Chronic haloperidol during development attenuates dopamine autoreceptor function in striatal and mesolimbic brain regions of young and older adult rats

1985 ◽  
Vol 85 (3) ◽  
pp. 271-276 ◽  
Author(s):  
Frank M. Scalzo ◽  
Linda Patia Spear
Keyword(s):  
Older Adult ◽  
Brain Regions ◽  
Adult Rats ◽  
Dopamine Autoreceptor ◽  
Chronic Haloperidol

scholarly journals Inflammation Biomarkers in Older Adult Rats Consuming Moderate Levels of Ethanol

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Lani Morales ◽  
Jacqueline Quigley ◽  
Jeremy Pascua ◽  
Natalie Pinkowski ◽  
Lama Almaiman ◽  
...  
Keyword(s):  
Older Adult ◽  
Adult Rats

Age-related susceptibility to muscle damage following mechanotherapy in rats recovering from disuse atrophy

2021 ◽  
Author(s):  
Zachary R Hettinger ◽  
Kyoko Hamagata ◽  
Amy L Confides ◽  
Marcus M Lawrence ◽  
Benjamin F Miller ◽  
...  
Keyword(s):  
Older Adults ◽  
Muscle Mass ◽  
Older Adult ◽  
Recovery Period ◽  
Male Rats ◽  
Hindlimb Suspension ◽  
Disuse Atrophy ◽  
Adult Rats ◽  
Transverse Stiffness ◽  
Age Related

Abstract The inability to fully recover lost muscle mass following periods of disuse atrophy predisposes older adults to lost independence and poor quality of life. We have previously shown that mechanotherapy at a moderate load (4.5 N) enhances muscle mass recovery following atrophy in adult, but not older adult rats. We propose that elevated transverse stiffness in aged muscle inhibits the growth response to mechanotherapy and hypothesize that a higher load (7.6 N) will overcome this resistance to mechanical stimuli. F344/BN adult and older adult male rats underwent 14-days of hindlimb suspension, followed by 7-days of recovery with (RE+M) or without (RE) mechanotherapy at 7.6 N on gastrocnemius muscle. The 7.6 N load was determined by measuring transverse passive stiffness and linearly scaling up from 4.5 N. No differences in protein turnover or mean fiber cross sectional area were observed between RE and RE+M for older adult rats or adult rats at 7.6 N. However, there was a higher number of small muscle fibers present in older adult, but not adult rats, which was explained by a 16-fold increase in the frequency of small fibers expressing embryonic myosin heavy chain. Elevated central nucleation, satellite cell abundance, and dystrophin -/laminin + fibers were present in older adult rats only following 7.6 N, while 4.5 N did not induce damage at either age. We conclude that age is an important variable when considering load used during mechanotherapy and age-related transverse stiffness may predispose older adults to damage during the recovery period following disuse atrophy.

scholarly journals Adrenergic-Induced Enhancement of Brain Barrier System Permeability to Small Nonelectrolytes: Choroid Plexus versus Cerebral Capillaries

1985 ◽  
Vol 5 (3) ◽  
pp. 401-412 ◽  
Author(s):  
Vincent A. Murphy ◽  
Conrad E. Johanson
Keyword(s):  
Choroid Plexus ◽  
Brain Regions ◽  
Volume Of Distribution ◽  
Brain Barrier ◽  
Sprague Dawley ◽  
Adult Rats ◽  
Acute Hypertension ◽  
Adrenergic Agents ◽  
Cerebral Capillaries ◽  
Choroid Plexuses

