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Introduction: Motor neurons (MNs) within the nucleus ambiguus innervate the skeletal muscles of the larynx, pharynx, and oesophagus. These muscles are activated during vocalisation and swallowing and must be coordinated with several respiratory and other behaviours. Despite many studies evaluating the projections and orientation of MNs within the nucleus ambiguus, there is no quantitative information regarding the dendritic arbours of MNs residing in the compact, and semicompact/loose formations of the nucleus ambiguus.. Methods: In female and male Fischer 344 rats, we evaluated MN number using Nissl staining, and MN and non-MN dendritic morphology using Golgi-Cox impregnation Brightfield imaging of transverse Nissl sections (15 µm) were taken to stereologically assess the number of nucleus ambiguus MNs within the compact and semicompact/loose formations. Pseudo-confocal imaging of Golgi-impregnated neurons within the nucleus ambiguus (sectioned transversely at 180 µm) was traced in 3D to determine dendritic arbourisation. Results: We found a greater abundance of MNs within the compact than the semicompact/loose formations. Dendritic lengths, complexity, and convex hull surface areas were greatest in MNs of the semicompact/loose formation, with compact formation MNs being smaller. MNs from both regions were larger than non-MNs reconstructed within the nucleus ambiguus. Conclusion: Adding HBLS to the diet could be a potentially effective strategy to improve horses' health.

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Introduction: Stress is a pervasive health concern known to induce physiological changes, particularly impacting the vulnerable hippocampus and the morphological integrity of its main residing cells, the hippocampal neurons. Eye Movement Desensitization and Reprocessing (EMDR), initially developed to alleviate emotional distress, has emerged as a potential therapeutic/preventive intervention for other stress-related disorders. This study aimed to investigate the impact of Acute Variable Stress (AVS) on hippocampal neurons and the potential protective effects of EMDR. Methods: Rats were exposed to diverse stressors for 7 days, followed by dendritic morphology assessment of hippocampal neurons using Golgi-Cox staining. Results: AVS resulted in significant dendritic atrophy, evidenced by reduced dendritic branches and length. In contrast, rats receiving EMDR treatment alongside stress exposure exhibited preserved dendritic morphology comparable to controls, suggesting EMDR's protective role against stressinduced dendritic remodeling. Conclusions: These findings highlight the potential of EMDR as a neuroprotective intervention in mitigating stress-related hippocampal alterations.

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Previous studies demonstrate that ethanol dependence induced by repeating cycles of chronic intermittent ethanol vapor exposure (CIE) followed by protracted abstinence produces significant gray matter damage via myelin dysfunction in the rodent medial prefrontal cortex (mPFC) and alterations in neuronal excitability in the mPFC and the dentate gyrus (DG) of the hippocampus. Specifically, abstinence-induced neuroadaptations have been associated with persistent elevated relapse to drinking. The current study evaluated the effects of forced abstinence for 1 day (d), 7 d, 21 d, and 42 d following seven weeks of CIE on synaptic plasticity proteins in the mPFC and DG. Immunoblotting revealed reduced expression of CaMKII in the mPFC and enhanced expression of GABAA and CaMKII in the DG at the 21 d time point, and the expression of the ratio of GluN2A/2B subunits did not change at any of the time points studied. Furthermore, cognitive performance via Pavlovian trace fear conditioning (TFC) was evaluated in 3 d abstinent rats, as this time point is associated with negative affect. In addition, the expression of the ratio of GluN2A/2B subunits and a 3D structural analysis of neurons in the mPFC and DG were evaluated in 3 d abstinent rats. Behavioral analysis revealed faster acquisition of fear responses and reduced retrieval of fear memories in CIE rats compared to controls. TFC produced hyperplasticity of pyramidal neurons in the mPFC under control conditions and this effect was not evident or blunted in abstinent rats. Neurons in the DG were unaltered. TFC enhanced the GluN2A/2B ratio in the mPFC and reduced the ratio in the DG and was not altered by abstinence. These findings indicate that forced abstinence from CIE produces distinct and divergent alterations in plasticity proteins in the mPFC and DG. Fear learning-induced changes in structural plasticity and proteins contributing to it were more profound in the mPFC during forced abstinence.

