Importance of Selected Nutrients and Additives in the Feed of Pregnant Sows for the Survival of Newborn Piglets.

This systematic review analyzed the effect of selected nutrients and additives in the feed of pregnant sows on the survival of newborn piglets. We analyzed 720 peer-reviewed publications in English in PubMed® and Web of Science®, dated July 2023 to January 2024, related to the effect of dietary supplementation with fatty acids and various percentages of protein, amino acids, and/or sources of dietary fiber on the offspring of gestating sows. While several papers evaluated the effect of nutrition on gestating sows, only a few delved into the distinct feeding strategies required at each stage of gestation to meet the NRC's nutritional requirements for maternal tissue gain and postnatal neonatal survival and growth. This body of research suggests that as gestation progresses the sow's nutritional requirements increase, as the NRC established, to satisfy their own metabolic needs and those of their fetuses. Additional research is needed to determine an optimal feeding strategy.

Alterations of learning and memory are accompanied by alterations in the expression of 5-HT receptors, glucocorticoid receptor and brain-derived neurotrophic factor in different brain regions of an animal model of depression generated by neonatally male treatment with clomipramine in male rats.

Depressive illness has been associated with impaired cognitive processes accompanied by reduced neurotrophin levels, especially brain-derived neurotrophic factor (BDNF), and dysfunctions in the hypothalamic-pituitary-adrenal (HPA) axis. In addition, depression is characterized by a decreased functioning of the serotonergic system due to changes in the activity or expression of its receptors including, most significantly, 5-HT1A, 5-HT2A, and 5-HT3 in brain regions that regulate mood, emotions, and memory, such as the prefrontal cortex, hippocampus, and amygdala. In this regard, rats treated with clomipramine (CMI) in the neonatal stage show depression-like behaviors that persist into adulthood; hence, this constitutes an adequate model of depression for exploring various molecular aspects associated with the etiology of this disorder. This, study, then, was designed to analyze the long-term effects of early postnatal exposure to CMI on the expression of 5-HT1A, 5-HT2A, and 5-HT3 receptors, as well as BDNF and GR in the following brain regions: PFC, amygdala, hippocampus, and hypothalamus, which could be related to alterations in memory and learning, as evaluated using the novel object recognition (NOR) and Morris water maze (MWM). Expression of the 5-HT1A, 5-HT2A, and 5-HT3 receptors, BDNF, and the glucocorticoid receptor (GR) was assessed by RT-qPCR in the four aforementioned brain regions, all of which play important roles in the control of memory and mood. Findings show that neonatal treatment with CMI causes alterations in memory and learning, as indicated by alterations in the results of the MWM and NOR tests. Expression of the 5-HT1A receptor increased in the hippocampus, amygdala, and hypothalamus, but decreased in the PFC, while the 5-HT2A and BDNF receptors decreased their expression in the PFC, amygdala, and hippocampus. There was no change in the expression of the 5-HT3 receptor. In addition, expression of GR in the hippocampus and PFC was low, but increased in the hypothalamus. Taken together, these data show that neonatal CMI treatment produces permanent molecular changes in brain regions related to learning and memory that could contribute to explaining the behavioral alterations observed in this model.

Effects of postnatal exposure to cadmium on male sexual incentive motivation and copulatory behavior: Estrogen and androgen receptors expression in adult brain rat.

There are numerous evidence showing that cadmium (Cd) is an endocrine disruptor that exerts multiple toxic effects at different reproductive levels, including male sexual behavior (MSB). The effect of early exposure to Cd on sexual incentive motivation (SIM) and MSB in adult stage, and the immunoreactivity of receptors for hormones such as estrogens and androgens in brain regions that are relevant for the SIM and MSB display, have not been studied until now. The present study evaluated the effects of 0.5 and 1 mg/kg CdCl2 from day 1-56 of postnatal life on SIM and MSB in adults rats, as well as serum testosterone concentrations, Cd concentration in blood, testis, and brain areas, and the immunoreactivity in estrogen receptors (ER-α and -ß), and androgen receptor (AR) in the olfactory bulbs (OB), medial preoptic area (mPOA), and medial amygdala (MeA). Our results showed that both doses of Cd decreased SIM and MSB, accompanied by low serum concentrations of testosterone. Also, there was a significant reduction in immunoreactivity of ER-α and AR in mPOA, and a significant reduction in AR in MeA on male rats treated with Cd 1 mg/kg. These results show that exposure to high doses of Cd in early postnatal life could alter the correct integration of hormonal signals in the brain areas that regulate and display SIM and MSB in adult male rats.

