In vivo Nuclear 3H-Estradiol Binding in Brain Areas of the Rat: Reduction by Endogenous and Exogenous Androgens

1976 ◽  
Vol 21 (4) ◽  
pp. 350-365 ◽  
Author(s):  
L. Ogren ◽  
M. Vértes ◽  
D. Woolley
Keyword(s):  
Brain Areas

scholarly journals Norepinephrine Protects against Methamphetamine Toxicity through β2-Adrenergic Receptors Promoting LC3 Compartmentalization

2021 ◽  
Vol 22 (13) ◽  
pp. 7232
Author(s):  
Gloria Lazzeri ◽  
Carla L. Busceti ◽  
Francesca Biagioni ◽  
Cinzia Fabrizi ◽  
Gabriele Morucci ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Light Chain ◽  
Adrenergic Receptors ◽  
Cell Damage ◽  
Protective Effects ◽  
Autophagy Flux ◽  
Brain Areas ◽  
Indirect Consequence

Norepinephrine (NE) neurons and extracellular NE exert some protective effects against a variety of insults, including methamphetamine (Meth)-induced cell damage. The intimate mechanism of protection remains difficult to be analyzed in vivo. In fact, this may occur directly on target neurons or as the indirect consequence of NE-induced alterations in the activity of trans-synaptic loops. Therefore, to elude neuronal networks, which may contribute to these effects in vivo, the present study investigates whether NE still protects when directly applied to Meth-treated PC12 cells. Meth was selected based on its detrimental effects along various specific brain areas. The study shows that NE directly protects in vitro against Meth-induced cell damage. The present study indicates that such an effect fully depends on the activation of plasma membrane β2-adrenergic receptors (ARs). Evidence indicates that β2-ARs activation restores autophagy, which is impaired by Meth administration. This occurs via restoration of the autophagy flux and, as assessed by ultrastructural morphometry, by preventing the dissipation of microtubule-associated protein 1 light chain 3 (LC3) from autophagy vacuoles to the cytosol, which is produced instead during Meth toxicity. These findings may have an impact in a variety of degenerative conditions characterized by NE deficiency along with autophagy impairment.

NE turnover in genetically hypertensive rats of Lyon strain. I. Brain nuclei

1988 ◽  
Vol 255 (4) ◽  
pp. H729-H735 ◽  
Author(s):  
M. Sautel ◽  
J. Sacquet ◽  
M. Vincent ◽  
J. Sassard
Keyword(s):  
Blood Pressure ◽  
Hypothalamic Nucleus ◽  
Primary Role ◽  
Hypertensive Rats ◽  
Brain Areas ◽  
Brain Nuclei ◽  
Genetically Hypertensive Rats ◽  
Low Blood Pressure ◽  
Genetically Hypertensive

Several indirect evidences of alterations in the central catecholaminergic structures were obtained in genetically hypertensive rats. Because they could be of pathogenetic value, we measured, in the present work, the in vivo turnover (TO) of norepinephrine (NE) in brain areas of 5- and 22-wk-old genetically hypertensive (LH) rats of the Lyon strain, and their simultaneously selected normotensive (LN) and low blood pressure (LL) controls. Among the changes observed, the increased TO of NE in the A2 and A6 regions of 5-wk-old LH rats and its decrease in the posteroventral hypothalamic nucleus of 22-wk-old LH animals appeared likely to compensate for hypertension. On the contrary, the decreased TO of NE in the anterior hypothalamic nucleus observed at 5 wk and in the A6 and A1 areas at 22 wk of age in LH rats could participate in the development or the maintenance of hypertension. Above all, it was postulated that the increased TO of NE found in the A7 region of 5-wk-old LH rats could play a primary role in the pathogenesis of hypertension in the Lyon model.

In vivo conversion of vasopressin after microinjection into limbic brain areas of rats

Peptides ◽  
1989 ◽  
Vol 10 (4) ◽  
pp. 717-720 ◽  
Author(s):  
Holger Stark ◽  
J.Peter H. Burbach ◽  
Arno A.M. Van Der Kleij ◽  
David De Wied
Keyword(s):  
Brain Areas

scholarly journals Neuronal spreading and plaque induction of intracellular Aβ and its disruption of Aβ homeostasis

2021 ◽  
Author(s):  
Tomas T. Roos ◽  
Megg G. Garcia ◽  
Isak Martinsson ◽  
Rana Mabrouk ◽  
Bodil Israelsson ◽  
...  
Keyword(s):  
Brain Homogenate ◽  
Fold Increase ◽  
Amyloid Beta Peptide ◽  
Intracellular Accumulation ◽  
Brain Areas ◽  
Cellular Models ◽  
Beta Peptide ◽  
The Brain

AbstractThe amyloid-beta peptide (Aβ) is thought to have prion-like properties promoting its spread throughout the brain in Alzheimer’s disease (AD). However, the cellular mechanism(s) of this spread remains unclear. Here, we show an important role of intracellular Aβ in its prion-like spread. We demonstrate that an intracellular source of Aβ can induce amyloid plaques in vivo via hippocampal injection. We show that hippocampal injection of mouse AD brain homogenate not only induces plaques, but also damages interneurons and affects intracellular Aβ levels in synaptically connected brain areas, paralleling cellular changes seen in AD. Furthermore, in a primary neuron AD model, exposure of picomolar amounts of brain-derived Aβ leads to an apparent redistribution of Aβ from soma to processes and dystrophic neurites. We also observe that such neuritic dystrophies associate with plaque formation in AD-transgenic mice. Finally, using cellular models, we propose a mechanism for how intracellular accumulation of Aβ disturbs homeostatic control of Aβ levels and can contribute to the up to 10,000-fold increase of Aβ in the AD brain. Our data indicate an essential role for intracellular prion-like Aβ and its synaptic spread in the pathogenesis of AD.