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The objective of this chapter is to provide an overview of the methods used to investigate the connectivity and structure of the nervous system. These methods allow neuronal cells to be categorized according to their location, shape, and connections to other cells. The Golgi-Cox staining gives a thorough picture of all significant neuronal structures found in the brain that may be distinguished from one another. The most significant characteristic is its three-dimensional integrity since all neuronal structures may be followed continuously from one part to the next. Successions of sections of the brain's neurons are seen with the Golgi stain. The Golgi method is used to serially segment chosen brain parts, and the resulting neurons are produced from those sections.

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The hippocampal complex of birds is a narrow-curved strip of tissue that plays a crucial role in learning, memory, spatial navigation, and emotional and sexual behavior. This study was conducted to evaluate the effect of unpredictable chronic mild stress in multipolar neurons of 3-, 5-, 7-, and 9-week-old chick's hippocampal complex. This study revealed that chronic stress results in neuronal remodeling by causing alterations in dendritic field, axonal length, secondary branching, corrected spine number, and dendritic branching at 25, 50, 75, and 100 µm. Due to stress, the overall dendritic length was significantly retracted in 3-week-old chick, whereas no significant difference was observed in 5- and 7-week-old chick, but again it was significantly retracted in 9-week-old chick along with the axonal length. So, this study indicates that during initial days of stress exposure, the dendritic field shows retraction, but when the stress continues up to a certain level, the neurons undergo structural modifications so that chicks adapt and survive in stressful conditions. The repeated exposure to chronic stress for longer duration leads to the neuronal structural disruption by retraction in the dendritic length as well as axonal length. Another characteristic which leads to structural alterations is the dendritic spines which significantly decreased in all age groups of stressed chicks and eventually leads to less synaptic connections, disturbance in physiology, and neurology, which affects the learning, memory, and coping ability of an individual.

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Over time, scientists have been fascinated by the complex connections among nutrition, brain development, and behavior. It's been well understood that the brain's peak performance relies on having the right nutrients available. Thus, nutritional insufficiency, where an organism lacks vital nutrients crucial for optimal growth and function, can upset the body's balance, potentially triggering stress responses. However, our grasp of how the brain reacts to insufficient nutrition, particularly in avian species like domestic chickens, has shown inconsistencies in our understanding. Domestic chickens have frequently served as subjects for studying memory and learning, primarily focusing on the hippocampus-a region highly responsive to environmental changes. Yet, another critical brain region, the parahippocampal region, integral to memory and spatial cognition, had received relatively little attention concerning the consequences of inadequate nutrition and hydration. To address this knowledge gap, our study sought to investigate the impact of stress induced by nutritional insufficiency on the neuronal cells within the region parahippocampalis in two distinct age groups of domestic chickens, Gallus gallus domesticus: fifteen and thirty days old. We employed the Golgi-Cox-Impregnation technique to explore whether the structural characteristics of neuronal cells, specifically the dendritic spines, underwent changes under transient stressful conditions during these crucial developmental stages. The results were intriguing. Stress evidently induced observable alterations in the dendritic spines of the parahippocampal neuronal cells, with the extent of these changes being age-dependent. In fifteen-day-old chickens, stress prompted substantial modifications in the dendritic spines of parahippocampal multipolar and pyramidal neurons. In contrast, among thirty-day-old chickens, the response to stress was less comprehensive, with only specific parahippocampal multipolar neurons displaying such alterations. These findings underscored the influential role of stress in reshaping the structure of parahippocampal neurons and emphasized the importance of considering age when studying the impact of stress on the brain. Through this research, we aim to enhance our understanding of the intricate interplay between stress, brain structure, and the critical role of adequate nutrition, especially during pivotal developmental stages. Our future research objectives include a deeper investigation into the intracellular events including cellular and molecular mechanisms precipitating these changes and determining whether these alterations have downstream effects on crucial brain functions like learning and memory.

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The avian dorsomedial surface of the cerebral hemisphere is occupied by the hippocampal complex (HCC), which plays an important role in learning, memory, cognitive functions, and regulating instinctive behavior patterns. The objective of the study was to evaluate the effect of chronic mild stress (CMS) in 4, 6, and 8 weeks and after chronic stress removal (CSR) in 6 and 8 weeks, on neuronal plasticity in HCC neurons of chicks through the Golgi-Cox technique. Further, behavioral study and open field test were conducted to test of exploration or of anxiety. The study revealed that the length of CMS and CSR groups shows a similar pattern as in nonstressed (NS) chicks, while weight shows nonsignificant decrease due to CMS as compared to NS and after CSR. The behavioral test depicts that the CMS group took more time to reach the food as compared to the NS and CSR groups. Due to CMS, the dendritic field of multipolar neurons shows significant decrease in 4 weeks, but in 6- and 8-week-old chicks, the multipolar, pyramidal, and stellate neurons depict significant decrease, whereas after CSR all neurons show significant increase in 8-week-old chicks. In 4- and 8-week-old chicks, all neurons depict significant decrease in their spine number, whereas in 6 weeks only multipolar neurons show significant decrease, but after CSR significant increase in 8-week-old chicks was observed. The study revealed that HCC shows continuous neuronal plasticity, which plays a significant role in normalizing and re-establishing the homeostasis in animals to survive.