Therapeutic treatment with fluoxetine using the chronic unpredictable stress model induces changes in neurotransmitters and circulating miRNAs in extracellular vesicles.

The most widely prescribed antidepressant, fluoxetine (FLX), is known for its antioxidant and anti-inflammatory effects when administered post-stress. Few studies have evaluated the effects of FLX treatment when chronic stress has induced deleterious effects in patients. Our objective was to evaluate FLX treatment (20 mg/kg/day, i.v.) once these effects are manifested, and the drug's relation to extracellular circulating microRNAs associated with inflammation, a hedonic response (sucrose intake), the forced swim test (FST), and corticosterone levels (CORT) and monoamine concentrations in limbic areas. A group of Wistar rats was divided into groups: Control; FLX; CUMS (for six weeks of exposure to chronic, unpredictable mild stress); and CUMS + FLX, a mixed group. After CUMS, the rats performed the FST, and serum levels of CORT and six microRNAs (miR-16, -21, -144, -155, -146a, -223) were analyzed, as were levels of dopamine, noradrenaline, and serotonin in the prefrontal cortex, hippocampus, and hypothalamus. CUMS reduced body weight, sucrose intake, and hippocampal noradrenaline levels, but increased CORT, immobility behavior on the FST, dopamine concentrations in the prefrontal cortex, and all miRNAs except miR-146a expression. Administering FLX during CUMS reduced CORT levels and immobility behavior on the FST and increased the expression of miR-16, -21, -146a, -223, and dopamine. FLX protects against the deleterious effects of stress by reducing CORT and has an antidepressant effect on the FST, with minimally-modified neurotransmitter levels. FLX increased the expression of miRNAs as part of the antidepressant effect. It also regulates both neuroinflammation and serotoninergic neurotransmission through miRNAs, such as the miR-16.

Role of the MicroRNAs in the Pathogenic Mechanism of Painful Symptoms in Long COVID: Systematic Review.

The ongoing pandemic of COVID-19 has caused more than 6.7 million tragic deaths, plus, a large percentage of people who survived it present a myriad of chronic symptoms that last for at least 6 months; this has been named as long COVID. Some of the most prevalent are painful symptoms like headache, joint pain, migraine, neuropathic-like pain, fatigue and myalgia. MicroRNAs are small non-coding RNAs that regulate genes, and their involvement in several pathologies has been extensively shown. A deregulation of miRNAs has been observed in patients with COVID-19. The objective of the present systematic review was to show the prevalence of chronic pain-like symptoms of patients with long COVID and based on the expression of miRNAs in patients with COVID-19, and to present a proposal on how they may be involved in the pathogenic mechanisms of chronic pain-like symptoms. A systematic review was carried out in online databases for original articles published between March 2020 to April 2022; the systematic review followed the PRISMA guidelines, and it was registered in PROSPERO with registration number CRD42022318992. A total of 22 articles were included for the evaluation of miRNAs and 20 regarding long COVID; the overall prevalence of pain-like symptoms was around 10 to 87%, plus, the miRNAs that were commonly up and downregulated were miR-21-5p, miR-29a,b,c-3p miR-92a,b-3p, miR-92b-5p, miR-126-3p, miR-150-5p, miR-155-5p, miR-200a, c-3p, miR-320a,b,c,d,e-3p, and miR-451a. The molecular pathways that we hypothesized to be modulated by these miRNAs are the IL-6/STAT3 proinflammatory axis and the compromise of the blood-nerve barrier; these two mechanisms could be associated with the prevalence of fatigue and chronic pain in the long COVID population, plus they could be novel pharmacological targets in order to reduce and prevent these symptoms.

Effect of thiamine pyrophosphate on the characteristics of farrowing and piglet vitality.

