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  • 11
    Electronic Resource
    Electronic Resource
    Increased expression of Nogo-A in hippocampal neurons of patients with temporal lobe epilepsy (2004)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 20 (2004), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Mesial temporal lobe epilepsy (TLE) is associated with pronounced anatomical and biochemical changes in the hippocampal formation including extensive neurodegeneration, reorganization of mossy fibres and sprouting of interneurons. Although the anatomical features and some of the physiological consequences of hippocampal remodeling have been well documented, the molecular mechanisms underlying the profound and orientated outgrowth of hippocampal neurons in TLE are not yet understood. The reticulon protein Nogo-A has been associated with an inhibitory action on axon growth and plasticity. Using immunohistochemistry and in situ hybridization, we investigated the expression of Nogo-A in specimens obtained at surgery from patients with TLE compared with those obtained from autopsy controls. In control specimens, Nogo-A immunoreactivity and mRNA were mainly confined to oligodendrocytes. Only ≈ 40% of the specimens revealed low expression of Nogo-A mRNA in neurons. In contrast, in TLE patients with and without Ammon's horn sclerosis, Nogo-A mRNA and immunoreactivity were markedly up-regulated in most neurons (3.6- and 4.4-fold increases in Nogo-A mRNA in granule cells of sclerotic and nonsclerotic specimens) and their processes throughout the hippocampal formation. Similar elevations in Nogo-A mRNA and protein levels were determined by quantitative RT-PCR and Western blotting. Since Nogo-A expression was also up-regulated in specimens without hippocampal sclerosis, it may be induced by seizures prior to progressing neurodegeneration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1460-9568.2004.03470.x
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  • 12
    Electronic Resource
    Electronic Resource
    Reduced anxiety and improved stress coping ability in mice lacking NPY-Y2 receptors (2003)
    Oxford, UK : Blackwell Science, Ltd
    European journal of neuroscience 18 (2003), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Neuropeptide Y (NPY) has been implicated in the pathophysiology of certain mood disorders, including depression and anxiety. It is, however, not known which of the five cloned NPY receptors mediate these functions. We investigated the effect of Y2 receptor deletion on anxiety and stress-related behaviours. In the elevated plus maze, Y2 knock out (Y2−/−) mice showed a 2.7-fold higher frequency of entering into, and spent 3.8 times more time within, the open arms compared to controls, while entries into the closed arms did not differ. Similarly Y2−/− mice entered the central area of the open field 1.7 times more frequently and also spent 1.8 times more time there. In the light/dark test Y2−/− mice had a 4.8-fold lower latency to enter the lit area but stayed there 2.6 times longer than control mice. Y2−/− mice displayed 3.2-fold less immobility in the forced swim test, indicating improved stress coping ability. Y2 receptors are predominantly located presynaptically where they mediate feedback inhibition of neurotransmitter release. Deletion of these receptors may result in enhanced release of NPY, GABA and/or glutamate in brain areas linked to the manifestation of anxiety, and stress-related behaviour such as the amygdala. Taken together, deletion of the Y2 receptor has revealed an important role of Y2 receptors in the generation of anxiety-related and stress-related behaviours in mice.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.2003.02725.x
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  • 13
    Electronic Resource
    Electronic Resource
    Serotonergic denervation partially protects rat striatum from kainic acid toxicity (1982)
    [s.l.] : Nature Publishing Group
    Nature 299 (1982), S. 254-256 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Half-maximal lesion of the striatum (with respect to marker enzymes for acetylcholine and y- aminobutyric acid neurones, see Fig. Ib; for enzyme assays, see Fig. 1 legend) was reproduc-ibly obtained by applying stereotaxically (David Kopf apparatus) 2 nmol of KA dissolved in 1 JJL! 0.9% buffered ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/299254a0
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  • 14
    Electronic Resource
    Electronic Resource