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Status Epilepticus (SE) is a distributed network disorder, which involves the hippocampus and extra-hippocampal structures. Epileptogenesis in SE is tightly associated with neurogenesis, plastic changes and neural network reorganization facilitating hyper-excitability. On the other hand, dendritic spines are known to be the excitatory synapse in the brain. Therefore, dendritic spine dynamics could play an intricate role in these network alterations. However, the exact reason behind these structural changes in SE are elusive. In the present study, we have investigated the aforementioned hypothesis in the lithium-pilocarpine treated rat model of SE. We have examined cytoarchitectural and morphological changes using hematoxylin-eosin and Golgi-Cox staining in three different brain regions viz. CA1 pyramidal layer of the dorsal hippocampus, layer V pyramidal neurons of anterior temporal lobe (ATL), and frontal neocortex of the same animals. We observed macrostructural and layer-wise alteration of the pyramidal layer mainly in the hippocampus and ATL of SE rats, which is associated with sclerosis in the hippocampus. Sholl analysis exhibited partial dendritic plasticity in apical and basal dendrites of pyramidal cells as compared to the saline-treated weight-/age-matched control group. These findings indicate that region-specific alterations in dendritogenesis may contribute to the development of independent epileptogenic networks in the hippocampus, ATL, and frontal neocortex of SE rats.

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Iron supplementation previously demonstrated antidepressant-like effects in post-partum rats. The present study evaluates the possible synergistic antidepressant effect of sub-therapeutic dose of iron co-administered with citalopram or imipramine in female Institute of Cancer Research mice. Depression-like symptoms were induced in the forced swim (FST), tail suspension (TST), and open space swim (OSST) tests while open field test (OFT) was used to assess locomotor activity. Mice (n = 8) received iron (0.8-7.2 mg/kg), citalopram (3-30 mg/kg), imipramine (3-30 mg/kg), desferrioxamine (50 mg/kg) or saline in the single treatment phase of each model and subsequently a sub-therapeutic dose of iron co-administered with citalopram or imipramine. Assessment of serum brain derived neurotrophic factor (BDNF) and dendritic spine density was done using ELISA and Golgi staining techniques respectively. Iron, citalopram and imipramine, unlike desferrioxamine, reduced immobility score in the TST, FST and OSST without affecting locomotor activity, suggesting antidepressant-like effect. Sub-therapeutic dose of iron in combination with citalopram or imipramine further enhanced the antidepressant-like effect, producing a more rapid effect when compared to the iron, citalopram or imipramine alone. Iron, citalopram and imipramine or their combinations increased serum BDNF concentration, hippocampal neuronal count and dendritic spine densities. Our study provides experimental evidence that iron has antidepressant-like effect and sub-therapeutic dose of iron combined with citalopram or imipramine produces more rapid antidepressant-like effect. We further show that iron alone or its combination with citalopram or imipramine attenuates the neuronal loss associated with depressive conditions, increases dendritic spines density and BDNF levels. These finding suggest iron-induced neuronal plasticity in the mice brain.

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Facial nerve injury in rats have been widely used to study functional and structural changes that occur in the injured motoneurons and other central nervous system structures related with sensorimotor processing. A decrease in long-term potentiation of hippocampal CA3-to-CA1 commissural synapse has recently been reported related to this peripheral injury. Additionally, it has been found increased corticosterone plasmatic levels, impairment in spatial memory consolidation, and hippocampal microglial activation in animals with facial nerve axotomy. In this work, we analyzed the neuronal morphology of hippocampal CA1 and CA3 pyramidal neurons in animals with either reversible or irreversible facial nerve injury. For this purpose, brain tissues of injured animals sacrificed at different postlesion times, were stained with the Golgi-Cox method and compared with control brains. It was found that both reversible and irreversible facial nerve injury-induced significant decreases in dendritic tree complexity, dendritic length, branch points, and spine density of hippocampal neurons. However, such changes' timing varied according to hippocampal area (CA1 vs. CA3), dendritic area (apical vs. basal), and lesion type (reversible vs. irreversible). In general, the observed changes were transient when animals had the possibility of motor recovery (reversible injury), but perdurable if the recovery from the lesion was impeded (irreversible injury). CA1 apical and CA3 basal dendritic tree morphology were more sensible to irreversible injury. It is concluded that facial nerve injury induced significant changes in hippocampal CA1 and CA3 pyramidal neurons morphology, which could be related to LTP impairments and microglial activation in the hippocampal formation, previously described.

