Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Protective effects of idebenone and α-tocopherol on β-amyloid-(1–42)-induced learning and memory deficits in rats: implication of oxidative stress in β-amyloid-induced neurotoxicity in vivo (1999)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 11 (1999), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Amyloid β-peptide (Aβ), the major constituent of the senile plaques in the brains of patients with Alzheimer's disease, is cytotoxic to neurons and has a central role in the pathogenesis of the disease. Previous studies have suggested that oxidative stress is involved in the mechanisms of Aβ-induced neurotoxicity in vitro. In the present study, we examined whether oxidative stress contributes to learning and memory deficits caused by continuous intracerebroventricular infusion of Aβ-(1–42). In the Aβ-(1–42)-infused rats, spontaneous alternation behaviour in a Y-maze and spatial memory in a water maze task were significantly impaired, as compared with Aβ-(40–1)-infused control rats. The retention of passive avoidance learning was also significantly impaired by treatment with Aβ-(1–42). Potent antioxidants idebenone and α-tocopherol prevented the behavioural deficits in Y-maze and water maze, but not passive avoidance, tasks in Aβ-(1–42)-infused rats when they were repeatedly administered by mouth once a day from 3 days before the start of Aβ infusion to the end of behavioural experiments. Lipid peroxide levels in the hippocampus and cerebral cortex of Aβ-(1–42)-infused rats did not differ from those in control animals, and neither idebenone nor α-tocopherol affected the lipid peroxide levels. These results suggest that treatment with antioxidants such as idebenone and α-tocopherol prevents learning and memory deficits caused by Aβ.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.1999.00408.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Effect of chronic administration of methamphetamine on the responsiveness of substantia nigra zona reticulata neurons to GABA or a GABA agonist in rats (1986)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 334 (1986), S. 458-462 
    Details
    ISSN: 1432-1912
    Keywords: GABA ; Muscimol ; Substantia nigra zona reticulata ; Long-term treatment ; Methamphetamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of chronic administration of methamphetamine on the responsiveness of neurons of the substantia nigra zona reticulata (SNR) to gammaaminobutyric acid (GABA) or to a GABA receptor agonist were examined. Neuronal activity was recorded from the SNR of rats that had been pretreated twice daily, for 6 consecutive days, with saline or with 5 mg/kg methamphetamine. Intravenous administration of the GABA receptor agonist, muscimol, caused a dose-dependent decrease in the unit activity of the SNR neurons and the SNR neurons became less sensitive to the depressant effects of the drug after chronic treatment with methamphetamine. Iontophoretic application, with increasing currents, of GABA produced a progressive inhibition of unit activity in control animals, an effect that was significantly reduced in rats pretreated with methamphetamine. These results support the hypothesis that long-term administration of methamphetamine increases the activity of the striatonigral GABA system and thereby reduces the sensitivity of postsynaptic GABA receptors in the SNR.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00569386
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    A role played by sigma receptors in the conditioned suppression of motility in mice (1988)
    Springer
    Psychopharmacology 94 (1988), S. 515-520 
    Details
    ISSN: 1432-2072
    Keywords: Conditioned suppression ; Sigma receptors ; Opioid receptor types ; Stress
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Mice exhibited marked suppression of motility (conditioned suppression) when placed in the same environment in which they had previously received an electric foot-shock. The conditioned suppression was attenuated by cyclazocine and N-allylnormetazocine (SKF-10047), sigma agonists. The effect of these drugs was reduced by chronic pretreatment with cyclazocine. This behavioral change was related to the change in binding activity of [3H]-phencyclidine to sigma receptors (defined using non-radioactive SKF-10047). In the chronic vehicle-pretreated conditioned suppression group, the Kd and Bmax values of [3H]-phencyclidine binding at the high affinity site were increased when compared to those in the chronic vehicle-pretreated control group. The increased values were restored to the control levels by acute treatment with cyclazocine and SKF-10047. On the other hand, in the chronic cyclazocine-pretreated conditioned suppression group, acute cyclazocine and SKF-10047 treatment failed to change the increased values of Kd and Bmax at the high affinity site. The present behavioral and receptor-binding experiments suggest that the activation of nervous system mediated by sigma receptors may be responsible for the attenuation of conditioned suppression of motility.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00212847