scholarly journals Amyloid-ß promotes neurotoxicity by Cdk5-induced p53 stabilization

2018 ◽  
Author(s):  
Rebeca Lapresa ◽  
Jesús Agulla ◽  
Irene Sánchez-Morán ◽  
Juan P. Bolaños ◽  
Angeles Almeida
Keyword(s):  
Neuronal Apoptosis ◽  
Therapeutic Strategy ◽  
Neuronal Damage ◽  
P53 Protein ◽  
Protein A ◽  
Tumor Suppressor Protein ◽  
Protein Accumulation ◽  
Brain Areas ◽  
P53 Tumor Suppressor Protein

ABSTRACTThe p53 tumor suppressor protein, a key regulator of cell apoptosis, has been described to accumulate in affected brain areas from Alzheimer’s disease (AD) patients. However, whether p53 plays any role in AD pathogenesis remains unknown. Here, we found that exposure of neurons to oligomers of the amyloidogenic fragment 25-35 of the Aß peptide (Aβ25-35) activated Cdk5, which promoted p53 protein phosphorylation and stabilization. Moreover, Aβ25-35-mediated mitochondrial dysfunction and neuronal apoptosis were prevented by both genetic and pharmacological inhibition of either p53 or Cdk5 activities. To confirm this mechanism in vivo, Aβ25-35 was stereotaxically injected in the cerebral right ventricle of mice, a treatment that caused p53 protein accumulation, dendrite disruption and neuronal death. Furthermore, these effects were prevented in p53 knockout mice or by pharmacologically inhibiting p53. Thus, Aβ25-35 triggers Cdk5 activation to induce p53 phosphorylation and stabilization, which leads to neuronal damage. Inhibition of the Cdk5-p53 pathway may therefore represent a novel therapeutic strategy against Aβ-induced neurodegeneration.

Targeting of Thymoquinone-loaded mesoporous silica nanoparticles to different brain areas: In vivo study

Life Sciences ◽  
2019 ◽  
Vol 222 ◽  
pp. 94-102 ◽  
Author(s):  
Heba M. Fahmy ◽  
Mohamed M. Fathy ◽  
Raghda A. Abd-elbadia ◽  
Wael M. Elshemey
Keyword(s):  
Mesoporous Silica ◽  
Silica Nanoparticles ◽  
Mesoporous Silica Nanoparticles ◽  
In Vivo Study ◽  
Brain Areas

Delayed differential alterations in human brain volume in affected and remote brain areas after cerebral infarction measured intraindividually in vivo by 3D-MRI volumetry

NeuroImage ◽  
2001 ◽  
Vol 13 (6) ◽  
pp. 804 ◽  
Author(s):  
Matthias Kraemer ◽  
Thorsten Schormann ◽  
Peter Bi ◽  
Georg Hagemann ◽  
Karl Zilles ◽  
...  
Keyword(s):  
Cerebral Infarction ◽  
Human Brain ◽  
Brain Volume ◽  
3D Mri ◽  
Brain Areas ◽  
Mri Volumetry

In vivo Conversion of 3H-L-Tryptophan into 3H-Serotonin in Brain Areas of Adrenalectomized Rats

Science ◽  
1970 ◽  
Vol 169 (3941) ◽  
pp. 201-203 ◽  
Author(s):  
E. C. Azmitia ◽  
S. Algeri ◽  
E. Costa
Keyword(s):  
Brain Areas ◽  
Adrenalectomized Rats

scholarly journals Multi-Neuromodulator Measurements across Fronto-Striatal Network Areas of the Behaving Macaque using Solid-Phase Microextraction

2019 ◽  
Author(s):  
Seyed-Alireza Hassani ◽  
Sofia Lendor ◽  
Ezel Boyaci ◽  
Janusz Pawliszyn ◽  
Thilo Womelsdorf
Keyword(s):  
Solid Phase Microextraction ◽  
Solid Phase ◽  
Brain Regions ◽  
Brain Areas ◽  
Brain States ◽  
High Consistency ◽  
Local Circuits ◽  
Collective Influence ◽  
Goal Directed Behavior

AbstractDifferent neuromodulators rarely act independent from each other to modify neural processes but are instead co-released, gated, or modulated. To understand this interdependence of neuromodulators and their collective influence on local circuits during different brain states, it is necessary to reliably extract local concentrations of multiple neuromodulators in vivo. Here we describe results using solid phase microextraction (SPME), a method providing sensitive, multi-neuromodulator measurements. SPME is a sampling method that is coupled with mass spectrometry to quantify collected analytes. Reliable measurements of glutamate, dopamine, acetylcholine and choline were made simultaneously within frontal cortex and striatum of two macaque monkeys (Macaca mulatta) during goal-directed behavior. We find glutamate concentrations several orders of magnitude higher than acetylcholine and dopamine in all brain regions. Dopamine was reliably detected in the striatum at tenfold higher concentrations than acetylcholine. Acetylcholine and choline concentrations were detected with high consistency across brain areas, within monkeys and between monkeys. These findings illustrate that SPME microprobes provide a versatile novel tool to characterize multiple neuromodulators across different brain areas in vivo to understand the interdependence and co-variation of neuromodulators during goal directed behavior. Such data will be important to better distinguish between different behavioral states and characterize dysfunctional brain states that may be evident in psychiatric disorders.

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