Asphyxia is considered the main non-infectious cause of prepartum mortality in swine, as well as an important factor that negatively affects neonatal vitality and can trigger physiological and metabolic disorders. Hence, the search for pharmacological protocols to reduce the harmful effects of asphyxia is a key area of research. Recent observations show that administering thiamine pyrophosphate (TPP) prior to a hypoxic event in certain species (rabbits, rats) has a neuroprotector effect that preserves energy metabolism under hypoxic conditions. Given this, the objective of this study was to evaluate a prophylactic protocol in high- and low-vitality neonate piglets based on TPP's effect on physiological and metabolic responses, body temperature, and weight. A total of 149 piglets born from 15 multiparous sows were used. The dams were randomly divided into two groups: control (NaCl 0.9%) and TPP (25 ml of TTP) administered 24 and 12 h before the expected farrowing date. The following reproductive variables of the sows were recorded: duration of farrowing, total number of piglets born per litter, number of liveborn piglets per litter, number of stillbirths and mummified fetuses at birth, and number of live piglets at weaning. In addition, the expulsion interval and vitality of all neonates were evaluated, body temperatures were recorded at ten intervals, and physiological profiles (blood gases, electrolytes, glucose) were registered for each neonate. Results show that the TPP-treated sows had shorter farrowing duration (P = 0.0060) and higher percentage of high-vitality neonates (60%). Moreover, their offspring exhibited greater vitality, fewer imbalances in their physiological and metabolic profiles, and greater weight gain at weaning (P < 0.0001). Findings suggest that administering TPP exerts a protective effect when hypoxic events occur, though this differs from results obtained with rat pups, where applying TPP after such events did not provide protection from asphyxia-induced damage. These differences may be due to the moment at which TPP was applied. The application time we selected was distinct from the procedure followed with rats because it was based on a dataset that describes the influence of administering TPP as a prophylactic treatment before a hypoxic event. Prophylactic administration of TPP to sows at the end of gestation exerted a neuroprotective effect on neonatal vitality and gas exchanges and energy metabolism in the offspring that were reflected in the greater weekly weight gain in those piglets.

Neuropathic Pain in Parkinson's Disease.

Pain is a well-recognized and important non-motor manifestation in Parkinson disease (PD). Painful or unpleasant sensations in PD can be classified as musculoskeletal, dystonia, akathisia, radicular, and central or primary pain; the last two are associated with neuropathic pain. Particularly, neuropathic pain in PD has not been fully clarified; therefore, it goes somewhat unnoticed, and the affected patients do not receive adequate pain treatment. The main purpose of this literature review was to identify the incidence of neuropathic pain in PD and the involvement of dopamine of this type of pain by the integration of different lines of investigation. In this review, a search was conducted using PubMed, ProQuest, EBSCO, Medline, EMBASE, and the Science Citation index for studies evaluating pain in patients with PD. The inclusion criteria were as follows: original articles that evaluated incidence and possible mechanism of neuropathic, central, and radicular pain in PD. Nine studies related to the incidence of neuropathic pain in PD suggest the activation of cerebral areas, such as the cortex, striatum, amygdala, thalamus, raphe nuclei, and locus coeruleus. Neuropathic pain is related to altered levels of dopamine, serotonin, and norepinephrine; these neurotransmitters are related to the sensitive and emotional dimensions of pain. Dopamine could cause hypersensitivity to pain, either indirectly through modulatory effects on affective pain processing and/or directly by affecting the neural activity in key areas of the brain that modulate pain. A considerable proportion of patients with PD suffer neuropathic pain; however, it has been disregarded, this has led to an inability to achieve an adequate treatment and a decrease in pain to improve the quality of life of these patients. We consider that neuropathic pain in PD is possibly induced by neurophysiological changes due to the degradation of dopaminergic neurons.

Sperm Dysfunction in the Testes and Epididymides due to Overweight and Obesity Is Not Caused by Oxidative Stress.

