A Narrative Review on the Clinical Relevance of Imaging the Circumventricular Brain Organs and Performing Their Anatomical and Histopathological Examination in Acute and Postacute COVID-19.

ABSTRACT: Autopsy followed by histopathological examination is foundational in clinical and forensic medicine for discovering and understanding pathological changes in disease, their underlying processes, and cause of death. Imaging technology has become increasingly important for advancing clinical research and practice, given its noninvasive, in vivo and ex vivo applicability. Medical and forensic autopsy can benefit greatly from advances in imaging technology that lead toward minimally invasive, whole-brain virtual autopsy. Brain autopsy followed by histopathological examination is still the hallmark for understanding disease and a fundamental modus operandi in forensic pathology and forensic medicine, despite the fact that its practice has become progressively less frequent in medical settings. This situation is especially relevant with respect to new diseases such as COVID-19 caused by the SARS-CoV-2 virus, for which our neuroanatomical knowledge is sparse. In this narrative review, we show that ad hoc clinical autopsies and histopathological analyses combined with neuroimaging of the principal circumventricular organs are critical to gaining insight into the reconstruction of the pathophysiological mechanisms and the explanation of cause of death (ie, atrium mortis) related to the cardiovascular effects of SARS-CoV-2 infection in forensic and clinical medicine.

Investigating the structural network underlying brain-immune interactions using combined histopathology and neuroimaging: a critical review for its relevance in acute and long COVID-19.

Current views on immunity support the idea that immunity extends beyond defense functions and is tightly intertwined with several other fields of biology such as virology, microbiology, physiology and ecology. It is also critical for our understanding of autoimmunity and cancer, two topics of great biological relevance and for critical public health considerations such as disease prevention and treatment. Central to this review, the immune system is known to interact intimately with the nervous system and has been recently hypothesized to be involved not only in autonomic and limbic bio-behaviors but also in cognitive function. Herein we review the structural architecture of the brain network involved in immune response. Furthermore, we elaborate upon the implications of inflammatory processes affecting brain-immune interactions as reported recently in pathological conditions due to SARS-Cov-2 virus infection, namely in acute and post-acute COVID-19. Moreover, we discuss how current neuroimaging techniques combined with ad hoc clinical autopsies and histopathological analyses could critically affect the validity of clinical translation in studies of human brain-immune interactions using neuroimaging. Advances in our understanding of brain-immune interactions are expected to translate into novel therapeutic avenues in a vast array of domains including cancer, autoimmune diseases or viral infections such as in acute and post-acute or Long COVID-19.

Early Regressive Development of the Subcommissural Organ of Two Human Fetuses with Non-Communicating Hydrocephalus.

Hydrocephalus is a central nervous system condition characterized by CSF buildup and ventricular hypertrophy. It is divided into two types: communicative and non-communicating hydrocephalus. Congenital hydrocephalus has been linked to several changes in the subcommissural organ (SCO). However, it is unclear whether these changes occur before or as a result of the hydrocephalic illness. This report presents three cases of human fetuses with hydrocephalus: one non-communicating case, two communicating cases, and two controls. Hematoxylin-Eosin (H&E) or cresyl violet and immunohistochemistry with anti-transthyretin were used to analyze SCO morphological and secretory changes. We conclude that in the cases presented here, there could be an early regression in the SCO of the communicating cases that is not present in the non-communicating case.

Altered Expression of AQP1 and AQP4 in Brain Barriers and Cerebrospinal Fluid May Affect Cerebral Water Balance during Chronic Hypertension.

Hypertension is the leading cause of cardiovascular affection and premature death worldwide. The spontaneously hypertensive rat (SHR) is the most common animal model of hypertension, which is characterized by secondary ventricular dilation and hydrocephalus. Aquaporin (AQP) 1 and 4 are the main water channels responsible for the brain's water balance. The present study focuses on defining the expression of AQPs through the time course of the development of spontaneous chronic hypertension. We performed immunofluorescence and ELISA to examine brain AQPs from 10 SHR, and 10 Wistar−Kyoto (WKY) rats studied at 6 and 12 months old. There was a significant decrease in AQP1 in the choroid plexus of the SHR-12-months group compared with the age-matched control (p < 0.05). In the ependyma, AQP4 was significantly decreased only in the SHR-12-months group compared with the control or SHR-6-months groups (p < 0.05). Per contra, AQP4 increased in astrocytes end-feet of 6 months and 12 months SHR rats (p < 0.05). CSF AQP detection was higher in the SHR-12-months group than in the age-matched control group. CSF findings were confirmed by Western blot. In SHR, ependymal and choroidal AQPs decreased over time, while CSF AQPs levels increased. In turn, astrocytes AQP4 increased in SHR rats. These AQP alterations may underlie hypertensive-dependent ventriculomegaly.

