scholarly journals Corticotropin-releasing factor distribution in the brain of the brown anole lizard

2021 ◽  
Author(s):  
David Kabelik
Keyword(s):  
Supraoptic Nucleus ◽  
Brain Regions ◽  
Corticotropin Releasing Factor ◽  
Cell Populations ◽  
Vertebrate Species ◽  
Anole Lizard ◽  
Reptile Species ◽  
Brown Anole ◽  
Crf Neurons ◽  
The Brain

AbstractCorticotropin-releasing factor (CRF) is best known for its involvement in peripheral glucocorticoid release across vertebrate species. However, CRF is also produced and released throughout various brain regions to regulate central aspects of the stress response. While these various CRF populations have been described extensively in mammals, less is known about their distributions in other amniotes, and only a handful of studies have ever examined CRF distributions in reptiles. Out study is the first to map CRF cell and fiber distributions in the brain of a lizard, the brown anole (Anolis sagrei). Our results indicate that brown anole CRF distributions are highly similar to those in snakes and turtles. However, unlike in these other reptile species, we find immunofluorescent CRF neurons in a few additional brown anole locations, most notably the supraoptic nucleus. The CRF distribution in the present study is also similar to published CRF descriptions in mammals and birds, although our findings, as well as the other published reports in reptiles, collectively suggest that reptiles possess a slightly more restricted distribution of CRF cell populations than do mammals and birds.

scholarly journals Involvement of different mesotocin (oxytocin homologue) populations in sexual and aggressive behaviours of the brown anole

2014 ◽  
Vol 10 (8) ◽  
pp. 20140566 ◽  
Author(s):  
David Kabelik ◽  
D. Sumner Magruder
Keyword(s):  
Neural Activity ◽  
Social Behaviour ◽  
Corticotropin Releasing Factor ◽  
Cell Populations ◽  
Cell Numbers ◽  
Mt Neurons ◽  
Anole Lizard ◽  
Brown Anole ◽  
Parvocellular Neurons ◽  
Aggressive Behaviours

The oxytocin (OT) family of neuropeptides are known to modulate social behaviours and anxiety in mammals and birds. We investigated cell numbers and neural activity, assessed as Fos induction, within magnocellular and parvocellular populations of neurons producing the OT homologue mesotocin (MT, Ile 8 -oxytocin). This was conducted within the male brown anole lizard, Anolis sagrei , following agonistic or courtship encounters with a conspecific. Both neurons colocalizing and not colocalizing corticotropin-releasing factor (CRF) were examined. Parvocellular neurons of the paraventricular nucleus exhibited a positive correlation between courtship frequency and Fos colocalization, regardless of whether they produce just MT or MT + CRF. Magnocellular populations showed only trends towards positive relationships with courtship and no cell populations showed aggression-related Fos induction. These findings are novel because they demonstrate the involvement of MT neurons in male social behaviour, especially in reptiles for whom the involvement of MT in social behaviour was previously unknown.

Stimuli and consequences of dendritic release of oxytocin within the brain

2007 ◽  
Vol 35 (5) ◽  
pp. 1252-1257 ◽  
Author(s):  
I.D. Neumann
Keyword(s):  
Paraventricular Nucleus ◽  
Stress Responses ◽  
Supraoptic Nucleus ◽  
Brain Regions ◽  
Model System ◽  
Intracerebral Microdialysis ◽  
Psychotherapeutic Intervention ◽  
Psychiatric Illnesses ◽  
Oxytocin Release ◽  
The Brain

The brain oxytocin system has served as a distinguished model system in neuroendocrinology to study detailed mechanisms of intracerebral release, in particular of somatodendritic release, and its behavioural and neuroendocrine consequences. It has been shown that oxytocin is released within various brain regions, but evidence for dendritic release is limited to the main sites of oxytocin synthesis, i.e. the hypothalamic SON (supraoptic nucleus) and PVN (paraventricular nucleus). In the present paper, stimuli of dendritic release of oxytocin and the related neuropeptide vasopressin are discussed, including parturition and suckling, i.e. the period of a highly activated brain oxytocin system. Also, exposure to various pharmacological, psychological or physical stressors triggers dendritic oxytocin release, as monitored by intracerebral microdialysis within the SON and PVN during ongoing behavioural testing. So far, dendritic release of the neuropeptide has only been demonstrated within the hypothalamus, but intracerebral oxytocin release has also been found within the central amygdala and the septum in response to various stimuli including stressor exposure. Such a locally released oxytocin modulates physiological and behavioural reproductive functions, emotionality and hormonal stress responses, as it exerts, for example, pro-social, anxiolytic and antistress actions within restricted brain regions. These discoveries make oxytocin a promising neuromodulator of the brain for psychotherapeutic intervention and treatment of numerous psychiatric illnesses, for example, anxiety-related diseases, social phobia, autism and postpartum depression.

