scholarly journals The cerebral amygdaloid body: Functional morphology and neuroendocrinology

1995 ◽  
Vol 41 (2) ◽  
pp. 44-44
Author(s):  
V. I. Kandror ◽  
I. G. Akmayev ◽  
L. B. Kalimullina
Keyword(s):  
Structural Organization ◽  
Reproductive Function ◽  
Brain Regions ◽  
Amygdaloid Body ◽  
Extensive Literature ◽  
Schematic Diagram ◽  
Volumetric Reconstruction ◽  
Almost All ◽  
The Brain ◽  
Illustrative Material

Due to the fact that endocrine functions are inherent in almost all areas of the brain, the hypothalamus ceases to be an exclusive object of research by neuroendocrinologists. An increasing number of brain regions are being drawn into the orbit of neuroendocrine research. Among them, the limbic region of the brain attracts the most attention, an important link of which, participating in the regulation of reproductive functions, is the amygdala complex (MC). Latest fundamental analysis, including structural, concerning histophysiologic and neuroendocrinological approaches are presented in the reviewed book. It must be admitted that the publication of this book is timely. Drawing on many years of experience of their own research and extensive literature, the authors analyze in detail the features of the structural organization of this region of the brain and the mechanisms of its interaction with the centers of the brain that control reproductive function. The book consists of a brief introduction, three main chapters and a conclusion. In addition to a large summary of the cited literature, attracts the attention of a rich and very illustrative material. The latter includes a volumetric reconstruction of the entire MC of the brain and its individual components, the reconstruction of the MC on a series of histological sections, each of which is further reproduced in the form of a schematic diagram, and finally, a series of the most informative sections of the MC, reflecting the main structures of this brain region on the frontal sections. Due to its uniqueness, the illustrative material can be used as an atlas of the structural organization of the MC, and therefore it is of independent value.

IGF-1 in the Brain as a Regulator of Reproductive Neuroendocrine Function

2005 ◽  
Vol 230 (5) ◽  
pp. 292-306 ◽  
Author(s):  
Shabrine S. Daftary ◽  
Andrea C. Gore
Keyword(s):  
Critical Role ◽  
Somatic Growth ◽  
Reproductive Function ◽  
Brain Regions ◽  
Pituitary Hormones ◽  
Somatotropic Axis ◽  
Gnrh Neurons ◽  
Close Relationship ◽  
The Brain ◽  
Neuroendocrine Functions

Given the close relationship among neuroendocrine systems, it Is likely that there may be common signals that coordinate the acquisition of adult reproductive function with other homeo-static processes. In this review, we focus on central nervous system insulin-like growth factor-1 (IGF-1) as a signal controlling reproductive function, with possible links to somatic growth, particularly during puberty. In vertebrates, the appropriate neurosecretion of the decapeptide gonadotropin-releas-ing hormone (GnRH) plays a critical role in the progression of puberty. Gonadotropin-releasing hormone is released in pulses from neuroterminals in the median eminence (ME), and each GnRH pulse triggers the production of the gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH). These pituitary hormones in turn stimulate the synthesis and release of sex steroids by the gonads. Any factor that affects GnRH or gonadotropin pulsatility is important for puberty and reproductive function and, among these factors, the neurotrophic factor IGF-1 is a strong candidate. Although IGF-1 is most commonly studied as the tertiary peripheral hormone in the somatotropic axis via its synthesis in the liver, IGF-1 Is also synthesIzed in the brain, within neurons and glia. In neuroendocrine brain regions, central IGF-1 plays roles in the regulation of neuroendocrine functions, including direct actions on GnRH neurons. Moreover, GnRH neurons themselves co-express IGF-1 and the IGF-1 receptor, and this expression is developmentally regulated. Here, we examine the role of IGF-1 acting in the hypothalamus as a critical link between reproductive and other neuroendocrine functions.

scholarly journals Characterization of GPR101 transcript structure and expression patterns

2016 ◽  
Vol 57 (2) ◽  
pp. 97-111 ◽  
Author(s):  
Giampaolo Trivellin ◽  
Ivana Bjelobaba ◽  
Adrian F Daly ◽  
Darwin O Larco ◽  
Leonor Palmeira ◽  
...  
Keyword(s):  
Expression Patterns ◽  
Adult Life ◽  
Cell Types ◽  
Brain Regions ◽  
Human Tissues ◽  
Specific Expression ◽  
Pituitary Development ◽  
Rapid Amplification ◽  
Almost All ◽  
The Brain