AQP4, Astrogenesis, and Hydrocephalus: A New Neurological Perspective.

Aquaporin 4 (AQP4) is a cerebral glial marker that labels ependymal cells and astrocytes' endfeet and is the main water channel responsible for the parenchymal fluid balance. However, in brain development, AQP4 is a marker of glial stem cells and plays a crucial role in the pathophysiology of pediatric hydrocephalus. Gliogenesis characterization has been hampered by a lack of biomarkers for precursor and intermediate stages and a deeper understanding of hydrocephalus etiology is needed. This manuscript is a focused review of the current research landscape on AQP4 as a possible biomarker for gliogenesis and its influence in pediatric hydrocephalus, emphasizing reactive astrogliosis. The goal is to understand brain development under hydrocephalic and normal physiologic conditions.

AQP4 labels a subpopulation of white matter-dependent glial radial cells affected by pediatric hydrocephalus, and its expression increased in glial microvesicles released to the cerebrospinal fluid in obstructive hydrocephalus.

Hydrocephalus is a distension of the ventricular system associated with ventricular zone disruption, reactive astrogliosis, periventricular white matter ischemia, axonal impairment, and corpus callosum alterations. The condition's etiology is typically attributed to a malfunction in classical cerebrospinal fluid (CSF) bulk flow; however, this approach does not consider the unique physiology of CSF in fetal and perinatal patients. The parenchymal fluid contributes to the glymphatic system, and plays a fundamental role in pediatric hydrocephalus, with aquaporin 4 (AQP4) as the primary facilitator of these fluid movements. Despite the importance of AQP4 in the pathophysiology of hydrocephalus, it's expression in human fetal life is not well-studied. This manuscript systematically defines the brain expression of AQP4 in human brain development under control (n = 13) and hydrocephalic conditions (n = 3). Brains from 8 postconceptional weeks (PCW) onward and perinatal CSF from control (n = 2), obstructive (n = 6) and communicating (n = 6) hydrocephalic samples were analyzed through immunohistochemistry, immunofluorescence, western blot, and flow cytometry. Our results indicate that AQP4 expression is observed first in the archicortex, followed by the ganglionic eminences and then the neocortex. In the neocortex, it is initially at the perisylvian regions, and lastly at the occipital and prefrontal zones. Characteristic astrocyte end-feet labeling surrounding the vascular system was not established until 25 PCW. We also found AQP4 expression in a subpopulation of glial radial cells with processes that do not progress radially but, rather, curve following white matter tracts (corpus callosum and fornix), which were considered as glial stem cells (GSC). Under hydrocephalic conditions, GSC adjacent to characteristic ventricular zone disruption showed signs of early differentiation into astrocytes which may affect normal gliogenesis and contribute to the white matter dysgenesis. Finally, we found that AQP4 is expressed in the microvesicle fraction (p < 0.01) of CSF from patients with obstructive hydrocephalus. These findings suggest the potential use of AQP4 as a diagnostic and prognostic marker of pediatric hydrocephalus and as gliogenesis biomarker.

AQP1 Overexpression in the CSF of Obstructive Hydrocephalus and Inversion of Its Polarity in the Choroid Plexus of a Chiari Malformation Type II Case.

The choroid plexus (ChP) is involved in the production of cerebrospinal fluid (CSF) and is intimately related to CSF physiopathology. Aquaporin-1 (AQP1) is the water channel directly implicated in CSF production and a potential therapeutic target in the management of CSF circulation disorders. Pathologies that present ventriculomegaly are associated with defective CSF turnover and AQPs are involved in both the production and reabsorption of CSF. This work examines the levels of AQP1 and its dynamics in ventriculomegaly conditions such as congenital hydrocephalus (communicating and obstructive) or type II lissencephaly versus control. We specifically address the expression of AQP1 in the CSF of 16 term-pregnancy infants where it was found to be significantly increased in obstructive cases when compared with communicating hydrocephalus or control patients. We also defined histologically the expression of AQP1 in the ChP from 6 nonsurvival preterm-pregnancy infants ranging ages between 20 and 25 gestational weeks in which AQP1 was mainly expressed at the apical pole of the ChP epithelium (ChPE) in control and lissencephalic patients. AQP1 expression from the Chiari malformation case showed an inverted polarity being expressed in the basal pole of the ChPE colocalizing with the glucose transporter 1 where this transporter is naturally located.

