scholarly journals Early Postnatal Hypoxia Induces Behavioral Deficits but not Morphological Damage in the Hippocampus in Adolescent Rats

2020 ◽  
pp. 165-179
Author(s):  
V. RILJAK ◽  
Z. LAŠTŮVKA ◽  
J. MYSLIVEČEK ◽  
V. BORBÉLYOVÁ ◽  
J. OTÁHAL

Hypoxia is one of the major pathological factors affecting brain function. The aim of the present study was to describe the effect of neonatal hypobaric hypoxia on the behavior of rats and to analyze its effect on hippocampal neurodegeneration. Hypobaric hypoxia at a simulated altitude of 9000 m was induced for one hour in neonatal rat pups (PND7 and PND9) of both sexes. Subsequently, the rats underwent behavioral testing on PND25 and PND35 using a LABORAS apparatus to assess spontaneous behavior. Hypoxia did not cause any morphological damage in the hippocampus of rats. However, hypoxia on PND7 led to less horizontal locomotor activity both in males (on PND25) and females (on PND35). Hypoxia on PND9 led to higher rearing in females on PND25. Hypoxic males exhibited higher grooming activity, while females lower grooming activity on PND35 following hypoxia induced on PND7. In females, hypoxia on PND9 resulted in higher grooming activity on PND25. Sex differences in the effect of hypoxia were observed on PND35, when hypoxic males compared to hypoxic females displayed more locomotor, rearing and grooming activity. Our data suggest that hypoxia on PND7 versus PND9 differently affects locomotion and grooming later in adolescence and these effects are sex-dependent.

2012 ◽  
pp. S111-S117
Author(s):  
K. JANDOVÁ ◽  
V. RILJAK ◽  
J. POKORNÝ ◽  
D. MAREŠOVÁ

The aim of our study was to test the hypothesis, whether repeated allopurinol pre-treatment (in dose of 135 mg/kg s.c.) can influence changes of brain excitability caused by long-term hypoxia exposition in young immature rats. Rat pups were exposed together with their mother in to an intermittent hypobaric hypoxia (simulated altitude of 7 000 m) since the day of birth till the 11th day (youngest experimental group) or 17th day for 8 hours a day. Allopurinol was administered daily immediately before each hypoxia exposition. The duration of evoked afterdischarges (ADs) and the shape of evoked graphoelements were evaluated in 12, 18, 25 and 35-day-old freely moving male pups. Hypobaric hypoxia prolonged the duration of ADs in 12, 18 and 25-day-old rats. The ADs were prolonged in 35-day-old rats only after the first stimulation. Allopurinol shorted the duration of ADs only in 12-day-old pups. In older experimental group the effect of allopurinol treatment was less pronounced.


1997 ◽  
Vol 21 (7) ◽  
pp. 1218-1225 ◽  
Author(s):  
Jennifer D. Thomas ◽  
Stephen P. Weinert ◽  
Sharerah Sharif ◽  
Edward P. Riley

1996 ◽  
Vol 82 (3) ◽  
pp. 903-911 ◽  
Author(s):  
Steven M. Specht ◽  
Richard G. Burright ◽  
Linda Patia Spear

Neonatal rat pups exhibit a complex constellation of behaviors in response to a variety of salient stimuli such as the odor of milk or maternal saliva, stroking with a soft brush, electrical brain stimulation, and intraoral infusions of milk. Although psychobiologists have used the term “behavioral activation” to refer to such behavioral displays, the exact nature of “behavioral activation” and its underlying neural substrates have yet to be elucidated. This study was undertaken to characterize “behavioral activation” quantitatively to describe and define this apparently global pattern of response in terms of possible underlying components. Principal components analysis suggested that “behavioral activation” may be comprised of separable ingestive, exploratory, and locomotor behavioral “assemblies.”


2011 ◽  
Vol 1425 ◽  
pp. 98-110 ◽  
Author(s):  
Filippos Karalis ◽  
Vassiliki Soubasi ◽  
Thomas Georgiou ◽  
Christos T. Nakas ◽  
Constantina Simeonidou ◽  
...  

2016 ◽  
Vol 120 (11) ◽  
pp. 1277-1287 ◽  
Author(s):  
Scott A. Givan ◽  
Kevin J. Cummings

5-HT neurons contribute to autoresuscitation and survival during intermittent severe hypoxia (IsH). In adults, catecholaminergic neurons in the ventrolateral medulla (VLM) contribute to the autonomic response to hypoxia. We hypothesized that 1) catecholaminergic neurons in the neonatal VLM are activated following IsH, 2) this activation is compromised following an acute loss of brain stem 5-HT, and 3) IsH induces cellular and/or transcriptomic plasticity within catecholaminergic and serotonergic neurons that are within or project to the VLM, respectively. To test these hypotheses, we treated rat pups with 6-fluorotryptophan, a tryptophan hydroxylase (TPH) inhibitor, and then exposed treated and vehicle controls to IsH or air. Along with immunohistochemistry to detect tyrosine hydroxylase (TH)- or Fos-positive neurons, we used RNA sequencing to resolve the effects of IsH and 5-HT deficiency on the expression of serotonergic and catecholaminergic system genes in the VLM. 5-HT deficiency compromised autoresuscitation and survival. IsH significantly increased the number of identifiable TH-positive VLM neurons, an effect enhanced by 5-HT deficiency ( P = 0.003). Contrary to our hypothesis, 5-HT-deficient pups had significantly more Fos-positive neurons following IsH ( P = 0.008) and more activated TH-positive neurons following IsH or air ( P = 0.04). In both groups the expression of the 5-HT transporter and TPH2 was increased following IsH. In 5-HT-deficient pups, the expression of the inhibitory 5-HT1A receptor was decreased following IsH, while the expression of DOPA decarboxylase was increased. These data show that the serotonergic and catecholaminergic systems in the VLM of the neonatal rat are dynamically upregulated by IsH, potentially adapting cardiorespiratory responses to severe hypoxia.