Fever-specific changes in central MSH and CRF concentrations

1985 ◽  
Vol 248 (1) ◽  
pp. R125-R129
Author(s):  
M. Holdeman ◽  
O. Khorram ◽  
W. K. Samson ◽  
J. M. Lipton
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Heat Exposure ◽  
Brain Regions ◽  
Corticotropin Releasing Factor ◽  
Melanocyte Stimulating Hormone ◽  
Septal Region ◽  
Tissue Extracts ◽  
Central Gray ◽  
The Brain

The concentration of melanocyte-stimulating hormone (melanotropin; MSH) within the septal region of the brain increases during the fever, and septal injections of MSH are antipyretic. Corticotropin-releasing factor (CRF), when injected intracerebroventricularly, is also antipyretic. Using sensitive radioimmunoassays of microdissected tissue extracts, we established the presence of immunoreactive MSH (IRMSH) and CRF (IRCRF) within discrete central nervous system sites of the rabbit. Leukocytic pyrogen-induced fever and hyperthermia due to heat exposure did not alter concentrations of IRMSH or IRCRF in tissue extracted from preoptic-anterior hypothalamic or midbrain central gray regions. However, significantly greater levels of IRMSH were detected in septal extracts of febrile rabbits than in similar extracts from afebrile controls or heat-stressed animals. A significant decrease in IRCRF was detected in paraventricular nucleus extracts from febrile animals compared with extracts from afebrile controls or heat-stressed rabbits. Our results support the hypothesis that these central peptides have a role in temperature control during fever. Since no changes were detected in extracts from hyperthermic rabbits, it appears that changes in concentration of these neuropeptides within particular brain regions are specific to the febrile state and are not caused by elevation of body temperature or by nonspecific stress.

Effects of central sodium on epithelial sodium channels in rat brain

2010 ◽  
Vol 299 (1) ◽  
pp. R222-R233 ◽  
Author(s):  
Hong-Wei Wang ◽  
Md Shahrier Amin ◽  
Esraa El-Shahat ◽  
Bing S. Huang ◽  
Balwant S. Tuana ◽  
...  
Keyword(s):  
Choroid Plexus ◽  
Supraoptic Nucleus ◽  
Third Ventricle ◽  
Brain Regions ◽  
Neural Precursor Cells ◽  
Epithelial Sodium Channels ◽  
Artificial Cerebrospinal Fluid ◽  
Hypothalamic Nuclei ◽  
Hypothalamic Tissue ◽  
The Brain

We evaluated the effects of intracerebroventricular (icv) infusion of Na+-rich artificial cerebrospinal fluid (aCSF), with or without the mineralocorticoid receptor (MR) blocker spironolactone, on epithelial Na+ channel (ENaC) subunits and regulators, such as MR, serum/glucocorticoid-inducible kinase 1, neural precursor cells expressed developmentally downregulated 4-like gene, 11β-hydroxylase, and aldosterone synthase, in brain regions of Wistar rats. The effects of icv infusion of the amiloride analog benzamil on brain tissue and CSF Na+ concentration ([Na+]) were also assessed. In the choroid plexus and ependyma of the anteroventral third ventricle, ENaC subunits are present in apical and basal membranes. Na+-rich aCSF increased β-ENaC mRNA and immunoreactivity in the choroid plexus and increased α- and β-ENaC immunoreactivities in the ependyma. Na+-rich aCSF increased α- and β-ENaC-gold-labeled particles in the microvilli of the choroid plexus and in basolateral membranes of the ependyma. Spironolactone only prevented the increase in β-ENaC immunoreactivity in the choroid plexus and ependyma. In the supraoptic nucleus, paraventricular nucleus, and subfornical organ, Na+-rich aCSF did not affect mRNA expression levels of the studied genes. Benzamil significantly increased CSF [Na+] in the control, but not Na+-rich, aCSF group. In contrast, benzamil prevented the increase in hypothalamic tissue [Na+] by Na+-rich aCSF. These results suggest that CSF Na+ upregulates ENaC expression in the brain epithelia, but not in the neurons of hypothalamic nuclei. ENaC in the choroid plexus and ependyma appear to contribute to regulation of Na+ homeostasis in the brain.

Brain activation following peripheral administration of the GLP-1 receptor agonist exendin-4

2011 ◽  
Vol 301 (4) ◽  
pp. R1011-R1024 ◽  
Author(s):  
Elena-Dana Baraboi ◽  
David H. St-Pierre ◽  
Julie Shooner ◽  
Elena Timofeeva ◽  
Denis Richard
Keyword(s):  
Vagus Nerve ◽  
Mrna Expression ◽  
Supraoptic Nucleus ◽  
Brain Activation ◽  
Brain Regions ◽  
Nodose Ganglion ◽  
Central Regions ◽  
The Brain ◽  
Pituitary Adrenal Axis

The aim of our study was to investigate the anorectic and brain stimulatory effects of various doses of exendin-4 (Ex-4) and to investigate the role of the vagus nerve in Ex-4-induced brain activation. A dose-related increase in c- fos mRNA expression was observed following Ex-4 administration (0.155–15.5 μg/kg). Doses of Ex-4 that caused anorexia without aversive effects (0.155, 0.775 μg/kg) induced c- fos expression in the hypothalamic arcuate and paraventricular (PVH; parvocellular) nuclei as well as in the limbic and brainstem structures. Doses of Ex-4 that caused aversion (1.55, 15.5 μg/kg) stimulated the same regions (in a more intense way) and additionally activated the magnocellular hypothalamic structures (supraoptic nucleus and PVH magnocellular). The brain c- fos pattern induced by Ex-4 showed both similarities and differences with that induced by refeeding. Subdiaphragmatic vagotomy significantly blunted the stimulation of c- fos mRNA expression induced by Ex-4 in the nodose ganglion, the medial part of nucleus of the solitary tract, and the parvocellular division of the PVH. Pretreatment with Ex-9-39 (330 μg/kg ip) impaired the neuronal activation evoked by Ex-4 in all brain regions and in the nodose ganglion. Effects of Ex-4 on hypothalamic-pituitary-adrenal axis activity were not altered by vagotomy. Results of this study demonstrate and relate the anorectic and brain stimulatory effects of aversive and nonaversive doses of Ex-4 and indicate that the activation of specific central regions induced by the peripheral administration of Ex-4 is, at least in part, dependent on the integrity of the vagus nerve.

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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