Systemic Hypertension Effects on the Ciliary Body and Iris. An Immunofluorescence Study with Aquaporin 1, Aquaporin 4, and Na⁺, K⁺ ATPase in Hypertensive Rats.

Aquaporin 1 (AQP1) and aquaporin 4 (AQP4) have been identified in the eye as playing an essential role in the formation of the aqueous humor along with the Na⁺/K⁺ ATPase pump. Different authors have described the relationship between blood pressure, aqueous humor production, and intraocular pressure with different conclusions, with some authors supporting a positive correlation between blood pressure and intraocular pressure while others disagree. The aim of this work was to study the effect of high blood pressure on the proteins involved in the production of aqueous humor in the ciliary body (CB) and iris. For this purpose, we used the eyes of spontaneously hypertensive rats (SHR) and their control Wistar-Kyoto rats (WKY). Immunofluorescence was performed in different eye structures to analyze the effects of hypertension in the expression of AQP1, AQP4, and the Na⁺/K⁺ ATPase α1 and α2 subunits. The results showed an increase in AQP1 and Na⁺/K⁺ ATPase α1 and a decrease in AQP4 and Na⁺/K⁺ ATPase α2 in the CB of SHR, while an increase in AQP4 and no significant differences in AQP1 were found in the iris. Therefore, systemic hypertension produced changes in the proteins implicated in the movement of water in the CB and iris that could influence the production rate of aqueous humor, which would be affected depending on the duration of systemic hypertension.

A Distal to Proximal Gradient of Human Choroid Plexus Development, with Antagonistic Expression of Glut1 and AQP1 in Mature Cells vs. Calbindin and PCNA in Proliferative Cells.

The choroid plexuses (ChP) are highly vascularized tissues suspended from each of the cerebral ventricles. Their main function is to secret cerebrospinal fluid (CSF) that fills the ventricles and the subarachnoid spaces, forming a crucial system for the development and maintenance of the CNS. However, despite the essential role of the ChP-CSF system to regulate the CNS in a global manner, it still remains one of the most understudied areas in neurobiology. Here we define by immunohistochemistry the expression of different proteins involved in the maturation and functionality of the ChP from the late embryological period to maturity. We found an opposite gradient of expression between aquaporin 1 (AQP1) and glucose transporter 1 (Glut 1) that define functional maturation in the ChP periphery, and proliferating cell nuclear antigen (PCNA) and calbindin (CB), present in the ChP root zone with proliferative activity. We conclude that the maturation of the ChP matures from distal to proximal, starting in the areas nearest to the cortex, expressing in the distal, mature areas AQP1 and Glut1 (related to ChP functionality to support cortex development), and in the proximal immature areas (ChP root) CB and PCNA related to progenitor activity and proliferation.

Cerebrospinal fluid levels of tumor necrosis factor alpha and aquaporin 1 in patients with mild cognitive impairment and idiopathic normal pressure hydrocephalus.

OBJECTIVE: The aim of the present work was to make a comparative analysis of the cerebrospinal fluid levels of Tumor necrosis factor (TNFα) and aquaporin 1 (AQP1) in (i) healthy elder control, (ii) patients with mild cognitive impairment and, (iii) patients with idiopathic normal pressure hydrocephalus. PATIENTS AND METHODS: Samples of CSF were taken from seven patients with MCI, 77 years average age; six patients with iNPH, 75 years average age; eleven healthy subjects, 60year average age, were used as controls. The cerebrospinal fluid levels of AQP1 and TNFα were studied by enzyme immunoassay (ELISA). RESULTS: In mild cognitive impairment the total protein content of the CSF and the relative CSF levels of AQP1 and TNFα were similar to those of control subjects and different from those of iNPH patients. On the other hand, in iNPH patients the CSF content of proteins was low and the levels of TNFα were significantly high while those of AQP1 were insignificantly high. CONCLUSION: These finding may help the differential diagnosis and prognosis of mild cognitive impairment and normal pressure hydrocephalus patients.

