Metabolic activity in the brain of juvenile and adult rats with a neonatal ventral hippocampal lesion

Hippocampus ◽  
2009 ◽  
pp. NA-NA ◽  
Author(s):  
Jennifer François ◽  
Estelle Koning ◽  
Arielle Ferrandon ◽  
Guy Sandner ◽  
Astrid Nehlig
Keyword(s):  
Metabolic Activity ◽  
Hippocampal Lesion ◽  
Adult Rats ◽  
The Brain ◽  
Neonatal Ventral Hippocampal Lesion

Histological correlates of N40 auditory evoked potentials in adult rats after neonatal ventral hippocampal lesion: animal model of schizophrenia

2014 ◽  
Vol 159 (2-3) ◽  
pp. 450-457 ◽  
Author(s):  
A.L. Romero-Pimentel ◽  
R.A. Vázquez-Roque ◽  
I. Camacho-Abrego ◽  
K.L. Hoffman ◽  
P. Linares ◽  
...  
Keyword(s):  
Animal Model ◽  
Evoked Potentials ◽  
Hippocampal Lesion ◽  
Auditory Evoked Potentials ◽  
Lesion Animal ◽  
Adult Rats ◽  
Neonatal Ventral Hippocampal Lesion

scholarly journals Intermittent Hypobaric Hypoxic Preconditioning Provides Neuroprotection by Increasing Antioxidant Activity, Erythropoietin Expression and Preventing Apoptosis and Astrogliosis in the Brain of Adult Rats Exposed to Acute Severe Hypoxia

2021 ◽  
Vol 22 (10) ◽  
pp. 5272
Author(s):  
Débora Coimbra-Costa ◽  
Fernando Garzón ◽  
Norma Alva ◽  
Tiago C. C. Pinto ◽  
Fernando Aguado ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hypobaric Hypoxia ◽  
Hypoxic Preconditioning ◽  
Severe Hypoxia ◽  
Efficient Tool ◽  
Adult Rats ◽  
Therapeutic Benefits ◽  
Background Exposure ◽  
The Brain ◽  
Apoptotic Cascade

Background: Exposure to intermittent hypoxia has been demonstrated to be an efficient tool for hypoxic preconditioning, preventing damage to cells and demonstrating therapeutic benefits. We aimed to evaluate the effects of respiratory intermittent hypobaric hypoxia (IHH) to avoid brain injury caused by exposure to acute severe hypoxia (ASH). Methods: biomarkers of oxidative damage, mitochondrial apoptosis, and transcriptional factors in response to hypoxia were assessed by Western blot and immunohistochemistry in brain tissue. Four groups of rats were used: (1) normoxic (NOR), (2) exposed to ASH (FiO2 7% for 6 h), (3) exposed to IHH for 3 h per day over 8 days at 460 mmHg, and (4) ASH preconditioned after IHH. Results: ASH animals underwent increased oxidative-stress-related parameters, an upregulation in apoptotic proteins and had astrocytes with phenotype forms compatible with severe diffuse reactive astrogliosis. These effects were attenuated and even prevented when the animals were preconditioned with IHH. These changes paralleled the inhibition of NF-κB expression and the increase of erythropoietin (EPO) levels in the brain. Conclusions: IHH exerted neuroprotection against ASH-induced oxidative injury by preventing oxidative stress and inhibiting the apoptotic cascade, which was associated with NF-κB downregulation and EPO upregulation.

scholarly journals Transfer of rhodamine-123 into the brain and cerebrospinal fluid of fetal, neonatal and adult rats

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Liam M. Koehn ◽  
Katarzyna M. Dziegielewska ◽  
Mark D. Habgood ◽  
Yifan Huang ◽  
Norman R. Saunders
Keyword(s):  
Cerebrospinal Fluid ◽  
Fetal Brain ◽  
Maternal Blood ◽  
Adult Brain ◽  
Rhodamine 123 ◽  
Patient Specific ◽  
Adult Rats ◽  
Blood Brain ◽  
The Brain ◽  
Brain Barriers