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Nootropic effect of nicotine on carbon monoxide (CO)-induced delayed amnesia in mice (1994)
    Springer
    Psychopharmacology 116 (1994), S. 33-39 
    Details
    ISSN: 1432-2072
    Keywords: (−)-Nicotine ; (+)-Nicotine ; Cholinergic neuronal system ; Carbon monoxide ; Delayed amnesia ; Learning ; Mecamylamine ; Passive avoidance ; Stereoisomer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of nicotine on carbon monoxide (CO)-induced amnesia in mice were investigated using a step-down type passive avoidance task. Mice were exposed to CO 3 times at 1-h intervals, 7 days before the first training and retention test and 24 h after the first training session. Memory deficiency occurred in mice when training commenced more than 3 days after CO exposure (delayed amnesia): the median step-down latency in the retention test of the CO-exposed group was significantly shorter than that of the control group. Administration of (−)-nicotine (15.6 and 31.3 nmol/kg, IP) 15 min before the first training session prolonged the step-down latency in the CO-exposed group, but (+)-nicotine did not. To determine whether this effect of (−)-nicotine was mediated via nicotinic cholinergic receptors, we attempted to block its action using a nicotinic acetylcholine receptor antagonist (mecamylamine). Mecamylamine (1.25 µmol/kg) blocked the effect of (−)-nicotine (31.3 nmol/kg) on delayed amnesia. Administration of (−)-nicotine (15.6–62.5 nmol/kg) immediately after the first training session failed to ameliorate learning ability in the CO-exposed group. These results suggest that (−)-nicotine potentiates the nicotinic cholinergic neuronal system and may potentiate acquisition of memory.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02244868
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Involvement of GABAergic systems in benzodiazepine-induced impairment of passive avoidance learning in mice (1991)
    Springer
    Psychopharmacology 105 (1991), S. 22-26 
    Details
    ISSN: 1432-2072
    Keywords: Chlordiazepoxide ; GABA antagonist ; GABA agonist ; Passive avoidance response ; Mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The possible involvement of GABAergic neuronal systems in benzodiazepine(BZP)-induced impairment of a passive avoidance response was investigated. Chlordiazepoxide(CDP) impaired passive avoidance when administered prior to training. The CDP-induced impairment was antagonized by pretreatment with picrotoxin, but not by pretreatment with bicuculline or posttraining administration of picrotoxin. On the contrary, when combined with muscimol, the dose at which CDP impaired the response was lower than the dose at which it did so alone. The synergy of muscimol and CDP was attenuated by pretreatment with flumazenil or bicuculline. From these results, we conclude that GABAergic systems play an important role in the BZP-induced impairment of passive avoidance.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02316859
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Effects of imipramine on auditory sensitivity in the rat in relation to initial sensitivity (1976)
    Springer
    Psychopharmacology 48 (1976), S. 199-204 
    Details
    ISSN: 1432-2072
    Keywords: Imipramine ; Auditory sensitivity ; Animal psychophysics ; Operant conditioning ; Animal temperament
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Rats were divided into 2 groups according to their absolute auditory thresholds, as measured by a psychophysical method of limits using an operant conditioning technique. The procedure required a water-deprived rat to bar press repeatedly until a 3 s pure tone (3 kHz) came on. VR-15 schedule was used to determine the frequency of occurrence of the tone. Only within 4 s after the tone onset could the rat get water reinforcement by sticking its nose into the dipper area. The descending method was used with tone intensities ranging from 120 to 40 dB, in 2 dB steps. Imipramine was then administered 3 times at 24-h intervals (40, 80 and 160 mg/kg, p.o., respectively), and each rat was tested at 4, 8, and 12 h after each administration. Rats with high initial thresholds showed a decrease in thresholds with the lower dose of imipramine, and those with low initial thresholds an increase with the higher dose. An analysis of variance of these data showed significant effects of the type of subject (in terms of the level of initial thresholds), dose and interval conditions, and their interaction. It was demonstrated that the lower the initial sensitivity the greater the increase in sensitivity by imipramine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00423261
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    Phencyclidine-induced retrograde amnesia in mice (1986)
    Springer
    Psychopharmacology 89 (1986), S. 334-337 
    Details
    ISSN: 1432-2072