We recently showed that Xq26.3 microduplications cause X-linked acrogigantism (X-LAG). X-LAG patients mainly present with growth hormone and prolactin-secreting adenomas and share a minimal duplicated region containing at least four genes. GPR101 was the only gene highly expressed in their pituitary lesions, but little is known about its expression patterns. In this work, GPR101 transcripts were characterized in human tissues by 5′-Rapid Amplification of cDNA Ends (RACE) and RNAseq, while the putative promoter was bioinformatically predicted. We investigated GPR101 mRNA and protein expression by RT-quantitative PCR (qPCR), whole-mount in situ hybridization, and immunostaining, in human, rhesus monkey, rat and zebrafish. We identified four GPR101 isoforms characterized by different 5′-untranslated regions (UTRs) and a common 6.1kb long 3′UTR. GPR101 expression was very low or absent in almost all adult human tissues examined, except for specific brain regions. Strong GPR101 staining was observed in human fetal pituitary and during adolescence, whereas very weak/absent expression was detected during childhood and adult life. In contrast to humans, adult monkey and rat pituitaries expressed GPR101, but in different cell types. Gpr101 is expressed in the brain and pituitary during rat and zebrafish development; in rat pituitary, Gpr101 is expressed only after birth and shows sexual dimorphism. This study shows that different GPR101 transcripts exist and that the brain is the major site of GPR101 expression across different species, although divergent species- and temporal-specific expression patterns are evident. These findings suggest an important role for GPR101 in brain and pituitary development and likely reflect the very different growth, development and maturation patterns among species.

Distribution of regional cerebral blood flow in voluntarily diving rats.

1998 ◽  
Vol 201 (4) ◽  
pp. 549-558
Author(s):  
G P Ollenberger ◽  
N H West
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Regional Cerebral Blood Flow ◽  
Regional Distribution ◽  
Detailed Examination ◽  
Brain Regions ◽  
Regional Cerebral Blood ◽  
Output Only ◽  
Almost All ◽  
The Brain

The distribution of regional cerebral blood flow (rCBF) was examined in conscious, voluntarily diving rats using the brain blood flow tracer N-[14C]isopropyl-p-iodoamphetamine and quantitative autoradiography. A detailed examination of the regional distribution of cerebral blood flow revealed that almost all brain regions were hyperperfused during diving. During diving, rCBF increased by an average of 1.7-fold in 29 of the 33 brain regions examined, despite a 69.2 % decrease in cardiac output. Only some regions of the basal ganglia (caudate-putamen and globus pallidus) and limbic areas (hippocampus and amygdala) did not increase rCBF significantly during diving. We determined that the increase in rCBF during diving is primarily due to a corresponding 20.9 % decrease in cerebrovascular resistance. A significant increase in perfusion pressure during diving also potentially contributed to the increase in rCBF. Because some brain regions did not increase flow significantly during diving, these results suggest that not all brain regions participate equally in the global cerebrovascular response to diving. This study provides evidence to support the view that the brain is preferentially perfused during conscious voluntary diving in the rat. The mechanism(s) that probably produce the cerebrovascular changes during diving are discussed.

Types of refractive errors and methods for their diagnosis

2020 ◽  
pp. 30-36
Author(s):  
Olga Lemzyakova
Keyword(s):  
Optical System ◽  
Contact Lenses ◽  
Vision Impairment ◽  
Refractive Errors ◽  
Vision Correction ◽  
Light Rays ◽  
Different Types ◽  
Almost All ◽  
Degrees Of Severity ◽  
The Brain

Refraction of the eye means its ability to bend (refract) light in its own optical system. In a normal state, which is called emmetropia, light rays passing through the optical system of the eye focus on the retina, from where the impulse is transmitted to the visual cortex of the brain and is analyzed there. A person sees equally well both in the distance and near in this situation. However, very often, refractive errors develop as a result of various types of influences. Myopia, or short-sightedness, occurs when the light rays are focused in front of the retina as a result of passing through the optical system of the eye. In this case, a person will clearly distinguish close objects and have difficulties in seeing distant objects. On the opposite side is development of farsightedness (hypermetropia), in which the focusing of light rays occurs behind the retina — such a person sees distant objects clearly, but outlines of closer objects are out of focus. Near vision impairment in old age is a natural process called presbyopia, it develops due to the lens thickening. Both myopia and hypermetropia can have different degrees of severity. The variant, when different refractive errors are observed in different eyes, is called anisometropia. In the same case, if different types of refraction are observed in the same eye, it is astigmatism, and most often it is a congenital pathology. Almost all of the above mentioned refractive errors require correction with spectacles or use of contact lenses. Recently, people are increasingly resorting to the methods of surgical vision correction.