Brain sexual development in Kallmann syndrome

Prenatal and one-two month postnatal testosterone influences human neural and behavioural development, since the prenatal and one-two month postnatal hormone environment clearly contributes to the development of sex-related variation in human behaviour, and plays a role in the development of the sexual brain and individual differences in behaviour within each sex, as well as differences between the sexes. Olfactory system development, brain sexual maturation and sexual behaviour in man and animals are closely related. Kallmann syndrome (KS) is a genetic disorder which combines hypogonadotropic hypogonadism and anosmia. Hypogonadism is characterized by the absence or reduced levels of gonadotropinreleasing hormone, and anosmia is due to aplasia of the olfactory bulb. The overlap between the formation of the olfactory system and the migration of neurons that synthesize the gonadotropinreleasing hormone (GnRH) is common knowledge. GnRH neurons migrate from the medial portion of the nasal epithelium through the olfactory nerves and the main olfactory bulb to the anterior hypothalamus. Furthermore, the clinical manifestations of KS are: anosmia, the absence of puberty, and modifications in sexual behaviour. The structures responsible for the maturation of the main and accessory olfactory systems, the sexual differentiation of the brain and its relationship with clinical manifestations and sexual behaviour in Kallmann syndrome are analyzed in this review. The importance of the treatment of KS at early ages is suggested in order to improve brain sexual development and its clinical and sexual behaviour manifestations

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Choroid plexus dysfunction impairs beta-amyloid clearance in a triple transgenic mouse model of Alzheimer's disease.

Compromised secretory function of choroid plexus (CP) and defective cerebrospinal fluid (CSF) production, along with accumulation of beta-amyloid (Aß) peptides at the blood-CSF barrier (BCSFB), contribute to complications of Alzheimer's disease (AD). The AD triple transgenic mouse model (3xTg-AD) at 16 month-old mimics critical hallmarks of the human disease: ß-amyloid (Aß) plaques and neurofibrillary tangles (NFT) with a temporal- and regional- specific profile. Currently, little is known about transport and metabolic responses by CP to the disrupted homeostasis of CNS Aß in AD. This study analyzed the effects of highly-expressed AD-linked human transgenes (APP, PS1 and tau) on lateral ventricle CP function. Confocal imaging and immunohistochemistry revealed an increase only of Aß42 isoform in epithelial cytosol and in stroma surrounding choroidal capillaries; this buildup may reflect insufficient clearance transport from CSF to blood. Still, there was increased expression, presumably compensatory, of the choroidal Aß transporters: the low density lipoprotein receptor-related protein 1 (LRP1) and the receptor for advanced glycation end product (RAGE). A thickening of the epithelial basal membrane and greater collagen-IV deposition occurred around capillaries in CP, probably curtailing solute exchanges. Moreover, there was attenuated expression of epithelial aquaporin-1 and transthyretin (TTR) protein compared to Non-Tg mice. Collectively these findings indicate CP dysfunction hypothetically linked to increasing Aß burden resulting in less efficient ion transport, concurrently with reduced production of CSF (less sink action on brain Aß) and diminished secretion of TTR (less neuroprotection against cortical Aß toxicity). The putative effects of a disabled CP-CSF system on CNS functions are discussed in the context of AD.

Relationships between bending and torsional strengths of the tibia and simple anthropometric variables among the prehispanic population of El Hierro (Canary Islands)

Assessment of skeletal robusticity is an important tool for the archaeologist and anthropologist, since it may be related to the intensity and type of activity performed by ancient population groups. Development of computed tomography (CT) allows determination of biomechanical properties of long bones. However, CT technology may not be easily available and is a relatively expensive procedure. Therefore, it is pertinent to estimate whether any of the parameters which can be easily measured in bare bones by simple anthropometry are useful to assess the torsional strength and bending strength of these bones. We included twenty one well preserved tibiae corresponding to prehispanic adult individuals (13 men) of El Hierro. These bones were anthropometrically measured following classical methods, and also subjected to CT analysis, and further calculation of minimum and maximum second moments and polar second moment of area, both at midshaft and at the nutrient foramen levels, using the software (www.hopkinsmedicine.org/FAE/mmacro.htm). The diaphyseal robusticity index showed a close relationship with minimum second moment of area at the nutrient foramen (r=0.824, p<0.001) and polar second moment of area at the nutrient foramen (r=0.824, p<0.001), whereas correlations with the epiphyseal robusticity index were weaker (r=0.628, p=0.005, and r=0.618, p=0.007, respectively). The variable which allows the best estimation of the torsional strength is the perimeter at the nutrient foramen, by the formula Polar second moment of area (in mm3) = -700.30 + 11.77 * perimeter at the nutrient foramen (in mm) for the whole population (standard error of the estimation=56.91; absolute range from-114.26 to 140.29), or Polar second moment of area (in mm3) = -897.93 + 13.74 * perimeter at the nutrient foramen (in mm) when only men were analyzed, with a standard error of the estimation of 32.17 (absolute range= from -44.53 to 50.32 mm3)

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Early treatment of Kallmann syndrome may prevent eunuchoid appearance and behavior.