Abstract Background Adenosine triphosphate binding cassette transporters such as P-glycoprotein (PGP) play an important role in drug pharmacokinetics by actively effluxing their substrates at barrier interfaces, including the blood-brain, blood-cerebrospinal fluid (CSF) and placental barriers. For a molecule to access the brain during fetal stages it must bypass efflux transporters at both the placental barrier and brain barriers themselves. Following birth, placental protection is no longer present and brain barriers remain the major line of defense. Understanding developmental differences that exist in the transfer of PGP substrates into the brain is important for ensuring that medication regimes are safe and appropriate for all patients. Methods In the present study PGP substrate rhodamine-123 (R123) was injected intraperitoneally into E19 dams, postnatal (P4, P14) and adult rats. Naturally fluorescent properties of R123 were utilized to measure its concentration in blood-plasma, CSF and brain by spectrofluorimetry (Clariostar). Statistical differences in R123 transfer (concentration ratios between tissue and plasma ratios) were determined using Kruskal-Wallis tests with Dunn’s corrections. Results Following maternal injection the transfer of R123 across the E19 placenta from maternal blood to fetal blood was around 20 %. Of the R123 that reached fetal circulation 43 % transferred into brain and 38 % into CSF. The transfer of R123 from blood to brain and CSF was lower in postnatal pups and decreased with age (brain: 43 % at P4, 22 % at P14 and 9 % in adults; CSF: 8 % at P4, 8 % at P14 and 1 % in adults). Transfer from maternal blood across placental and brain barriers into fetal brain was approximately 9 %, similar to the transfer across adult blood-brain barriers (also 9 %). Following birth when placental protection was no longer present, transfer of R123 from blood into the newborn brain was significantly higher than into adult brain (3 fold, p < 0.05). Conclusions Administration of a PGP substrate to infant rats resulted in a higher transfer into the brain than equivalent doses at later stages of life or equivalent maternal doses during gestation. Toxicological testing of PGP substrate drugs should consider the possibility of these patient specific differences in safety analysis.

scholarly journals The path from trigeminal asymmetry to cognitive impairment: a behavioral and molecular study

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Maria Paola Tramonti Fantozzi ◽  
Giulia Lazzarini ◽  
Vincenzo De Cicco ◽  
Angela Briganti ◽  
Serena Argento ◽  
...  
Keyword(s):  
Pupil Size ◽  
Muscle Spindles ◽  
Molecular Study ◽  
Contralateral Side ◽  
Acute Effects ◽  
Adult Rats ◽  
Afferent Inputs ◽  
Acute And Chronic Effects ◽  
The Brain ◽  
Mandibular Branch

AbstractTrigeminal input exerts acute and chronic effects on the brain, modulating cognitive functions. Here, new data from humans and animals suggest that these effects are caused by trigeminal influences on the Locus Coeruleus (LC). In humans subjects clenching with masseter asymmetric activity, occlusal correction improved cognition, alongside with reductions in pupil size and anisocoria, proxies of LC activity and asymmetry, respectively. Notably, reductions in pupil size at rest on the hypertonic side predicted cognitive improvements. In adult rats, a distal unilateral section of the trigeminal mandibular branch reduced, on the contralateral side, the expression of c-Fos (brainstem) and BDNF (brainstem, hippocampus, frontal cortex). This counterintuitive finding can be explained by the following model: teeth contact perception loss on the lesioned side results in an increased occlusal effort, which enhances afferent inputs from muscle spindles and posterior periodontal receptors, spared by the distal lesion. Such effort leads to a reduced engagement of the intact side, with a corresponding reduction in the afferent inputs to the LC and in c-Fos and BDNF gene expression. In conclusion, acute effects of malocclusion on performance seem mediated by the LC, which could also contribute to the chronic trophic dysfunction induced by loss of trigeminal input.