Obesity is a condition that has been linked to male infertility. The current hypothesis regarding the cause of infertility is that sperm are highly sensitive to reactive oxygen species (ROS) during spermatogenesis in the testes and transit through the epididymides, so the increase in ROS brought on by obesity could cause oxidative stress. The aim of this study was to evaluate whether the activity of the enzymes catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPX) is capable of counteracting oxidative stress in sperm. The male Wistar rat was used as an overweight and obesity model, and analysis of fertility in these groups was carried out including the control group. Serum testosterone levels were determined, and the scrotal fat, testes, and epididymides were extracted. The epididymides were separated ini0 3 principal parts (caput, corpus, and cauda) before evaluating sperm viability, sperm morphology, damage to desoxyribonucleic acid of the sperm, and ROS production. The protein content and specific activity of the three enzymes mentioned above were evaluated. Results showed a gain in body weight and scrotal fat in the overweight and obese groups with decreased parameters for serum testosterone levels and sperm viability and morphology. Fertility was not greatly affected and no DNA integrity damage was found, although ROS in the epididymal sperm increased markedly and Raman spectroscopy showed a disulfide bridge collapse associated with DNA. The specific activities of CAT and GPX increased in the overweight and obesity groups, but those of SOD did not change. The amounts of proteins in the testes and epididymides decreased. These findings confirm that overweight and obesity decrease concentrations of free testosterone and seem to decrease protein content, causing poor sperm quality. Implications. An increase in scrotal fat in these conditions fosters an increase of ROS, but the increase of GPX and CAT activity seems to avoid oxidative stress increase in the sperm without damaging your DNA.

Potential Neuroprotective Effect of Cannabinoids in COVID-19 Patients.

The global pandemic caused by the SARS-CoV-2 virus began in early 2020 and is still present. The respiratory symptoms caused by COVID-19 are well established. However, neurological manifestations that may result from direct or indirect neurological damage after SARS-CoV-2 infection have been reported frequently. The main proposed pathophysiological processes leading to neurological damage in COVID-19 are cerebrovascular disease and indirect inflammatory/ autoimmune origin mechanisms. A growing number of studies confirm that neuroprotective measures should be maintained in COVID-19 patients. On the other hand, cannabinoids have been the subject of various studies that propose them as potentially promising drugs in chronic neurodegenerative diseases due to their powerful neuroprotective potential. In this review, we addresses the possible mechanism of action of cannabinoids as a neuroprotective treatment in patients infected by SARS-CoV-2. The endocannabinoid system is found in multiple systems within the body, including the immune system. Its activation can lead to beneficial results, such as a decrease in viral entry, a reduction of viral replication, and a reduction of pro-inflammatory cytokines such as IL-2, IL-4, IL-6, IL-12, TNF-α, or IFN-c through CB2R expression induced during inflammation by SARS-CoV-2 infection in the central nervous system.

Depression and Pain: Use of Antidepressants.

BACKGROUND: Emotional disorders are common comorbid affectations that exacerbate the severity and persistence of chronic pain. Specifically, depressive symptoms can lead to an excessive duration and intensity of pain. Clinical and preclinical studies have been focused on the underlying mechanisms of chronic pain and depression comorbidity and the use of antidepressants to reduce pain. AIM: This review provides an overview of the comorbid relationship of chronic pain and depression, the clinical and pre-clinical studies performed on the neurobiological aspects of pain and depression, and the use of antidepressants as analgesics. METHODS: A systematic search of literature databases was conducted according to pre-defined criteria. The authors independently conducted a focused analysis of the full-text articles. RESULTS: Studies suggest that pain and depression are highly intertwined and may co-exacerbate physical and psychological symptoms. One important biochemical basis for pain and depression focuses on the serotonergic and norepinephrine system, which have been shown to play an important role in this comorbidity. Brain structures that codify pain are also involved in mood. It is evident that using serotonergic and norepinephrine antidepressants are strategies commonly employed to mitigate pain Conclusion: Literature indicates that pain and depression impact each other and play a prominent role in the development and maintenance of other chronic symptoms. Antidepressants continue to be a major therapeutic tool for managing chronic pain. Tricyclic antidepressants (TCAs) are more effective in reducing pain than Selective Serotonin Reuptake Inhibitors (SSRIs) and Serotonin- Noradrenaline Reuptake Inhibitors (SNRIs).