RAS in the Central Nervous System: Potential Role in Neuropsychiatric Disorders

2018 ◽  
Vol 25 (28) ◽  
pp. 3333-3352 ◽  
Author(s):  
Natalia Pessoa Rocha ◽  
Ana Cristina Simoes e Silva ◽  
Thiago Ruiz Rodrigues Prestes ◽  
Victor Feracin ◽  
Caroline Amaral Machado ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Therapeutic Potential ◽  
Neuropsychiatric Disorders ◽  
Extensive Literature ◽  
Ang Ii ◽  
Mas Receptor ◽  
The Central Nervous System ◽  
The Brain

Background: The Renin-Angiotensin System (RAS) is a key regulator of cardiovascular and renal homeostasis, but also plays important roles in mediating physiological functions in the central nervous system (CNS). The effects of the RAS were classically described as mediated by angiotensin (Ang) II via angiotensin type 1 (AT1) receptors. However, another arm of the RAS formed by the angiotensin converting enzyme 2 (ACE2), Ang-(1-7) and the Mas receptor has been a matter of investigation due to its important physiological roles, usually counterbalancing the classical effects exerted by Ang II. Objective: We aim to provide an overview of effects elicited by the RAS, especially Ang-(1-7), in the brain. We also aim to discuss the therapeutic potential for neuropsychiatric disorders for the modulation of RAS. Method: We carried out an extensive literature search in PubMed central. Results: Within the brain, Ang-(1-7) contributes to the regulation of blood pressure by acting at regions that control cardiovascular functions. In contrast with Ang II, Ang-(1-7) improves baroreflex sensitivity and plays an inhibitory role in hypothalamic noradrenergic neurotransmission. Ang-(1-7) not only exerts effects related to blood pressure regulation, but also acts as a neuroprotective component of the RAS, for instance, by reducing cerebral infarct size, inflammation, oxidative stress and neuronal apoptosis. Conclusion: Pre-clinical evidence supports a relevant role for ACE2/Ang-(1-7)/Mas receptor axis in several neuropsychiatric conditions, including stress-related and mood disorders, cerebrovascular ischemic and hemorrhagic lesions and neurodegenerative diseases. However, very few data are available regarding the ACE2/Ang-(1-7)/Mas receptor axis in human CNS.

Management of Glioblastoma Multiforme by Phytochemicals: Applications of Nanoparticle Based Targeted Drug Delivery System

2020 ◽  
Vol 21 ◽  
Author(s):  
Sayed Md Mumtaz ◽  
Gautam Bhardwaj ◽  
Shikha Goswami ◽  
Rajiv Kumar Tonk ◽  
Ramesh K. Goyal ◽  
...  
Keyword(s):  
Drug Delivery ◽  
Glioblastoma Multiforme ◽  
Drug Delivery System ◽  
Delivery System ◽  
Genetic Disorder ◽  
Drug Regimen ◽  
Brain Regions ◽  
Radio Therapy ◽  
Novel Drug ◽  
The Brain

: The Glioblastoma Multiforme (GBM; grade IV astrocytoma) exhort tumor of star-shaped glial cell in the brain. It is a fast-growing tumor that spreads to nearby brain regions specifically to cerebral hemispheres in frontal and temporal lobes. The etiology of GBM is unknown, but major risk factors are genetic disorder like neurofibromatosis and schwanomatosis which develop the tumor in the nervous system. The management of GBM with chemo-radio therapy leads to resistance and current drug regimen like Temozolomide (TMZ) is less efficacious. The reasons behind failure of drugs are due to DNA alkylation in cell cycle by enzyme DNA guanidase and mitochondrial dysfunction. Naturally occurring bio-active compounds from plants known as phytochemicals, serve as vital sources for anti-cancer drugs. Some typical examples include taxol analogs, vinca alkaloids such as vincristine, vinblastine, podophyllotoxin analogs, camptothecin, curcumin, aloe emodin, quercetin, berberine e.t.c. These phytochemicals often act via regulating molecular pathways which are implicated in growth and progression of cancers. However the challenges posed by the presence of BBB/BBTB to restrict passage of these phytochemicals, culminates in their low bioavailability and relative toxicity. In this review we integrated nanotech as novel drug delivery system to deliver phytochemicals from traditional medicine to the specific site within the brain for the management of GBM.