    BIOCHEMICAL, BEHAVIORAL, AND PHARMACOLOGIC STUDIES OF THE EFFECTS OF DIHYDROXYTRYPTAMINES IN THE RODENT BRAIN (1978)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 305 (1978), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1978.tb31524.x
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  • 15
    Electronic Resource
    Electronic Resource
    Receptor mechanisms in increased sensitivity to serotonin agonists after dihydroxytryptamine shown by electronic monitoring of muscle twitches in the rat (1979)
    Springer
    Psychopharmacology 60 (1979), S. 281-289 
    Details
    ISSN: 1432-2072
    Keywords: Denervation ; Dihydroxytryptamines ; Muscle spasms ; Myoclonus ; Serotonin ; Super-sensitivity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Muscle twitches and autonomic changes were induced by systemic injections of L-5-hydroxytryptophan (5-HTP) or the serotonin agonist 5-methoxy-N,N-dimethyltryptamine (5-MeO-DMT) in rats previously lesioned with intracranial 5,7-dihydroxytryptamine (5,7-DHT) after desmethylimipramine. Movements were recorded sensitively and continuously by an electronic activity monitor. Spontaneous locomotor activity was strongly reduced after 5-HTP in both intact and lesioned rats, so that electronically recorded activity correlated very closely with disordered jerking movements scored by a behavioral rating scale. This myoclonus was dependent on the doses of 5-HTP and of 5,7-DHT and was strongly inhibited by serotonin antagonists. In lesioned rats, myoclonus occurred with unaltered activity of monoamine oxidase (MAO) and after only small increases in serotonin levels after 5-HTP, but even large increases in availability of serotonin in intact rats, or strong inhibition of serotonin uptake failed to induce myoclonus unless MAO was first inhibited. The response to 5-HTP in lesioned rats was attenuated by repeated injections of 5-HTP or 5-MeO-DMT. This decreased response was in turn blocked by repeated doses of a serotonin antagonist, but appeared not to be due to altered metabolism of 5-HTP or of serotonin; repeated pretreatment with cyproheptadine potentiated the myoclonic response to 5-HTP after DHT. Changes in postsynaptic receptors may be important in the behavioral supersentivity following 5,7-DHT, and restitution of serotonin or stimulation of its receptors after presynaptic denervation may suppress an evolving supersensitivity at receptive postsynaptic membranes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00426669
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  • 16
    Electronic Resource
    Electronic Resource
    Kainic acid seizures in the rat: differential expression of chromogranin A, carboxypeptidase H and peptidylglycine α-amidating monooxigenase in subfields of the hippocampal formation (1993)
    Springer
    Acta neuropathologica 86 (1993), S. 590-595 
    Details
    ISSN: 1432-0533
    Keywords: Epilepsy ; Limbic system ; Neuropeptides ; Neuropeptide processing ; Synaptic vesicles
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Using in situ hybridization histochemistry concentrations of mRNAs encoding chromogranin A (ChA), carboxypeptidase H (CPH) and peptidylglycine α-amidating monooxigenase (PAM) have been investigated in the hippocampus after kainic acid (KA)-induced limbic seizures in the rat. Increased concentrations (by 150%) of ChA and CPH mRNAs were found in the granule cell layer 24 h after KA injection. At the same time PAM mRNA levels were only slightly elevated (by 50%). Whereas the increases in CPH and PAM transcripts were only transient, ChA mRNA concentrations in the granule cell layer were elevated up to 2 months after the initial seizures. In contrast, in the pyramidal cell layers of all hippocampal subfields (CA1 to CA3) ChA mRNA concentrations were significantly reduced (by 40–70%) 1–60 days after KA. PAM and CPH messages were slightly reduced in the pyramamidal cell layer of CA1 but not in CA2 and CA3. The experiments demonstrate that KA-induced limbic seizures cause sustained changes in the expression of ChA mRNA. At the same time the expression of two enzymes involved in post-translational processing of neuropeptides, PAM and CPH, becomes only transiently altered. Synthesis of ChA may be regulated differently in the strata granulosum and pyramidale during epileptic seizures.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294297
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  • 17
    Electronic Resource
    Electronic Resource
    Neuropeptide Y and somatostatin immunoreactivity in the rat hippocampus after moderate hypoxia (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 354 (1996), S. 67-71 