Sleep Disruption Worsens Seizures: Neuroinflammation as a Potential Mechanistic Link.

Sleep disturbances, such as insomnia, obstructive sleep apnea, and daytime sleepiness, are common in people diagnosed with epilepsy. These disturbances can be attributed to nocturnal seizures, psychosocial factors, and/or the use of anti-epileptic drugs with sleep-modifying side effects. Epilepsy patients with poor sleep quality have intensified seizure frequency and disease progression compared to their well-rested counterparts. A better understanding of the complex relationship between sleep and epilepsy is needed, since approximately 20% of seizures and more than 90% of sudden unexpected deaths in epilepsy occur during sleep. Emerging studies suggest that neuroinflammation, (e.g., the CNS immune response characterized by the change in expression of inflammatory mediators and glial activation) may be a potential link between sleep deprivation and seizures. Here, we review the mechanisms by which sleep deprivation induces neuroinflammation and propose that neuroinflammation synergizes with seizure activity to worsen neurodegeneration in the epileptic brain. Additionally, we highlight the relevance of sleep interventions, often overlooked by physicians, to manage seizures, prevent epilepsy-related mortality, and improve quality of life.

Sleep deprivation induces oxidative stress in the liver and pancreas in young and aging rats.

The aging process is characterized by a gradual impairment generally caused by oxidative stress and, more specifically, sleep deprivation, which induces oxidative stress in the brain. The objective of this study was to assess the effect of three types of paradoxical sleep deprivation (PSD): 96 h of PSD (96PSD group); 192 h of PSD (192PSD group); 192 h of PSD followed by a recovery period of 20 days (192PSD + Recovery group) on an oral glucose tolerance test (OGTT), lipid peroxidation (LPO), and superoxide dismutase (SOD) and catalase (CAT) activities in the liver and pancreas of young (3-month-old) and adult (14-month-old) rats. The 96PSD and 192PSD groups of young rats showed lower glucose levels on the OGTT than the control group. In the adult rats, only the 96PSD group had lower glucose levels than the control group. However, the areas under the curve for the young and adult 192 and 192PSD + Recovery groups showed significant differences. Both LPO and SOD increased in the 192PSD and 192PSD + Recovery groups, but CAT decreased in the liver of young rats in the 192PSD group. Regarding the pancreas, LPO and SOD levels increased after 96 h of PSD. In adult animals, CAT decreased in the liver after 96 and 192 h of PSD, while LPO and SOD increased in the pancreas of the 192PSD and PSD + Recovery groups. Differences in the SOD and CAT activities in the liver and SOD activities in the pancreas were also observed between the young and adult rats and maintained across all the PSD groups. In conclusion, PSD induced differential responses that appeared to depend on the duration of the induced condition, the animals' age, and the tissue analyzed. It was found that adult rats were more susceptible to the effects of PSD than young rats.

Low frequency vortex magnetic field reduces amyloid ß aggregation, increase cell viability and protect from amyloid ß toxicity.

Plaques formed by abnormal accumulation of amyloid ß-peptide (Aß) lead to onset of Alzheimer's disease (AD). Pharmacological treatments do not reduce Aß aggregation neither restore learning and memory. Noninvasive techniques have emerged as an alternative to treat AD, such as stimulation with electromagnetic fields (EMF) that decrease Aß deposition and reverses cognitive impairment in AD mice, even though some studies showed side effects on parallel magnetic fields stimulation. As a new approach of magnetic field (MF) stimulation, vortex magnetic fields (VMF) have been tested inducing a random movement of charged biomolecules in cells, promoting cell viability and apparently safer than parallel magnetic fields. In this study we demonstrate the effect of VMF on Aß aggregation. The experimental strategy includes, i) design and construction of a coil capable to induce VMF, ii) evaluation of VMF stimulation on Aß peptide induced-fibrils-formation, iii) evaluation of VMF stimulation on SH-SY5Y neuroblastoma cell line in the presence of Aß peptide. We demonstrated for the first time that Aß aggregation exposed to VMF during 24 h decreased ~ 86% of Aß fibril formation compared to control. Likewise, VMF stimulation reduced Aß fibrils-cytotoxicity and increase SH-SY5Y cell viability. These data establish the basis for future investigation that involve VMF as inhibitor of Aß-pathology and indicate the therapeutic potential of VMF for AD treatment.

