Heide Hörtnagl

ORCID: 0000-0003-0608-0382
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About
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Research Areas
  • Neuroscience and Neuropharmacology Research
  • Receptor Mechanisms and Signaling
  • Neurotransmitter Receptor Influence on Behavior
  • Neuropeptides and Animal Physiology
  • Nerve injury and regeneration
  • Neuroendocrine regulation and behavior
  • Stress Responses and Cortisol
  • Liver Disease and Transplantation
  • Cholinesterase and Neurodegenerative Diseases
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Memory and Neural Mechanisms
  • Neurogenesis and neuroplasticity mechanisms
  • Hormonal Regulation and Hypertension
  • Nicotinic Acetylcholine Receptors Study
  • Electrolyte and hormonal disorders
  • Parkinson's Disease Mechanisms and Treatments
  • Neurological disorders and treatments
  • Lipid Membrane Structure and Behavior
  • Glycosylation and Glycoproteins Research
  • Liver Disease Diagnosis and Treatment
  • Hemoglobin structure and function
  • Tryptophan and brain disorders
  • Drug-Induced Hepatotoxicity and Protection
  • Anesthesia and Neurotoxicity Research
  • Cellular transport and secretion

Universität Innsbruck
1980-2022

Innsbruck Medical University
1981-2022

Charité - Universitätsmedizin Berlin
2004-2014

Humboldt-Universität zu Berlin
1997-2007

Institute of Pharmacology
2000-2005

Humboldt State University
1998-2002

University of Vienna
1989-2000

Universitätsklinikum Knappschaftskrankenhaus Bochum
2000

Freie Universität Berlin
1994

University Hospital Innsbruck
1992

The neurotransmitter serotonin [5-hydroxytryptamine (5-HT)] is causally involved in multiple central nervous facets of mood control and regulating sleep, anxiety, alcoholism, drug abuse, food intake, sexual behavior ([1][1]). In peripheral tissues, 5-HT regulates vascular tone, gut motility,

10.1126/science.1078197 article EN Science 2003-01-02

Altered glucocorticoid receptor (GR) signaling is a postulated mechanism for the pathogenesis of major depression. To mimic human situation altered GR function claimed depression, we generated mouse strains that underexpress or overexpress GR, but maintain regulatory genetic context controlling gene. achieve this goal, used following: (1) GR-heterozygous mutant mice (GR +/- ) with 50% gene dose reduction, and (2) overexpressing by yeast artificial chromosome resulting in twofold elevation....

10.1523/jneurosci.0736-05.2005 article EN cc-by-nc-sa Journal of Neuroscience 2005-06-29

Serotonin synthesis in mammals is initiated by 2 distinct tryptophan hydroxylases (TPH), TPH1 and TPH2. By genetically ablating TPH2, we created mice ( Tph2 −/− ) that lack serotonin the central nervous system. Surprisingly, these can be born survive until adulthood. However, depletion of signaling brain leads to growth retardation 50% lethality first 4 weeks postnatal life. Telemetric monitoring revealed more extended daytime sleep, suppressed respiration, altered body temperature control,...

10.1073/pnas.0810793106 article EN Proceedings of the National Academy of Sciences 2009-06-12

The GABAA receptor is the main inhibitory in brain and its subunits originate from different genes or gene families (α1-α6, β1-β3, γ1-γ3, δ, ε, θ, π, ρ1-3). In mouse anatomical distribution of subunit mRNAs so far investigated restricted to forming benzodiazepine-sensitive complexes (α1-α3, α5, β2, β3 γ2) forebrain midbrain as assessed by situ hybridization (ISH). present study α1-α6, γ1-γ2 δ was analyzed (excluding stem) ISH immunohistochemistry (IHC). several areas such hippocampus,...

10.1016/j.neuroscience.2013.01.008 article EN cc-by-nc-nd Neuroscience 2013-01-18

Several lines of clinical and experimental evidence suggest an important role the renin-angiotensin system in ischemic brain injury although cellular regulation angiotensin AT1 AT2 receptors their potential relevance this condition have not yet been clearly defined. We first assessed response to transient unilateral medial cerebral artery occlusion rats by real-time RT-PCR, Western blot, immunofluorescence labeling. peri-infarct zone were significantly upregulated 2 days after focal...

10.1096/fj.04-2960fje article EN The FASEB Journal 2005-01-21

After mild ischemic insults, many neurons undergo delayed neuronal death. Aberrant activation of the cell cycle machinery is thought to contribute apoptosis in various conditions including ischemia. We demonstrate that loss endogenous cyclin-dependent kinase (Cdk) inhibitor p16 INK4a an early and reliable indicator death striatal after cerebral ischemia vivo . Loss p27 Kip1 , another Cdk inhibitor, precedes neocortical subjected oxygen–glucose deprivation vitro The inhibitors followed by...

10.1523/jneurosci.21-14-05045.2001 article EN cc-by-nc-sa Journal of Neuroscience 2001-07-15

Abstract Statins [3‐hydroxy‐3‐methylglutaryl‐coenzyme A (HMG‐CoA) reductase inhibitors] exert cholesterol‐independent pleiotropic effects that include anti‐thrombotic, anti‐inflammatory, and anti‐oxidative properties. Here, we examined direct protective of atorvastatin on neurones in different cell damage models vitro . Primary cortical were pre‐treated with then exposed to (i) glutamate, (ii) oxygen–glucose deprivation or (iii) several apoptosis‐inducing compounds. Atorvastatin...