Neuro-Clinical Signatures of Language Impairments: A Theoretical Framework for Function-to-structure Mapping in Clinics

2020 ◽  
Vol 20 (9) ◽  
pp. 800-811 ◽  
Author(s):  
Ferath Kherif ◽  
Sandrine Muller
Keyword(s):  
Brain Mapping ◽  
Theoretical Framework ◽  
Brain Regions ◽  
Language Impairments ◽  
Structure Mapping ◽  
Language Functions ◽  
The Past ◽  
Language Recovery ◽  
The Brain ◽  
Bow Tie

In the past decades, neuroscientists and clinicians have collected a considerable amount of data and drastically increased our knowledge about the mapping of language in the brain. The emerging picture from the accumulated knowledge is that there are complex and combinatorial relationships between language functions and anatomical brain regions. Understanding the underlying principles of this complex mapping is of paramount importance for the identification of the brain signature of language and Neuro-Clinical signatures that explain language impairments and predict language recovery after stroke. We review recent attempts to addresses this question of language-brain mapping. We introduce the different concepts of mapping (from diffeomorphic one-to-one mapping to many-to-many mapping). We build those different forms of mapping to derive a theoretical framework where the current principles of brain architectures including redundancy, degeneracy, pluri-potentiality and bow-tie network are described.

scholarly journals Neuroinflammation and protein pathology in Parkinson’s disease dementia

2020 ◽  
Vol 8 (1) ◽  
Author(s):  
Antonina Kouli ◽  
Marta Camacho ◽  
Kieren Allinson ◽  
Caroline H. Williams-Gray
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
T Lymphocytes ◽  
Substantia Nigra ◽  
Amyloid Β ◽  
Brain Regions ◽  
Parkinson’S Disease Dementia ◽  
Activated Microglia ◽  
Cell Counts ◽  
The Brain

AbstractParkinson’s disease dementia is neuropathologically characterized by aggregates of α-synuclein (Lewy bodies) in limbic and neocortical areas of the brain with additional involvement of Alzheimer’s disease-type pathology. Whilst immune activation is well-described in Parkinson’s disease (PD), how it links to protein aggregation and its role in PD dementia has not been explored. We hypothesized that neuroinflammatory processes are a critical contributor to the pathology of PDD. To address this hypothesis, we examined 7 brain regions at postmortem from 17 PD patients with no dementia (PDND), 11 patients with PD dementia (PDD), and 14 age and sex-matched neurologically healthy controls. Digital quantification after immunohistochemical staining showed a significant increase in the severity of α-synuclein pathology in the hippocampus, entorhinal and occipitotemporal cortex of PDD compared to PDND cases. In contrast, there was no difference in either tau or amyloid-β pathology between the groups in any of the examined regions. Importantly, we found an increase in activated microglia in the amygdala of demented PD brains compared to controls which correlated significantly with the extent of α-synuclein pathology in this region. Significant infiltration of CD4+ T lymphocytes into the brain parenchyma was commonly observed in PDND and PDD cases compared to controls, in both the substantia nigra and the amygdala. Amongst PDND/PDD cases, CD4+ T cell counts in the amygdala correlated with activated microglia, α-synuclein and tau pathology. Upregulation of the pro-inflammatory cytokine interleukin 1β was also evident in the substantia nigra as well as the frontal cortex in PDND/PDD versus controls with a concomitant upregulation in Toll-like receptor 4 (TLR4) in these regions, as well as the amygdala. The evidence presented in this study show an increased immune response in limbic and cortical brain regions, including increased microglial activation, infiltration of T lymphocytes, upregulation of pro-inflammatory cytokines and TLR gene expression, which has not been previously reported in the postmortem PDD brain.

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