Delay in puberty indices of Wistar rats caused by Cadmium. Focus on the redox system in reproductive organs.

Puberty is a transitional period from juvenile stage to adulthood, followed by the functional maturation of gonads and reproductive organs. This period is sensitive to environmental pollutants like cadmium (Cd), a heavy metal that represents a serious health risk. Cd is an endocrine disruptor that interferes with reproduction by causing oxidative stress in the reproductive organs, affecting the sexual function and decreasing testosterone (T) levels. However, little research has been done on the effects of Cd on puberty markers and antioxidant systems. In this study, we evaluated the effects of Cd on puberty markers: preputial separation, testes descent and T levels, and the antioxidant activity (SOD, CAT, GSH/GSSG and TAC) in the seminal vesicles, testis and epididymis. Male Wistar pups were treated with 1 mg/kg Cd or saline solution by i.p. injection from day 1 to 35; the other treatment was administrated for 49 days. At the end of treatment, the animals were sacrificed, and the tissues of interest dissected, weighed and prepared for the respective assays. Cd treated rats from birth to puberty showed a delay onset in the puberty markers and a low weight in reproductive organs. Also, Cd induced differential effects on the redox system in reproductive organs and decreased T levels, these effects played a pivotal role in the delay of puberty markers onset (testes descent and preputial separation), affecting the development and sexual maturity of the male rats.

Neuroendocrine effects of cadmium exposure on male reproductive functions.

In industrialized countries, the use of Cadmium (Cd) produces a form of anthropogenic pollution. Hence, exposure by human populations is becoming a public health problem. With a half-life of up to 40 years, cadmium is now a topic of great interest due to its role as an endocrine disruptor and its effects on male reproduction. Cd's diverse toxic mechanisms are based on its capacity to mimic divalent ions -calcium, zinc, iron- that participate in physiological processes. It alters the mitochondrial function and generates the production of free radicals that can induce apoptosis. In male reproduction, Cd alters the precise coordination of the hypothalamic-hypophysis-testis axis (HHT), resulting in the loss of testicular functions like steroidogenesis, spermatogenesis and the onset of puberty, sexual maturity, sexual behavior and fertility. Exposure to Cd may even cause changes in the immune system that are associated with the reproductive system. This review analyses the state of the question regarding Cd's cellular and physiological mechanisms and the effects of this heavy metal on the neuroendocrine regulation of male reproduction.

Pubertal stress decreases sexual motivation and supresses the relation between cerebral theta rhythms and testosterone levels in adult male rats.

This study evaluated the effect of stress during puberty on sexual motivation and the correlation between serum testosterone levels (T) and the absolute power of the theta electroencephalographic rhythms, recorded in the medial prefrontal cortex (mPFC) and basolateral amygdala (BLA) of adult male rats. Thirty males of the stressed group (SG, housed 1 per cage from days 25-50) and 30 controls (CG, housed 5 per cage), were tested in copulatory interactions at 90 days of age. The above mentioned physiological parameters were obtained during the awake-quiet state in a sub-group without sexual motivation (WSM, n = 15, stimulated with a nonreceptive female) and a sub-group with sexual motivation (SM, n = 15, stimulated with a receptive-female). Pearson correlations (r) between these parameters were calculated for each sub-group and brain structure and then compared between sub-groups. SG presented higher mount and intromission latencies than CG. While CG-WSM showed a positive r between T levels and theta band (0.23-0.59), those CG-SM presented a negative r (-0.23 to -0.67). An r that tended towards zero (-0.31 to 0.29) was obtained in both stressed sub-groups. This study shows that pubertal stress suppresses the relation between serum T levels and theta rhythms in the mPFC and BLA in adult male rats. This is one of the first studies evaluating the association between these two physiological parameters specifically in the context of sexual motivation; thus increasing our understanding of the effect of pubertal stress on prefrontal-amygdaline functioning during the sexually-motivated state in male rats.