Acute hypertension induced by adrenergic agents opens up the blood–CSF barrier (choroid plexus) to nonelectrolyte and protein tracers. Sprague-Dawley adult rats anesthetized with ketamine were given an intravenous bolus of either epinephrine (10 μg/kg), phenylephrine (100 μg/kg), isoproterenol (10 μg/kg), or d,l-amphetamine (2 mg/kg). Tracers were injected simultaneously with test agents, and the animals killed 10 min later. Epinephrine raised MABP by 57 mm Hg, to a peak pressure of 160 mm Hg; and it increased the volume of distribution ( Vd) of urea, mannitol, and 125I-bovine serum albumin in CSF by 1.5-, 2.7-, and 30-fold, respectively. There was enhanced uptake by lateral and fourth ventricle choroid plexuses, cerebral cortex, cerebellum, medulla, and thalamus. Phenylephrine also elevated MABP to 160 mm Hg, but it increased permeation of tracers into CSF (and several brain regions) to a lesser extent than epinephrine, attributable to protective vasoconstriction associated with α-agonist activity. Ratio analysis of Vd data provides evidence that augmented permeation of nonelectrolyte tracers in acute hypertension occurs predominantly by diffusion rather than vesicular transport. It is postulated that elevated MABP distends the central cores of choroid plexus villi and cerebral capillaries, with resultant stretching and opening of tight junctions in both barrier systems; with less hindrance to diffusion, urea and mannitol are cleared at rates closer to free diffusion. Neither isoproterenol (decreased MABP by 40 mm Hg) nor amphetamine (did not alter MABP) significantly opened the choroid plexus or blood–brain barrier to tracers.

scholarly journals Ketosis Proportionately Spares Glucose Utilization in Brain

2013 ◽  
Vol 33 (8) ◽  
pp. 1307-1311 ◽  
Author(s):  
Yifan Zhang ◽  
Youzhi Kuang ◽  
Kui Xu ◽  
Donald Harris ◽  
Zhenghong Lee ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Ketone Bodies ◽  
Meta Analysis ◽  
Brain Regions ◽  
Primary Energy ◽  
Diet Group ◽  
Standard Diet ◽  
Metabolic Rates ◽  
Adult Rats ◽  
Ketogenic Diets

The brain is dependent on glucose as a primary energy substrate, but is capable of utilizing ketones such as β-hydroxybutyrate and acetoacetate, as occurs with fasting, starvation, or chronic feeding of a ketogenic diet. The relationship between changes in cerebral metabolic rates of glucose (CMRglc) and degree or duration of ketosis remains uncertain. To investigate if CMRglc decreases with chronic ketosis, 2-[18F]fluoro-2-deoxy-D-glucose in combination with positron emission tomography, was applied in anesthetized young adult rats fed 3 weeks of either standard or ketogenic diets. Cerebral metabolic rates of glucose (μmol/min per 100 g) was determined in the cerebral cortex and cerebellum using Gjedde-Patlak analysis. The average CMRglc significantly decreased in the cerebral cortex (23.0 ±4.9 versus 32.9 ±4.7) and cerebellum (29.3 ± 8.6 versus 41.2 ±6.4) with increased plasma ketone bodies in the ketotic rats compared with standard diet group. The reduction of CMRg|c in both brain regions correlates linearly by ∼9% for each 1 mmol/L increase of total plasma ketone bodies (0.3 to 6.3 mmol/L). Together with our meta-analysis, these data revealed that the degree and duration of ketosis has a major role in determining the corresponding change in CMRglc with ketosis.

scholarly journals Cortical Neurogenesis in Adult Rats after Reversible Photothrombotic Stroke

2000 ◽  
Vol 20 (8) ◽  
pp. 1166-1173 ◽  
Author(s):  
WeiGang Gu ◽  
Thomas Brännström ◽  
Per Wester
Keyword(s):  
At Risk ◽  
Cell Proliferation ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Three Dimensional ◽  
Brain Regions ◽  
Specific Marker ◽  
Cortical Region ◽  
Adult Rats ◽  
Adult Rat