Kallmann syndrome (KS) is a genetic disorder which combines hypogonadotropic hypogonadism and anosmia. Hypogonadism is characterized by the absence or reduced levels of gonadotropin-releasing hormone and anosmia due to olfactory bulb aplasia. KS treatment usually begins just before puberty, but brain sexual maturation occurs long before puberty normally at perinatal age. As brain cells implicated in the development of the olfactory and reproductive system have a rostral and a caudal origin, and the rostral origin is affected by aplasia in KS and the caudal origin does not seem to be affected, the early treatment of KS, as proposed in this paper, is to attain brain sexual maturation at the most appropriate age possible to prevent the eunuchoid behavior and appearance observed in KS.

The Neuroepithelium Disruption Could Generate Autoantibodies against AQP4 and Cause Neuromyelitis Optica and Hydrocephalus.

Neuromyelitis optica is an inflammatory disease characterized by neuritis and myelitis of the optic nerve. Its physiopathology is connected with the aquaporin-4 water channel, since antibodies against aquaporin-4 have been found in the cerebrospinal fluid and blood of neuromyelitis optica patients. The seropositivity for aquaporin-4 antibodies is used for the diagnosis of neuromyelitis optica or neuromyelitis optica spectrum disease. On the other hand, aquaporin-4 is expressed in astrocyte feet in the brain-blood barrier and subventricular zones of the brain ventricles. Aquaporin-4 expression is high in cerebrospinal fluid in hydrocephalus. Furthermore, neuroepithelial denudation precedes noncommunicating hydrocephalus and this neuroepithelial disruption could allow aquaporin-4 to reach anomalous brain areas where it is unrecognized and induce the generation of aquaporin-4 antibodies which could cause the neuromyelitis optica and certain types of hydrocephalus.

What is relationship between the medial preoptic area, the organum vasculosum of the lamina terminalis and Kallmann syndrome?

The medial preoptic area is a structure located in the hypothalamic anteroventral third ventricle region, and is closely related to the olfactory brain development and sexual differentiation of the brain. The medial preoptic area surrounds the organum vasculosum of the lamina terminalis, and both structures are the main areas where synthesis of gonadotropin-releasing hormone occurs in the brain. Neurons synthesizing gonadotropin-releasing hormone migrate from the medial nasal epithelium to the rostral brain and reach the organum vasculosum of the lamina terminalis and the medial preoptic area. Kallmann syndrome is a genetic disorder which combines hypogonadotropic hypogonadism and anosmia. Hypogonadism is characterized by the absence or reduced levels of gonadotropin-releasing hormone and anosmia due to olfactory bulb aplasia. This paper speculates on the connection between the development of the medial preoptic area, the organum vasculosum of the lamina terminalis and olfactory bulbs with Kallmann syndrome, since the anteroventral third ventricle region is crucial for the normal development of these structures and its connection with the olfactory nerves and sexual maturation.

Aquaporin-4 expression in the cerebrospinal fluid in congenital human hydrocephalus.

BACKGROUND: Aquaporin-4 (AQP4) is a water channel mainly located in the ventricular ependymal cells (brain-CSF barrier), the sub-ependymal glia, glia limitans and in end-feet of astrocytes in at the blood-brain barrier (BBB). METHODS: In the present work, the expression of AQP4 in the cerebrospinal fluid (CSF) in control and congenital human hydrocephalus infants (obstructive and communicating), was analysed by Western-blot and enzyme immunoassay (ELISA). RESULTS: AQP4 was found to be high compared to the control in the CSF in congenital hydrocephalus patients. Western-blot showed higher values for AQP4 than controls in communicating hydrocephalus (communicating: 38.3%, control: 6.9% p < 0.05) although the increase was not significant in obstructive hydrocephalus (obstructive: 14.7%). The AQP4 quantification by ELISA also showed that, the mean concentration of AQP4 in CSF was significantly higher in communicating hydrocephalus (communicating: 11.32 ± 0.69 ng/ml, control: 8.61 ± 0.31 ng/ml; p < 0.05). However, there was no increase over control in obstructive hydrocephalus (obstructive: 8.65 ± 0.80 ng/ml). CONCLUSIONS: AQP4 has a modulatory effect on ependyma stability and acts in CSF production and reabsorption. Therefore, the increase of AQP4 in the CSF in congenital hydrocephalus could be due to the fact that AQP4 passes from the parenchyma to the CSF and this AQP4 movement may be a consequence of ependyma denudation.

