Water maze and radial maze learning and the density of binding sites of glutamate, GABA, and serotonin receptors in the hippocampus of inbred mouse strains

Zilles, Karl; Wu, Jang‐Yen; Crusio, Wim E.; Schwegler, Herbert

doi:10.1002/1098-1063(2000)10:3<213::aid-hipo2>3.0.co;2-q

Cited by 56 publications

(18 citation statements)

References 111 publications

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“…In the present study, reduced excitation in the hippocampal circuit was further potentiated by an increase of ligand binding densities of the inhibitory GABA A receptor resulting in a relative shift in favor of inhibition and impaired behavioral performance. Our results differ from findings by Zilles et al (2000), who were not able to detect a correlation between NMDA receptor density and behavioral performance in a Morris water test in seven different mouse strains. In their study naive strain means were used for analysis, whereas the present study drew on mean values resulting from individual animals and previous testing.…”

Section: Discussioncontrasting

confidence: 99%

“…Moreover, reduced ligand binding to inhibitory GABA A receptors in the hippocampus may also play a crucial role for the poorer performance in the skilled motor test. In fact, GABA A receptor binding density has recently been shown to negatively correlate with activity-dependent scores resulting from the swimming speed in a water maze test (Zilles et al, 2000). The enhancement of motor function after G-CSF treatment as seen in earlier studies might be the result of enhanced motor skill learning and thereby exceeding growth factor enhanced recovery processes.…”

Section: Discussionmentioning

confidence: 83%

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The Role of Granulocyte-Colony Stimulating Factor (G-CSF) in the Healthy Brain: A Characterization of G-CSF-Deficient Mice

Diederich¹,

Sevimli²,

Dörr³

et al. 2009

J. Neurosci.

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Granulocyte-colony stimulating factor (G-CSF) is a hematopoietic growth factor that controls proliferation and differentiation of neural stem cells. Although recent studies have begun to explore G-CSF-related mechanisms of action in various disease models, little is known about its function in the healthy brain. In the present study, the effect of G-CSF deficiency on memory formation and motor skills was investigated. The impact of G-CSF deficiency on the structural integrity of the hippocampus was evaluated by analyzing the generation of doublecortin-expressing cells, the amount of bromodeoxyurine-labeled cells, the dendritic complexity in hippocampal neurons, the binding densities of NMDA and GABA A receptors and the induction of long-term potentiation (LTP). G-CSF deficiency caused a disruption in memory formation and in the development of motor skills. These impairments were associated with reduced ligand binding densities of NMDA receptors in hippocampal subfields CA3 and the dentate gyrus. The reduced excitation was potentiated by increased ligand binding densities of GABA A receptors resulting in a relative shift in favor of inhibition and impaired behavioral performance. These alterations were accompanied by impaired induction of LTP in the CA1 region. Moreover, G-CSF deficiency led to decreased dendritic complexity in hippocampal neurons in the dentate gyrus and the CA1 region. G-CSF deficiency also caused a reduction of neuronal precursor cells in the dentate gyrus. These findings confirm G-CSF as an essential neurotrophic factor, and point to a role in the proliferation, differentiation and functional integration of neural cells necessary for the structural and functional integrity of the hippocampal formation.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 83%

The Role of Granulocyte-Colony Stimulating Factor (G-CSF) in the Healthy Brain: A Characterization of G-CSF-Deficient Mice

Diederich¹,

Sevimli²,

Dörr³

et al. 2009

J. Neurosci.

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“…These include the content of brain noradrenaline (NA) (Kempf et al, 1974), the number of noradrenaline uptake sites in the locus ceruleus (Hwang et al, 1999), and the density of hippocampal glutamate, GABA, and 5-HT receptors (Zilles et al, 2000). Although we cannot exclude an effect of these differences, the results suggest that the failure of citalopram to reduce immobility in DBA/2J and BALB/c mice is mainly attributable to the genotype-dependent impairment of 5-HT synthesis.…”

Section: Discussionmentioning

confidence: 81%

Genotype-Dependent Activity of Tryptophan Hydroxylase-2 Determines the Response to Citalopram in a Mouse Model of Depression

Cervo¹,

Canetta²,

Calcagno³

et al. 2005

J. Neurosci.

129

132

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“…Ligands were purchased from Perkin Elmer (Boston, MA). Labeling of and incubation procedures for the AMPA and GABA A binding sites were performed according to the protocols by Zilles et al (16,17). Autoradiographies were scanned under equal lighting conditions using the digital CoolSNAP camera (Photometrics CoolSNAP; Roper Scientific, Ottobrunn, Munich, Germany) and were then digitized with an image analysis system (Imaging Research, St. Catharines, ON, Canada).…”

Section: Histologic Analysis Of Neuronal Injurymentioning

confidence: 99%

Systemic PaO2 Oscillations Cause Mild Brain Injury in a Pig Model

Klein

Johannes

Brückner

et al. 2016

Critical Care Medicine

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OBJECTIVE: Systemic PaO2 oscillations occur during cyclic recruitment and derecruitment of atelectasis in acute respiratory failure and might harm brain tissue integrity. DESIGN: Controlled animal study. SETTING: University research laboratory. SUBJECTS: Adult anesthetized pigs. INTER-VENTIONS: Pigs were randomized to a control group (anesthesia and extracorporeal circulation for 20 hr with constant PaO2, n = 10) or an oscillation group (anesthesia and extracorporeal circulation for 20 hr with artificial PaO2 oscillations [3 cycles min¹], n = 10). Five additional animals served as native group (n = 5). MEASUREMENTS AND MAIN RESULTS: Outcome following exposure to artificial PaO2 oscillations compared with constant PaO2 levels was measured using 1) immunohistochemistry, 2) real-time polymerase chain reaction for inflammatory markers, 3) receptor autoradiography, and 4) transcriptome analysis in the hippocampus. Our study shows that PaO2 oscillations are transmitted to brain tissue as detected by novel ultrarapid oxygen sensing technology. PaO2 oscillations cause significant decrease in NISSL-stained neurons (p < 0.05) and induce inflammation (p < 0.05) in the hippocampus and a shift of the balance of hippocampal neurotransmitter receptor densities toward inhibition (p < 0.05). A pathway analysis suggests that cerebral immune and acute-phase response may play a role in mediating PaO2 oscillation-induced brain injury. CONCLUSIONS: Artificial PaO2 oscillations cause mild brain injury mediated by inflammatory pathways. Although artificial PaO2 oscillations and endogenous PaO2 oscillations in lung-diseased patients have different origins, it is likely that they share the same noxious effect on the brain. Therefore, PaO2 oscillations might represent a newly detected pathway potentially contributing to the crosstalk between acute lung and remote brain injury.

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Water maze and radial maze learning and the density of binding sites of glutamate, GABA, and serotonin receptors in the hippocampus of inbred mouse strains

Cited by 56 publications

References 111 publications

The Role of Granulocyte-Colony Stimulating Factor (G-CSF) in the Healthy Brain: A Characterization of G-CSF-Deficient Mice

The Role of Granulocyte-Colony Stimulating Factor (G-CSF) in the Healthy Brain: A Characterization of G-CSF-Deficient Mice

Genotype-Dependent Activity of Tryptophan Hydroxylase-2 Determines the Response to Citalopram in a Mouse Model of Depression

Systemic PaO2 Oscillations Cause Mild Brain Injury in a Pig Model

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