    Details
    ISSN: 1432-1912
    Keywords: Protection ; Neuropeptide Y (NPY) ; Somatostatin ; Hippocampus ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Transient moderate hypoxia has been previously shown to exert a potent protective role to subsequently applied convulsant drugs. We now investigated neuropeptide Y and somatostatin immunoreactivities seven days after moderate hypoxia (9% O2 in N2 for two times 8 h) in the hippocampus of the rat. A slight reduction of somatostatin immunoreactive cells was observed in the hilus of the dorsal and ventral hippocampus. At the same time, the total number of neuropeptide Y immunoreactive neurons was increased in this area due to a pronounced increase in staining of presumable basket cells. There was also increased staining of neuropeptide Y positive fibers in the outer molecular layer. Our data suggest activation of neuropeptide Y containing interneurons after a moderate or a mild transient hypoxia. Activation of these inhibitory neurons may contribute to the protective effect of this treatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00168708
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  • 18
    Electronic Resource
    Electronic Resource
    Neuropeptide Y and somatostatin immunoreactivity in the rat hippocampus after moderate hypoxia (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 354 (1996), S. 67-71 
    Details
    ISSN: 1432-1912
    Keywords: Key words Hypoxia ; Protection ; Neuropeptide Y (NPY) ; Somatostatin ; Hippocampus ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Transient moderate hypoxia has been previously shown to exert a potent protective role to subsequently applied convulsant drugs. We now investigated neuropeptide Y and somatostatin immunoreactivities seven days after moderate hypoxia (9% O2 in N2 for two times 8 h) in the hippocampus of the rat. A slight reduction of somatostatin immunoreactive cells was observed in the hilus of the dorsal and ventral hippocampus. At the same time, the total number of neuropeptide Y immunoreactive neurons was increased in this area due to a pronounced increase in staining of presumable basket cells. There was also increased staining of neuropeptide Y positive fibers in the outer molecular layer. Our data suggest activation of neuropeptide Y containing interneurons after a moderate or a mild transient hypoxia. Activation of these inhibitory neurons may contribute to the protective effect of this treatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00168708
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  • 19
    Electronic Resource
    Electronic Resource
    Differential increases in brain levels of neuropeptide Y and vasoactive intestinal polypeptide after kainic acid-induced seizures in the rat (1989)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 339 (1989), S. 173-177 
    Details
    ISSN: 1432-1912
    Keywords: Epilepsy ; Kainic acid ; Neuropeptide Y ; Somatostatin ; Vasoactive intestinal polypeptide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Changes in immunoreactivities of neuropeptide Y (NPY) and vasoactive intestinal polypeptide (VIP) were investigated in the brain of rats after severe kainic acid (KA, 10 mg/kg, i.p.) induced limbic seizures. Decreased levels of both neuropeptides were observed in the frontal cortex, striatum, dorsal hippocampus and amygdala/pyriform cortex subsequently to the period of acute seizures (3 h after injection of the toxin). Then NPY increased consistently in the frontal cortex, hippocampus and amygdala/pyriform cortex. Highest levels (290% of controls) were found in the frontal cortex after two months. Anticonvulsant therapy with phenobarbital (20 mg/kg, i.p., twice daily for three weeks) partially suppressed the rise in NPY levels. Immunoreactivity of VIP increased (to 150%) in the frontal cortex only transiently 3 days after injection of kainic acid. At the subsequently examined time intervals (10–60 days after kainic acid) it declined to control values. Levels decreasing subsequently to acute seizures reflect increased release and degradation of the respective peptide. Increased NPY levels suggest “upregulation” of NPY/ somatostatin/GABA neurons due to the decreased seizure threshold of the animals. The early, reversible rise of VIP in the cortex points to a short-lasting activation of this peptide system contained in local cholinergic neurons. This may be a consequence either of the acute seizures or subsequent neuropathological changes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00165140
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