High blood pressure effects on the blood to cerebrospinal fluid barrier and cerebrospinal fluid protein composition: a two-dimensional electrophoresis study in spontaneously hypertensive rats.

The aim of the present work is to analyze the cerebrospinal fluid proteomic profile, trying to find possible biomarkers of the effects of hypertension of the blood to CSF barrier disruption in the brain and their participation in the cholesterol and ß-amyloid metabolism and inflammatory processes. Cerebrospinal fluid (CSF) is a system linked to the brain and its composition can be altered not only by encephalic disorder, but also by systemic diseases such as arterial hypertension, which produces alterations in the choroid plexus and cerebrospinal fluid protein composition. 2D gel electrophoresis in cerebrospinal fluid extracted from the cistern magna before sacrifice of hypertensive and control rats was performed. The results showed different proteomic profiles between SHR and WKY, that α-1-antitrypsin, apolipoprotein A1, albumin, immunoglobulin G, vitamin D binding protein, haptoglobin and α-1-macroglobulin were found to be up-regulated in SHR, and apolipoprotein E, transthyretin, α-2-HS-glycoprotein, transferrin, α-1ß-glycoprotein, kininogen and carbonic anhidrase II were down-regulated in SHR. The conclusion made here is that hypertension in SHR produces important variations in cerebrospinal fluid proteins that could be due to a choroid plexus dysfunction and this fact supports the close connection between hypertension and blood to cerebrospinal fluid barrier disruption.

Tibial marks in bare tibiae: relationship with robusticity indices

In bare bones, transverse lines may have several origins. Defleshing of a prey generates cutmarks, which can also appear in relation with traumatic events, post-mortem changes such as marks of animal teeth, rodent gnawing, or impact of stones, or even bone decoration. We hypothesize that in some instances they may be due to hyperplastic vessels beating on the bone surface, as expression of increased blood flow demand imposed by hypertrophied muscles. We analyzed 140 well-preserved tibiae which belonged to pre-Hispanic individuals from El Hierro, in the Canary Archipelago, currently kept at the Department of Archaeology and Prehistory of the University of La Laguna, and determined robusticity indices. Tibial marks were found in 53 out of 140 cases. Epiphyseal and diaphyseal robusticity indices were significantly higher in the first case among those with marks than among those without marks (T=3.13; p=0.002), and nearly significantly in the latter case (T=1.88; p=0.063). Considering only men, similar differences were observed regarding epiphyseal robusticity index (T=2.90; p=0.005) and diaphyseal robusticity index (T=2.11; p=0.039). There were also differences regarding the depth of the tibial marks: a higher epiphyseal robusticity index was associated with a more marked depth of the lines (T=2.11; p=0.042). An association was also observed between depth of the marks and sex (?2=4.12; p=0.042), more profound marks being observed among men. In conclusion, we here describe subtle bone marks in tibiae, which seem to correspond to vascular imprinting and are related to bone robustness. Whether or not they really represent an adaptation to an increased blood flow demand by hypertrophied muscles in relation with increased weight-bearing activity remains speculative, but this hypothesis may explain their presence (AU)

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Luteinizing hormone-releasing hormone distribution in the anterior hypothalamus of the female rats.

Luteinizing hormone-releasing hormone (LHRH) neurons and fibers are located in the anteroventral hypothalamus, specifically in the preoptic medial area and the organum vasculosum of the lamina terminalis. Most luteinizing hormone-releasing hormone neurons project to the median eminence where they are secreted in the pituitary portal system in order to control the release of gonadotropin. The aim of this study is to provide, using immunohistochemistry and female brain rats, a new description of the luteinizing hormone-releasing hormone fibers and neuron localization in the anterior hypothalamus. The greatest amount of the LHRH immunoreactive material was found in the organum vasculosum of the lamina terminalis that is located around the anterior region of the third ventricle. The intensity of the reaction of LHRH immunoreactive material decreases from cephalic to caudal localization; therefore, the greatest immunoreaction is in the organum vasculosum of the lamina terminalis, followed by the dorsomedial preoptic area, the ventromedial preoptic area, and finally the ventrolateral medial preoptic area, and in fibers surrounding the suprachiasmatic nucleus and subependymal layer on the floor of the third ventricle where the least amount immunoreactive material is found.