exposure affects zebrafish behavior during the initial growth phase. Methods Fish eggs were exposed to 0.0 (control), 0.25 and 0.5% ethanol at 24 h post-fertilization. Later, fry zebrafish (10 days old) were tested in a novel tank task and an inhibitory avoidance protocol to inquire about morphology and behavioral alterations. Results Analysis of variance showed that ethanol doses of 0.25 and 0.5% do not cause morphological malformations and did not impair associative learning but increased anxiety-like behavior responses and lower exploratory behavior when compared to the control. Conclusion Our results demonstrate that one can detect behavioral abnormalities in the zebrafish induced by embryonic ethanol as early as 10 days post-fertilization and that alcohol increases anxious behavior during young development in zebrafish.

scholarly journals Lipid Profile Changes Induced by Chronic Administration of Anabolic Androgenic Steroids and Taurine in Rats

Medicina ◽  
2019 ◽  
Vol 55 (9) ◽  
pp. 540 ◽  
Author(s):  
A.E. Rosca ◽  
Camelia Sorina Stancu ◽  
Corin Badiu ◽  
Bogdan Ovidiu Popescu ◽  
Radu Mirica ◽  
...  
Keyword(s):  
Lipid Profile ◽  
Therapeutic Potential ◽  
Low Density Lipoprotein ◽  
Plasma Lipid ◽  
Density Lipoprotein ◽  
Chronic Administration ◽  
Lipoprotein Cholesterol ◽  
Anabolic Androgenic Steroids ◽  
Endocrine Disorders ◽  
Androgenic Steroids

Background and Objectives: Anabolic androgenic steroids (AAS), used as a therapy in various diseases and abused in sports, are atherogenic in supraphysiological administration, altering the plasma lipid profile. Taurine, a conditionally-essential amino acid often used in dietary supplements, was acknowledged to delay the onset and progression of atherogenesis, and to mitigate hyperlipidemia. The aim of the present study was to verify if taurine could prevent the alterations induced by concomitant chronic administration of high doses of AAS nandrolone decanoate (DECA) in rats. Materials and Methods: Thirty-two male Wistar rats, assigned to 4 equal groups, were treated for 12 weeks either with DECA (A group), taurine (T group), both DECA and taurine (AT group) or vehicle (C group). Plasma triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), hepatic triglycerides (TGh) and liver non-esterified fatty acids (NEFA) were then determined. Results: DECA elevated TG level in A group vs. control (p = 0.01), an increase prevented by taurine association in AT group (p = 0.04). DECA decreased HDL-C in A group vs. control (p = 0.02), while taurine tended to increase it in AT group. DECA decreased TGh (p = 0.02) in A group vs. control. Taurine decreased TGh in T (p = 0.004) and AT (p < 0.001) groups vs. control and tended to lower NEFA (p = 0.08) in AT group vs. A group. Neither DECA, nor taurine influenced TC and LDL-C levels. Conclusions: Taurine partially prevented the occurrence of DECA negative effects on lipid profile, suggesting a therapeutic potential in several conditions associated with chronic high levels of plasma androgens, such as endocrine disorders or AAS-abuse.

scholarly journals Ginsenoside Rg1 Prevents Chronic Stress-Induced Depression-Like Behaviors and Neuronal Structural Plasticity in Rats

2018 ◽  
Vol 48 (6) ◽  
pp. 2470-2482 ◽  
Author(s):  
Hongluan Yu ◽  
Cuiqin Fan ◽  
Lejin Yang ◽  
Shuyan Yu ◽  
Qiqi Song ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Rat Model ◽  
Basolateral Amygdala ◽  
Therapeutic Potential ◽  
Chronic Administration ◽  
Ultrastructural Changes ◽  
Mild Stress ◽  
Ginsenoside Rg1 ◽  
Neuroprotective Effects ◽  
Neuronal Mechanisms

Background/Aims: Ginsenoside Rg1 has been demonstrated to exhibit neuroprotective effects in various studies. This study aimed to investigate the neuronal mechanisms underlying the neuroprotective and antidepressant-like effects of ginsenoside Rg1 in a rat model of depression. Methods: Chronic unpredictable mild stress was used to induce depression-like behaviors in rats. Transmission electron microscopy was used to observe neuronal synapses within the basolateral amygdala (BLA). The expression of microRNA (miR)-134 in the BLA was verified by real-time quantitative PCR. Finally, the synaptic plasticity-associated proteins CAMP-response element binding protein (CREB) and brain-derived neurotrophic factor (BDNF) were detected by immunoblotting. Results: Results showed that chronic stress effectively induced depression-like behaviors in rats, which were associated with significant ultrastructural changes within BLA neurons. Moreover, chronic stress decreased the expression of miR-134 in the BLA, which was accompanied by decreased phosphorylation of CREB and decreased expression of BDNF. Remarkably, chronic administration of ginsenoside Rg1 (40 mg/kg, i.p., 5 weeks) significantly ameliorated the neuronal structural abnormalities and biochemical changes induced by chronic stress, as well as preventing depression-like behaviors in these rats. Conclusion: Results suggested that ginsenoside Rg1 may exhibit neuroprotection and antidepressant-like effects by activating the CREB-BDNF system within the BLA in this rat model of depression. Amelioration of depression-like behaviors by ginsenoside Rg1 appears to involve modulation of the synapse-associated factor miR-134 within the BLA. Therefore, these findings demonstrate some of the neuronal mechanisms associated with depression and the therapeutic potential of ginsenoside Rg1 for use in the treatment of depression in clinical trials.

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