Acute administration of levetiracetam in tonic pain model modulates gene expression of 5HT1A and 5HT7 receptors in the thalamus of rats (Rattus norvergicus).

The nociceptive effect of Levetiracetam (LEV) on the expression of 5-HT1A and 5-HT7 receptors found in the thalamus was evaluated. Thirty-six male rats (Wistar) were randomized into six groups: in the Control group without treatment; LEV50 group LEV was administered in a single dose of 50 mg/kg i.g.; in the LEV300 group LEV dose of 300 mg/kg i.g.; in the FORMALIN group the formalin test was performed; in the LEV50/FORMALIN group LEV dose of 50 mg/kg i.g and the formalin test was performed; in the LEV300/FORMALIN group LEV dose of 300 mg/kg i.g and the formalin test was performed, subsequently the thalamus was dissected in all groups. In the formalin tests LEV exhibited an antinociceptive effect in the LEV300/FORMALIN group (p < 0.05) and a pronociceptive effect in the LEV50/FORMALIN group (p < 0.001). The results obtained by Real-time PCR confirmed the expression of the 5-HT1A and 5-HT7 receptors in the thalamus, 5-HT1A receptors increased significantly in the FORMALIN group and the LEV300/FORMALIN group (p < 0.05). 5-HT7 receptors are only over expressed at a dose of 300 mg/Kg of LEV with formalin (p < 0.05). This suggests that LEV modulates the sensation of pain by controlling the expression of 5-HT1A and 5-HT7 in a tonic pain model, and that changes in the expression of 5-HT1A and 5-HT7 receptors are associated with the sensation of pain, furthermore its possibility to be used in clinical treatments for pain.

Electroencephalographic changes and testosterone levels in a pubertal stress animal model: effects on adult sexual motivation / Cambios electroencefalográficos y niveles de testosterona en un modelo animal de estrés puberal: efectos sobre la motivación sexual adulta

Abstract Introduction Stress during puberty exerts long-term effects on endocrine systems and brain structures, such as the prefrontal cortex (PFC) and basolateral amygdala (BLA), two cerebral areas that participate in modulating sexual behavior and whose functioning is regulated by androgenic hormones. Objective To evaluate the effect of pubertal stress due to social isolation on the sexual motivation, serum testosterone levels, and electroencephalographic activity (EEG) of the PFC and BLA in male rats. Method Sixty sexually-experienced male rats were used. Thirty were stressed by social isolation during puberty (SG, housed 1 per cage, postnatal days 25-50); the other 30 formed the control group (CG, 5 per cage). All rats were implanted bilaterally with stainless steel electrodes in the PFC and BLA. EEGs were recorded during the awake-quiet state in two conditions: without sexual motivation (WSM), and with sexual motivation (SM). After EEG recording, the rats were sacrificed by decapitation to measure their testosterone levels. Results SG showed lower sexual motivation and testosterone levels, but higher amygdaline EEG activation in the presence of a receptive female, while CG showed higher prefrontal EEG activation. Discussion and conclusion It is probable that the decreased testosterone levels resulting from pubertal stress affected prefrontal and amygdaline functionality and, hence, sexual motivation. These data could explain some of the hormonal and cerebral changes associated with stress-induced sexual alterations, though this suggestion requires additional clinical and animal research.

Resumen Introducción El estrés durante la pubertad ejerce efectos a largo plazo sobre sistemas endocrinos y estructuras cerebrales como corteza prefrontal (CPF) y amígdala basolateral (ABL). Ambas estructuras participan en la modulación de la conducta sexual y su funcionamiento es regulado por andrógenos. Objetivo Evaluar los efectos del estrés puberal por aislamiento social sobre la motivación sexual, los niveles séricos de testosterona y la actividad electroencefalográfica (EEG) de la CPF y ABL en ratas macho. Método Se utilizaron sesenta ratas macho sexualmente expertas, 30 fueron estresadas por aislamiento social durante la pubertad (GE, hospedados 1 por caja, días 25 al 50 postnatal), y el resto conformó el grupo control (GC, hospedados 5 por caja). Las ratas fueron implantadas bilateralmente en la CPF y ABL y el EEG fue registrado durante estado vigilia-quieto en dos condiciones: sin motivación sexual (SMS) y con motivación sexual (MS). Finalmente, las ratas se sacrificaron por decapitación para medir los niveles de testosterona. Resultados El GE presentó menor motivación sexual, menores niveles de testosterona y, en presencia de una hembra receptiva, presentaron una mayor activación EEG amigdalina, mientras que el GC mostró una mayor activación EEG prefrontal. Discusión y conclusión Es probable que la disminución de los niveles de testosterona como resultado del estrés puberal haya afectado la funcionalidad prefrontal y amigdalina y, por ende, la motivación sexual. Estos datos pudieran explicar algunos de los cambios hormonales y cerebrales asociados con alteraciones sexuales producidas por estrés. Esta propuesta deberá explorarse en futuras investigaciones animales y clínicas.