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In rats reared without play, or with limited access to play during the juvenile period, the dendrites of pyramidal neurons of the medial prefrontal cortex (mPFC) exhibit more branching than rats reared with more typical levels of play. This suggests that play is critical for pruning the dendritic arbor of these neurons. However, the rearing paradigms typically used to limit play involve physical separation from a peer or sharing a cage with an adult, causing stress that may disrupt pruning. To limit this potentially confounding source of stress, we used an alternative approach in this study: pairing playful Long Evans rats (LE) with low playing Fischer 344 (F344) rats throughout the juvenile period. We then examined the morphology of medial prefrontal cortex (mPFC) neurons, predicting that pruning should be reduced. LE rats reared with another LE rat had significantly greater pruning of mPFC pyramidal neurons compared to LE rats reared with a F344 partner. Furthermore, in previous studies, only one sex or the other was used, whereas in the present rearing paradigm, both sexes were tested, showing that play influences neuronal pruning in both. The neurons of the play deficient LE rats not only occupied more space, as determined by convex hull analyses, but the dendrites were also longer than in rats with more typical play experiences. Unlike studies using more stressful rearing paradigms, the present effects were limited to the apical dendritic projections, suggesting that the previously reported effects on the basilar dendrites may have resulted from developmental disruptions caused by stress. If correct, the present findings indicate that play experienced over the juvenile period affects how mPFC neurons develop and function.

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Objective To study the effect and mechanism of estradiol (E

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Alzheimer´s disease (AD), the most common form of dementia in industrialized countries, severely targets the hippocampal formation in humans and mouse models of this condition. The adult hippocampus hosts the continuous addition of new dentate granule cells (DGCs) in numerous mammalian species, including humans. Although the morphology and positioning of DGCs within the granule cell layer (GCL) match their developmental origin in rodents, a similar correlation has not been reported in humans to date. Our data reveal that DGCs located in inner portions of the human GCL show shorter and less complex dendrites than those found in outer portions of this layer, which are presumably generated developmentally. Moreover, in AD patients, DGCs show early morphological alterations that are further aggravated as the disease progresses. An aberrantly increased number of DGCs with several primary apical dendrites is the first morphological change detected in patients at Braak-Tau I/II stages. This alteration persists throughout AD progression and leads to generalized dendritic atrophy at late stages of the disease. Our data reveal the distinct vulnerability of several morphological characteristics of DGCs located in the inner and outer portions of the GCL to AD and support the notion that the malfunction of the hippocampus is related to cognitive impairments in patients with AD.

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Mild traumatic brain injuries (mTBI) plague the human population and their prevalence is increasing annually. More so, repeated mTBIs (RmTBI) are known to manifest and compound neurological deficits in vulnerable populations. Age at injury and sex are two important factors influencing RmTBI pathophysiology, but we continue to know little about the specific effects of RmTBI in youth and females. In this study, we directly quantified the effects of RmTBI on adolescent and adult, male and female mice, with a closed-head lateral impact model. We report age- and sex-specific neurobehavioural deficits in motor function and working memory, microglia responses to injury, and the subsequent changes in dendritic spine density in select brain regions. Specifically, RmTBI caused increased footslips in adult male mice as assessed in a beam walk assay and significantly reduced the time spent with a novel object in adolescent male and female mice. RmTBIs caused a significant reduction in microglia density in male mice in the motor cortex, but not female mice. Finally, RmTBI significantly reduced dendritic spine density in the agranular insular cortex (a region of the prefrontal cortex in mice) and increased dendritic spine density in the adolescent male motor cortex. Together, the data provided in this study sheds new light on the heterogeneity in RmTBI-induced behavioural, glial, and neuronal architecture changes dependent on age and sex.