Neurogenesis occurs throughout life in the dentate gyrus of hippocampus and subventricular zone, but this phenomenon has rarely been observed in other brain regions of adult mammals. The aim of the current study was to investigate the cell proliferation process in the ischemically challenged region-at-risk after focal cerebral ischemia in the adult rat brain. A reversible photothrombotic ring stroke model was used, which features sustained hypoperfusion followed by late spontaneous reperfusion and a remarkable morphologic tissue recovery in the anatomically well defined somatosensory cortical region-at-risk. Twelve-week-old male Wistar rats received repeated intraperitoneal injections of the cell proliferation specific marker 5-bromodeoxyuridine (BrdU) after stroke induction. Immunocytochemistry of coronal brain sections revealed that the majority of BrdU-positive cells were of glial, macrophage, and endothelial origin, whereas 3% to 6% of the BrdU-positive cells were double-labeled by BrdU and the neuron-specific marker Map-2 at 7 and 100 days after stroke onset in the region-at-risk. They were distributed randomly in cortical layers II-VI. Three-dimensional confocal analyses of BrdU and the neuronal-specific marker Neu N by double immunofluorescence confirmed their colocalization within the same cells at 72 hours and 30 days after stroke induction. This study suggests that, as a potential pathway for brain repair, new neurons can be generated in the cerebral cortex of adult rats after sublethal focal cerebral ischemia.

scholarly journals Allergic Rhinitis in Rats Is Associated with an Inflammatory Response of the Hippocampus

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Shasha Yang ◽  
Jing Wu ◽  
Qinxiu Zhang ◽  
Xinrong Li ◽  
Daien Liu ◽  
...  
Keyword(s):  
Allergic Rhinitis ◽  
Inflammatory Responses ◽  
Brain Regions ◽  
Abnormal Behavior ◽  
Neurological Deficits ◽  
Glial Fibrillary Acid Protein ◽  
Adult Rats ◽  
Memory Decline ◽  
Acid Protein ◽  
And Behavior

Allergic rhinitis (AR) is a major concern in personal and public health, which negatively affects emotions and behavior, leading to cognitive deficits, memory decline, poor school performance, anxiety, and depression. Several cellular and molecular mediators are released in the inflammatory process of AR and activate common neuroimmune mechanisms, involving emotionally relevant circuits and the induction of anxiety. Responsiveness of the hypothalamic-pituitary-adrenal (HPA) axis to allergic processes have been reported, which may also include responsiveness of the hippocampus, cortex, and other brain regions. Here, we have used an optimized rat model of AR to explore whether the disease has a relationship with inflammatory responses in the hippocampus. AR was established in adult rats by ovalbumin sensitization, and the expression of various inflammatory substances in the hippocampus was measured by specific assays. Comparison between experimental and various control groups of animals revealed an association of AR with significant upregulation of substance P, microglia surface antigen (CD11b), glial fibrillary acid protein (GFAP), tumor necrosis factor-α (TNF-α), and interleukin 6 (IL-6) in the hippocampus. Thus, we hypothesize that the AR challenge may activate these inflammatory mediators in the hippocampus, which in turn contribute to the abnormal behavior and neurological deficits associated with AR.

scholarly journals Transfer Constants for Blood-Brain Barrier Permeation of the Neuroexcitatory Shellfish Toxin, Domoic Acid

1991 ◽  
Vol 18 (1) ◽  
pp. 39-44 ◽  
Author(s):  
Edward Preston ◽  
Ivo Hynie
Keyword(s):  
Blood Brain Barrier ◽  
Domoic Acid ◽  
Carrier Transport ◽  
Polar Compounds ◽  
Brain Regions ◽  
Brain Barrier ◽  
Adult Rats ◽  
Mean Values ◽  
Blood Brain ◽  
The Brain