1990 ◽  
Vol 12 (2) ◽  
pp. 169-172 ◽  
Author(s):  
Kornélia Lehotzky ◽  
György Ungváry ◽  
Dezsö Polinák ◽  
Anna Kiss

1990 ◽  
Vol 259 (4) ◽  
pp. C654-C659 ◽  
Author(s):  
L. E. Costa

Hepatic cytochrome P-450 content in adaptation to hypobaric hypoxia was studied in three groups of rats and in their respective controls at sea level atmospheric pressure. The experimental groups were as follows: 1) young male and female rats submitted to 4,400 m (simulated altitude) for 6-8 mo, 2) the same animal model of group 1 submitted to 5,500 m (simulated altitude) for a subsequent period of 2-3 mo, and 3) adult males exposed to 5,500 m for 35 days. Hypoxia caused a marked polycythemia in all three groups, body weight loss in males of the three groups and at 5,500 m also in females, whereas liver weight was normal in groups 1 and 2 and slightly decreased in group 3. Cytochrome P-450 content measured in microsomal suspensions of groups 1 and 2 was unchanged. In liver homogenates, cytochrome P-450 content was normal at 4,400 m (group 1) and decreased at 5,500 m (groups 2 and 3). Therefore, endoplasmic reticulum mass, calculated as the ratio of cytochrome P-450 in the homogenates and in the isolated microsomes, was unchanged in group 1 (4,400 m) and decreased in group 2 (5,500 m). The content of antioxidant enzymes superoxide dismutase, catalase, and glutathione peroxidase, measured in liver homogenates of group 3, were markedly decreased (by 40, 30, and 35%, respectively). Results do not support the hypothesis that an increase in cytochrome P-450 content plays a role in adaptation to hypoxia.


2019 ◽  
Vol 87 (5) ◽  
Author(s):  
Alex J. McCarthy ◽  
George M. H. Birchenough ◽  
Peter W. Taylor

ABSTRACTGastrointestinal (GI) colonization of 2-day-old (P2) rat pups withEscherichia coliK1 results in translocation of the colonizing bacteria across the small intestine, bacteremia, and invasion of the meninges, with animals frequently succumbing to lethal infection. Infection, but not colonization, is strongly age dependent; pups become progressively less susceptible to infection over the P2-to-P9 period. Colonization leads to strong downregulation of the gene encoding trefoil factor 2 (Tff2), preventing maturation of the protective mucus barrier in the small intestine. Trefoil factors promote mucosal homeostasis. We investigated the contribution of Tff2 to protection of the neonatal rat fromE. coliK1 bacteremia and tissue invasion. Deletion oftff2, using clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9, sensitized P9 pups toE. coliK1 bacteremia. There were no differences betweentff2−/−homozygotes and the wild type with regard to the dynamics of GI colonization. Loss of the capacity to elaborate Tff2 did not impact GI tract integrity or the thickness of the small-intestinal mucus layer but, in contrast to P9 wild-type pups, enabledE. coliK1 bacteria to gain access to epithelial surfaces in the distal region of the small intestine and exploit an intracellular route across the epithelial monolayer to enter the blood circulation via the mesenteric lymphatic system. Although primarily associated with the mammalian gastric mucosa, we conclude that loss of Tff2 in the developing neonatal small intestine enables the opportunistic neonatal pathogenE. coliK1 to enter the compromised mucus layer in the distal small intestine prior to systemic invasion and infection.


1997 ◽  
Vol 272 (4) ◽  
pp. H1690-H1695 ◽  
Author(s):  
M. Pissarek ◽  
X. Bigard ◽  
P. Mateo ◽  
C. Y. Guezennec ◽  
J. A. Hoerter

The effects of chronic hypobaric hypoxia (CHH, 28 days, simulated altitude 5,500 m) on the cardiac expression of myosin heavy chain (MHC) and creatine kinase (CK) was studied in rat left (LV) and right (RV) ventricle. To separate the effects of hypoxia from its associated perturbations, anorexia and pulmonary hypertension (resulting in RV hypertrophy), CHH animals were compared with normoxic controls (C) and with rats restricted in food supply (pair fed, PF). In RV, the increased proportion of beta-MHC in CHH (20 +/- 3%) vs. C (7 +/- 2%, P < 0.01) and vs. PF (12 +/- 2%, P < 0.05) rats was mainly attributed to hypertension. In contrast, the higher beta-MHC of CHH (23 +/- 2%) vs. C (13 +/- 2%, P < 0.05) in LV was mainly ascribed to anorexia (PF = 21 +/- 3%, not significant). A major contribution of anorexia was also evidenced in the isozymic profile of CK; anorexia accounted for a 25% decrease in mito-CK specific activity in LV, whereas hypertension partly accounted for the threefold increase in BB-CK in RV. CHH specifically induced a twofold rise in LV BB-CK. This suggests that both the expression of slow myosin, improving the economy of contraction, and the changes in CK isozymic profile could provide a biochemical basis for the CHH resistance to ischemia.


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