10.1111/j.1471-4159.2004.02980.x article EN Journal of Neurochemistry 2005-02-17

An imbalance of excitatory and inhibitory amino acid-ergic neurotransmission has been suggested to play a role in the pathogenesis hepatic encephalopathy. For further evaluation this hypothesis, several parameters were studied rats with acute liver failure induced by administration 300 mg per kg thioacetamide gavage on two consecutive days. By appropriate supportive care, hypoglycemia, renal hypothermia avoided. Rats monitored clinically neurologically. Hepatic encephalopathy evolved four...

10.1002/hep.1840090414 article EN Hepatology 1989-04-01

Washed membranes of bovine adrenal chromaffin granules contained most the cholesterol and phospholipids particle 22% total protein. The protein/lipid ratio was about 0.45 (w/w). Dopamine(3,4-dihydroxyphenethylamine)beta-hydroxylase, Mg(2+)-activated nucleoside triphosphatase cytochrome b-559 activities were present in membrane. ATP best substrate for triphosphatase, whose pH optimum 6.4, K(m) 7x10(-4)m V(max.) 1.8mumol/h per mg Treatment with various detergents caused a preferential...

10.1042/bj1180303 article EN Biochemical Journal 1970-06-01

The major goal of this study was to compare mechanisms the neuroprotective potential 17 β-estradiol in two models for oxidative stress-independent apoptotic neuronal cell death with that necrotic primary cultures derived from rat hippocampus, septum, or cortex. Neuronal apoptosis induced either by staurosporine ethylcholine aziridinium (AF64A), as glutamate exposure oxygen–glucose deprivation (OGD) were applied. Long-term (20 hr) pretreatment (0.1 μ m β-estradiol) AF64A (40 ) only...

10.1523/jneurosci.21-08-02600.2001 article EN cc-by-nc-sa Journal of Neuroscience 2001-04-15

If high sodium intake is involved in the pathogenesis of essential hypertension, effects changing should be demonstrable susceptible part normotensive population. Therefore, we have investigated moderate salt restriction 52 young subjects with and without a family history hypertension; 22 (42%) responded to (200 50 mmol/day) over 2 weeks, significant fall blood pressure shown by continuous automatic recordings. Accordingly, these were classified as salt-sensitive, remainder salt-resistant....

10.1161/01.hyp.6.2.152 article EN Hypertension 1984-03-01

Recent evidence indicates that glutamate homeostasis and neurotransmission are altered in major depressive disorder, but the nature of disruption mechanisms by which it contributes to syndrome unclear. Glutamate can act via AMPA, NMDA, or metabotropic receptors. Using targeted mutagenesis, we demonstrate here mice with deletion main AMPA receptor subunit GluR-A represent a depression model good face construct validity, showing behavioral neurochemical features also postulated for human...

10.1096/fj.08-106450 article EN The FASEB Journal 2008-05-20

Abstract Serotonergic neurones are among the first to develop in central nervous system. Their survival and maturation is promoted by a variety of factors, including serotonin itself, brain‐derived neurotrophic factor (BDNF) S100β, an astrocyte‐specific Ca 2+ binding protein. Here, we used BDNF‐deficient mice cell cultures embryonic raphe determine whether or not BDNF effects on developing serotonergic influenced its action glial cells. In BDNF–/– mice, number serotonin‐immunoreactive...

10.1111/j.1471-4159.2004.02911.x article EN Journal of Neurochemistry 2004-12-23

Ceftriaxone has been reported to reduce neuronal damage in amyotrophic lateral sclerosis and an in-vitro model of ischaemia through increased expression activity the glutamate transporter, GLT1. We tested effects ceftriaxone on mortality, neurological outcome, infarct size experimental stroke rats looked for underlying mechanisms.Male normotensive Wistar received (200 mg/kg intraperitoneal) as a single injection 90 min after middle cerebral artery occlusion (90 with reperfusion). Forty-eight...

10.1097/hjh.0b013e328313e403 article EN Journal of Hypertension 2008-11-07

1. Soluble lysates and membranes were prepared from chromaffin granules isolated bovine adrenal medulla. The detergent N-cetylpyridinium chloride was used for solubilizing the membrane proteins, including membrane-bound dopamine (2,4-dihydroxyphenethylamine) beta-hydroxylase. solubilized proteins fractionated by Sephadex chromatography in presence of chloride. major component i.e. chromomembrin A, identified as enzyme 2. addition to soluble lysate caused precipitation up 96% but only a small...

10.1042/bj1290187 article EN Biochemical Journal 1972-08-01

Folate deficiency and resultant increased homocysteine levels have been linked experimentally epidemiologically with neurodegenerative conditions like stroke dementia. Moreover, folate has implicated in the pathogenesis of psychiatric disorders, most notably depression. We hypothesized that pathogenic mechanisms include uracil misincorporation and, therefore, analyzed effects mice lacking DNA glycosylase ( Ung −/−) versus wild-type controls. depletion nuclear mutation rates −/− embryonic...

10.1523/jneurosci.0940-08.2008 article EN cc-by-nc-sa Journal of Neuroscience 2008-07-09
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