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Conventional camera lucida (CL) aided neuronal tracing technique for studying neural plasticity is a demanding procedure. Stereo Investigator-Neurolucida enabled neuronal tracing system is not accessible to all researchers. This necessitates alternate simple and less challenging digitised neuronal tracing methods. This report describes a novel digitised neuronal tracing method using widefield microscopy, and its effectiveness is compared with the traditional camera lucida aided neuronal tracing method. Golgi-Cox stained hippocampal cornu ammonis area-3 (CA3) pyramidal neuron photomicrographs were serially captured at a depth of every 2µm in the z-axis by a wide field microscope from the point of appearance to the disappearance. These images were stacked along the axis perpendicular to the image plane to reconstruct the neuron in its entirety, digitally traced and dendritic quantification was performed using open source software. The same neurons were manually traced using camera lucida, and Sholl analysis was done manually to quantify the dendritic arborisation pattern. The dendritic quantification data were not significantly different in both methods. Hence, the technology-enabled, less demanding, and equally accurate neuronal tracing can be adopted instead of manual tracing and analysis of neurons. •A simple digitised neuronal tracing method is described.•It is fast, rigorous, and comparable to traditional tracing techniques.•Helps the researcher to repeatedly probe data to reduce errors.

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Obtaining fine neuron morphology and connections data is extraordinarily useful in understanding the brain's functionality. Golgi staining is a widely used method for revealing neuronal morphology. However, Golgi-Cox-stained tissue is difficult to image in three dimensions and lacks cell-type specificity, limiting its use in neuronal circuit studies. Here, we describe an expansion-based method for rapidly clearing Golgi-Cox-stained tissue. The results show that 1 mm thick Golgi-Cox-stained tissue can be cleared within 6 hours with a well preserved Golgi-Cox-stained signal. At the same time, we found for the first time that the cleared Golgi-Cox-stained samples were compatible with three-dimensional (3D) immunostaining and multi-round immunostaining. By combining the Golgi-Cox staining with tissue clearing and immunostaining, Golgi-Cox-stained tissue could be used for large-volume 3D imaging, identification of cell types of Golgi-Cox-stained cells, and reconstruction of the neural circuits at dendritic spines level. More importantly, these methods could also be applied to samples from human brains, providing a tool for analyzing the neuronal circuit of the human brain.

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Introduction: Streptococcus pneumoniae (pneumococcus) meningitis is a serious disease with substantial lethality and long-term disability in survivors. Loss of synaptic staining in the superficial layers of the neocortex in rodent models and in humans, and pneumolysin (a major pneumococcal toxin)-dependent dendritic spine collapse in brain slices have been described. It remains unclear how deep in the neocortex more discrete changes are present, how soon after disease onset these changes occur, and whether other properties of dendrites are also affected. Methods: Using a mouse model of pneumococcal meningitis, we studied changes in the neocortex shortly (3-6 h) after the onset of clinical symptoms via modified Golgi-Cox silver staining. Results: Dendritic changes were present in areas with otherwise unchanged cell numbers and no signs of necrosis or other apparent neuronal pathology. Mature dendritic spines were reduced in the pyramidal neurons running through layers 1-5. Additionally, spine morphology changes (swelling, spine neck distortion), were also observed in the deeper layers 4 and 5 of the neocortex. Immature spines (filopodia) remained unchanged between groups, as well as the dendritic arborization of the analyzed neurons. In a third of the animals with meningitis, massive mechanical distortion of the primary dendrites of most of the pyramidal neurons through layers 1-5 was observed. This distortion was reproduced in acute brain slices after exposure to pneumolysin-containing bacterial lysates (S. pneumoniae D39 strain), but not to lysates of pneumolysin-deficient bacteria, which we explain by the tissue remodeling effect of the toxin. Experimental mechanical dendrite distortion in primary neural cultures demonstrated diminished FRAP diffusion of neuronally-expressed enhanced green fluorescent protein (eGFP), indicative of disturbed dendritic diffusion. Discussion: Our work extends earlier knowledge of synaptic loss in the superficial cortical layers during meningitis to deeper layers. These changes occurred surprisingly early in the course of the disease, substantially limiting the effective therapeutic window. Methodologically, we demonstrate that the dendritic spine collapse readout is a highly reliable and early marker of neural damage in pneumococcal meningitis models, allowing for reduction of the total number of animals used per a group due to much lower variation among animals.