Neonatal treatment with clomipramine modifies the expression of estrogen receptors in brain areas of male adult rats.

The participation of estrogens in depression has been well recognized. To exert its effects, estradiol binds mainly to estrogen receptors ESR1 and ESR2 (α and ß, respectively), expressed in brain regions including the hippocampus, limbic regions and hypothalamic nuclei. In rodents, modified estrogen receptors expression in brain areas have been implicated in different signs similar to those observed in depressive patients. Neonatal clomipramine (CMI) treatment is a pharmacological manipulation that generates behavioral and neurochemical changes that persist throughout adulthood and resemble human depression. The aim of this study was to analyze whether CMI neonatal treatment modifies the expression of nuclear ESR1 and ESR2 in the hippocampus, amygdala basolateral (BLA), amygdala medial (MeA), hypothalamic medial preoptic area (mPOA) and raphe nucleus in male rats. Our results indicate that CMI treatment significantly induced an mRNA increase of ESR1 in the hypothalamus, additionally produce a reduction in the mRNA ESR2 expression in raphe accompanied of an increase in hypothalamus and amygdala. CMI treated rats show more immunorreactive cells to ESR1 (ESR1-ir) in mPOA, BLA, MeA, together with a reduction of these cells in the hippocampal CA1 region. Moreover, an increase in the number of immunorreactive cells to ESR2 (ESR2-ir), in BLA and MeA, was observed in CMI treated rats. Additionally, the hippocampal CA2 region and raphe nucleus showed a decrease in these cells. Also, neonatal CMI treatment induced a decrease in the number of cells of the pyramidal layer in CA1. Overall, the results suggest that neonatal CMI treatment in rats (during brain development) induces changes in estrogen receptors in different brain areas involved with the regulation of depressive-like behaviors.

Caffeine administered to pregnant sows improves piglet vitality, gas exchange and body weight gain.

Intra-partum asphyxia is the most common non-infectious etiology limiting the performance of neonate piglets. Previous studies indicate caffeine (orally and subcutaneously) reverses the effects of intra-partum asphyxia in neonate piglets. In this study, there was investigation of whether use of a novel therapeutic protocol for administering caffeine subcutaneously to pregnant sows would improve the newborn piglets' vitality, physio-metabolic profiles and body weight gain. Sows were randomly divided into two groups (n = 10 each). Caffeine or NaCl 0.9% was administered 2 days pre-farrowing. Physio-metabolic profiles were measured using blood from the anterior vena cava. The vitality of piglets was evaluated immediately after birth. Piglets (n = 180) were weighed at birth and on days 7, 14 and 21 of lactation. Caffeine positively affected the vitality of the piglets, as indicated by greater vitality scores than that for the control group (8.72 ±â€¯0.12 compared with 7.28 ±â€¯0.16, P < 0.001). Metabolic values were similar between groups, but pO2 values were greater in the piglets with greater vitality scores treated with caffeine (19.10 ±â€¯0.82 compared with 14.49 ±â€¯1.42, P < 0.01), indicating increased respiratory rates. Body weight gain at day 21 was greater in the piglets treated with caffeine that had greater vitality scores than the control piglets having greater vitality scores (6.87 ±â€¯0.18 compared with 6.52 ±â€¯0.25 kg, P < 0.05). Caffeine administration before birth improves the vitality and respiratory capacity of piglets, increasing their adaptation to extra-uterine environment.