Effects of ventral hippocampal lesion on thermal and mechanical nociception in neonates and adult rats

2004 ◽  
Vol 20 (11) ◽  
pp. 3027-3034 ◽  
Author(s):  
Hassen A. Al Amin ◽  
Samir F. Atweh ◽  
Suhayl J. Jabbur ◽  
Nayef E. Saadé
Keyword(s):  
Hippocampal Lesion ◽  
Adult Rats

Expression of Human Neurofilament-light Transgene in Mouse Neurons Transplanted into the Brain of Adult Rats

1991 ◽  
Vol 3 (8) ◽  
pp. 758-763 ◽  
Author(s):  
Manuel Vidal-Sanz ◽  
Maria P. Villegas-Perez ◽  
David A. Carter ◽  
Jean-Pierre Julien ◽  
Alan Peterson ◽  
...  
Keyword(s):  
Adult Rats ◽  
Neurofilament Light ◽  
The Brain

Hippocampal glutamine synthetase: insensitivity to glucocorticoids and stress

1990 ◽  
Vol 258 (5) ◽  
pp. E894-E897 ◽  
Author(s):  
G. C. Tombaugh ◽  
R. M. Sapolsky
Keyword(s):  
Skeletal Muscle ◽  
Central Nervous System ◽  
Nervous System ◽  
Glutamine Synthetase ◽  
Glutamate Metabolism ◽  
Glutamatergic Synapses ◽  
Adult Rats ◽  
Glucocorticoid Induction ◽  
The Central Nervous System ◽  
The Brain

Glucocorticoids enhance the neurotoxic potential of several insults to the rat hippocampus that involve overactivation of glutamatergic synapses. These hormones also stimulate the synthesis of glutamine synthetase (GS) in peripheral tissue. Because this enzyme helps regulate glutamate metabolism in the central nervous system, glucocorticoid induction of GS in the brain may underlie the observed synergy. We have measured GS activity in the hippocampus and skeletal muscle (plantaris) of adult rats after bilateral adrenalectomy (ADX), corticosterone (Cort) replacement, or stress. No significant changes in GS were observed in hippocampal tissue, whereas muscle GS was significantly elevated after Cort treatment or stress and was reduced after ADX. These results suggest that Cort-induced shifts in GS activity probably do not explain Cort neurotoxicity, although the stress-induced rise in muscle GS may be relevant to certain types of myopathy.

scholarly journals NeuroRoots, a bio-inspired, seamless Brain Machine Interface device for long-term recording

2018 ◽  
Author(s):  
Marc D. Ferro ◽  
Christopher M. Proctor ◽  
Alexander Gonzalez ◽  
Eric Zhao ◽  
Andrea Slezia ◽  
...  
Keyword(s):  
Neurological Diseases ◽  
Signal Amplitude ◽  
Brain Machine Interface ◽  
Behavioral Experiments ◽  
Adult Rats ◽  
Integrative Level ◽  
Machine Interface ◽  
Freely Moving ◽  
The Brain

AbstractMinimally invasive electrodes of cellular scale that approach a bio-integrative level of neural recording could enable the development of scalable brain machine interfaces that stably interface with the same neural populations over long period of time.In this paper, we designed and created NeuroRoots, a bio-mimetic multi-channel implant sharing similar dimension (10µm wide, 1.5µm thick), mechanical flexibility and spatial distribution as axon bundles in the brain. A simple approach of delivery is reported based on the assembly and controllable immobilization of the electrode onto a 35µm microwire shuttle by using capillarity and surface-tension in aqueous solution. Once implanted into targeted regions of the brain, the microwire was retracted leaving NeuroRoots in the biological tissue with minimal surgical footprint and perturbation of existing neural architectures within the tissue. NeuroRoots was implanted using a platform compatible with commercially available electrophysiology rigs and with measurements of interests in behavioral experiments in adult rats freely moving into maze. We demonstrated that NeuroRoots electrodes reliably detected action potentials for at least 7 weeks and the signal amplitude and shape remained relatively constant during long-term implantation.This research represents a step forward in the direction of developing the next generation of seamless brain-machine interface to study and modulate the activities of specific sub-populations of neurons, and to develop therapies for a plethora of neurological diseases.

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