    Keywords: Phencyclidine ; Amnesia ; Passive avoidance ; Escape-learning ; Physostigmine ; Naloxone ; Memory ; Mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The amnesic action of phencyclidine (PCP) was investigated in mice using a passive avoidance- and escape-learning method. PCP (10–30 mg/kg) administered immediately after the training test dose-dependently shortened and prolonged the step-down latency and escape latency, respectively in the retention test. There was a significant inverse relationship between the step-down and escape latencies, indicating that PCP had induced amnesia. The amnesic actions of PCP were retrograde, being observed when mice were given PCP within 10 min but not more than 30 min after the training test. The amnesic effects of PCP on both variables were antagonized significantly by physostigmine and naloxone, whereas cyproheptadine and haloperidol had no effect. None of these drugs by themselves affected passive avoidance- or escape-learning performance. These results suggest that the retrograde amnesic actions of PCP were produced via either the cholinergic or the opioidergic systems or both, but not through the serotonergic and the dopaminergic systems.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00174370
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    Low dose of 1,3-di(2-tolyl)guanidine (DTG) attenuates MK-801-induced spatial working memory impairment in mice (1994)
    Springer
    Psychopharmacology 114 (1994), S. 520-522 
    Details
    ISSN: 1432-2072
    Keywords: DTG (1,3-di(2-tolyl)guanidine) ; Sigma (σ) receptor ; MK-801 ; Spatial working memory
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract MK-801 (30–100 µg/kg, SC) impaired spontaneous alternation behavior of mice, a behavior related to the spatial working memory. 1,3-Di-(2-tolyl)guanidine (DTG),(+)-pentazocine and (+)-SKF 10,047 (100 µg/kg, SC), putative σ agonists, administered 10 min before MK-801, partially but significantly reversed the impairment, without affecting the concomitant hyperlocomotion. The antagonizing effects by DTG were prevented by BMY-14802 (5 mg/kg, IP), a purported σ antagonist. These findings suggest that, at low doses, σ ligands may modulate theN-methyl-d-aspartate dependent memory processes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02249345
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 9
    Electronic Resource
    Electronic Resource
    Utility of an elevated plus-maze for the evaluation of memory in mice: effects of nootropics, scopolamine and electroconvulsive shock (1990)
    Springer
    Psychopharmacology 101 (1990), S. 27-33 
    Details
    ISSN: 1432-2072
    Keywords: Memory ; Elevated plus-maze ; Aniracetam ; Tacrine (tetrahydroaminoacridine) ; Scopolamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract An elevated plus-maze consisting of two open and two enclosed arms was employed for an evaluation of memory in mice. Mice in the plus-maze escaped from the open arm to the enclosed arm because mice apparently dislike open and high spaces. The time it took for the mice to move from the open arm to the enclosed arm (transfer latency) was recorded. The transfer latency after the 2nd day was significantly shorter than that on the 1st day when it was recorded at a rate of one trial a day for 5 days. The transfer latency on the 2nd day was significantly prolonged in the mice administered electroconvulsive shock (300 V, 1 s) or scopolamine (20 µg, ICV) immediately after the first trial compared to the transfer latency in the control group. The prolongation of transfer latency in the mice administered an electroconvulsive shock was reversed by pretreatment with aniracetam (20 mg/kg, PO), but not tacrine and physostigmine. The prolongation of transfer latency in the mice administered scopolamine was reversed by pretreatment with aniracetam (10 and 20 mg/kg, PO) tacrine (1 and 3 mg/kg, PO), or physostigmine (0.025–0.2 mg/kg, IP). These results suggest that transfer latency may be one of the parameters of learning and memory.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02253713
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 10
    Electronic Resource
    Electronic Resource
    Antinociceptive action of tizanidine in mice and rats (1985)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 330 (1985), S. 93-96 
    Details
    ISSN: 1432-1912
    Keywords: Anticociceptive action ; Mouse ; Nonopioid ; Rat ; Tizanidine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The antinociceptive action of tizanidine [5-chloro-(2-imidazolin-2-yl-amino)-2,1,3-benzothiadiazole], a centrally acting muscle relaxant, was evaluated after subcutaneous or peroral administration in mice and rats. Tizanidine strongly inhibited the writhing response induced by acetic acid, phenyl-p-benzoquinone and acetylcholine in mice, and its potency was found to be greater than that of morphine. Tizanidine showed antinociceptive action like morphine not only in tail pressure and electrical stimulation tests in mice but also in tail-flick tests in mice and rats. The antinociceptive action of tizanidine was unaffected by pretreatment with naloxone. These findings suggest that tizanidine develops relatively strong antinociceptive action by a nonopioid mechanism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00499900
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...