ABSTRACT:The cause of the toxic mussel poisoning episode in 1987 was traced to a plankton-produced excitotoxin, domoic acid. Experiments were undertaken to quantitate the degree to which blood-borne domoic acid can permeate the microvasculature to enter the brain. Pentobarbital-anesthetized, adult rats received an i.v. injection of 3H-domoic acid which was permitted to circulate for 3-60 min. Transfer constants (Ki) describing blood-to-brain diffusion of tracer were calculated from analysis of the relationship between brain vs plasma radioactivity with time. Mean values (mL.g-1.s-1 x 106) for permeation into 7 brain regions (n = 10 rats) ranged from 1.60 ± 0.13 (SE) to 1.86 ± 0.33 (cortex, ponsmedulla respectively), and carrier transport or regional selectivity in uptake were not evident. Nephrectomy prior to domoic acid injection resulted in the elevation of circulating plasma tracer level and brain uptake. The Ki values are comparable to those for other polar compounds such as sucrose, and indicate that the blood-brain barrier greatly limits the amount of toxin that enters the brain. Together with absorbed dosage, integrity of the cerebrovascular barrier and normal kidney function are important to the outcome of accidentally ingesting domoic acid.

scholarly journals Regional Brain Blood Flow, Blood Volume, and Haematocrit Values in the Adult Rat

1983 ◽  
Vol 3 (2) ◽  
pp. 254-256 ◽  
Author(s):  
Jill E. Cremer ◽  
Malcolm P. Seville
Keyword(s):  
Blood Flow ◽  
Blood Volume ◽  
Brain Regions ◽  
Adult Rats ◽  
Adult Rat ◽  
Systemic Artery ◽  
Significant Difference ◽  
Total Body ◽  
The Brain ◽  
Made In

Measurements of red cell volume, plasma volume, and tissue haematocrit (Hct) were made in 14 brain regions in adult rats using 51Cr-tagged red cells and 125I-labeled human serum albumin. The mean large vessel (systemic artery) Hct was 41.8, total body Hct was 35.3, and of the brain regions, the lowest value (septal nucleus) was 25.91 and the highest (visual cortex) was 32.05. The lowest blood volume was 6.29 μl g−1 (caudate putamen) and the highest was 14.44 μl g−1 (inferior colliculus). There was a significant difference between regions in both blood volume and tissue blood Hct. When brain regions were ranked in order of blood volume, this did not coincide with the order for blood flow.

scholarly journals Energy Drink Administration in Combination with Alcohol Causes an Inflammatory Response and Oxidative Stress in the Hippocampus and Temporal Cortex of Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Alfonso Díaz ◽  
Samuel Treviño ◽  
Jorge Guevara ◽  
Guadalupe Muñoz-Arenas ◽  
Eduardo Brambila ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Inflammatory Response ◽  
Temporal Cortex ◽  
Energy Drink ◽  
Brain Regions ◽  
Adult Rats ◽  
Mechanisms Of Toxicity ◽  
The Brain ◽  
And Oxidative Stress

Energy drinks (EDs) are often consumed in combination with alcohol because they reduce the depressant effects of alcohol. However, different researches suggest that chronic use of these psychoactive substances in combination with alcohol can trigger an oxidative and inflammatory response. These processes are regulated by both a reactive astrogliosis and an increase of proinflammatory cytokines such as IL-1β, TNF-α, and iNOS, causing cell death (apoptosis) at the central and peripheral nervous systems. Currently, mechanisms of toxicity caused by mixing alcohol and ED in the brain are not well known. In this study, we evaluated the effect of chronic alcohol consumption in combination with ED on inflammatory response and oxidative stress in the temporal cortex (TCx) and hippocampus (Hp) of adult rats (90 days old). Our results demonstrated that consuming a mixture of alcohol and ED for 60 days induced an increase in reactive gliosis, IL-1β, TNF-α, iNOS, reactive oxygen species, lipid peroxidation, and nitric oxide, in the TCx and Hp. We also found immunoreactivity to caspase-3 and a decrease of synaptophysin in the same brain regions. The results suggested that chronic consumption of alcohol in combination with ED causes an inflammatory response and oxidative stress, which induced cell death via apoptosis in the TCx and Hp of the adult rats.

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