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Gerbrandus Jelgersma published extensively on the (pathological) anatomy of the cerebellum between 1886 and 1934. Based on his observations on the double innervation of the Purkinje cells, he formulated a hypothesis on the function of the cerebellum. Both afferent systems of the cerebellum, the mossy fiber-parallel fiber system and the climbing fibers terminate on the Purkinje cell dendrites. According to Jelgersma, the mossy fiber-parallel fiber system is derived from the pontine nuclei and the inferior olive, and would transmit the movement images derived from the cerebral cortex. Spinocerebellar climbing fibers would transmit information about the execution of the movement. When the Purkinje cell compares these inputs and notices a difference between instruction and execution, it sends a correction through the descending limb of the superior cerebellar peduncle to the anterior horn cells. Jelgersma postulates that this cerebro-cerebellar coordination system shares plasticity with other nervous connections because nerve cell dendritic protrusions possess what he called amoeboid mobility: dendritic protrusions can be extended or retracted and are so able to create new connections or to abolish them. Jelgersma's theories are discussed against the background of more recent theories of cerebellar function that, similarly, are based on the double innervation of the Purkinje cells. The amoeboid hypothesis is traced to its roots in the late nineteenth century.

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Plasticity in the dentate gyrus (DG) is strongly influenced by ethanol, and ethanol experience alters long-term memory consolidation dependent on the DG. However, it is unclear if DG plasticity plays a role in dysregulation of long-term memory consolidation during abstinence from chronic ethanol experience. Outbred male Wistar rats experienced 7 weeks of chronic intermittent ethanol vapor exposure (CIE). Seventy-two hours after CIE cessation, CIE and age-matched ethanol-naïve Air controls experienced auditory trace fear conditioning (TFC). Rats were tested for cue-mediated retrieval in the fear context either twenty-four hours (24 hr), ten days (10 days), or twenty-one days (21 days) later. CIE rats showed enhanced freezing behavior during TFC acquisition compared to Air rats. Air rats showed significant fear retrieval, and this behavior did not differ at the three time points. In CIE rats, fear retrieval increased over time during abstinence, indicating an incubation in fear responses. Enhanced retrieval at 21 days was associated with reduced structural and functional plasticity of ventral granule cell neurons (GCNs) and reduced expression of synaptic proteins important for neuronal plasticity. Systemic treatment with the drug Isoxazole-9 (Isx-9; small molecule that stimulates DG plasticity) during the last week and a half of CIE blocked altered acquisition and retrieval of fear memories in CIE rats during abstinence. Concurrently, Isx-9 modulated the structural and functional plasticity of ventral GCNs and the expression of synaptic proteins in the ventral DG. These findings identify that abstinence-induced disruption of fear memory consolidation occurs via altered plasticity within the ventral DG, and that Isx-9 prevented these effects.

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Anxiety, hippocampus synaptic plasticity deficit, as well as pro-inflammatory cytokines, are involved in Alzheimer's disease (AD). The present study is designed to evaluate the possible therapeutic effect of crocin on anxiety-like behaviours, hippocampal synaptic plasticity and neuronal shape, as well as pro-inflammatory cytokines in the hippocampus using in vivo amyloid-beta (Aß) models of AD. The Aß peptide (1-42) was bilaterally injected into the frontal-cortex. Five hours after the surgery, the rats were given intraperitoneal (IP) crocin (30 mg/kg) daily up to 12 days. Elevated plus maze results showed that crocin treatment after bilateral Aß injection significantly increased the percentage of spent time into open arms, frequency of entries, and percentage of entries into open arms as compared with the Aß group. In the open field test, the Aß+crocin group showed a higher percentage of spent time in the centre and frequency of entries into central zone as compare with the Aß treated animals. Administering crocin increased the number of soma, dendrites and axonal arbores in the CA1 neurons among the rats with Aß neurotoxicity. Cresyl violet (CV) staining showed that crocin increased the number of CV-positive cells in the CA1 region of the hippocampus compared with the Aß group. Silver-nitrate staining indicated that crocin reduced neurofibrillary tangle formation induced by Aß. Crocin treatment attenuated the expression of TNF-α and IL-1ß mRNA in the hippocampus compared with the Aß group. Our results suggest that crocin attenuated Aß-induced anxiety-like behaviours and neuronal damage, and synaptic plasticity loss in hippocampal CA1 neurons may via its anti-inflammatory effects.

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