The effects of ladasten on dopaminergic neurotransmission and hippocampal synaptic plasticity in rats

  title={The effects of ladasten on dopaminergic neurotransmission and hippocampal synaptic plasticity in rats},
  author={Marina Mikhaylova and Julia V. Vakhitova and Renat S. Yamidanov and M. Kh. Salimgareeva and Sergey B. Seredenin and Thomas Behnisch},
Effects of the Novel Anti-Asthenic Drug Ladasten on Behavior and T-Cell Subsets Alterations in a Social Defeat Animal Model of Depression
The notion that depression is accompanied by cell-mediated immune activation and that targeting this pathway may be a new therapeutic approach for treatment is supported and further investigations of ladasten as a potent anti-depressive drug which can be used alone as well as in combination with other anti-Depressants are supported.
Changes in CREB (SER133) Content and DNA-Binding Activity of Transcriptional Factors in Rat Brain Cells against the Background of Ladasten Exposure
We studied the effects of single administration of ladasten (50 mg/kg) on the level of transcriptional factor CREB (cyclic AMP response binding element protein) phosphorylated by Ser133 in rat
Two‐Step Synthesis of Heptacyclo[,6.03,13.04,11.05,9.010,14] tetradecane from Norbornadiene: Mechanism of the Cage Assembly and Post‐synthetic Functionalization
Abstract A selective and scalable two‐step approach to the dimerization of norbornadiene (NBD) into its thermodynamically most stable dimer, heptacyclo[,6.03,13.04,11.05,9.010,14]


[The mechanisms of the neurotropic action of bromantan].
The main components of bromantan central neurotropic effect is its dopamine-positive activity: antagonism (5 mg/kg) to the effects of neuroleptics in rats, blocking (50 microM) of dopamine
[The effect of bromantane on the dopamin- and serotoninergic systems of the rat brain].
Bromantan induced a significant increase in the 5-HT and 5-HIAA content in the frontal cortex and delayed an increase in their content in subcortical brain regions, suggesting an important role of dopaminergic system in the mechanism of pharmacological effects of the drug.
Drugs abused by humans preferentially increase synaptic dopamine concentrations in the mesolimbic system of freely moving rats.
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    Proceedings of the National Academy of Sciences of the United States of America
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The effect of various drugs on the extracellular concentration of dopamine in two terminal dopaminergic areas, the nucleus accumbens septi (a limbic area) and the dorsal caudate nucleus (a
When Are Class I Metabotropic Glutamate Receptors Necessary for Long-Term Potentiation?
The functional significance of class I mGluRs in LTP is confined to certain types of potentiation, which are induced by weak tetanization protocols and require the release of Ca2+ from ICSs for induction.
Effects of the Uncompetitive NMDA Receptor Antagonist Memantine on Hippocampal Long‐term Potentiation, Short‐term Exploratory Modulation and Spatial Memory in Awake, Freely Moving Rats
These studies provide the first electrophysiological evidence that memantine can increase the durability of synaptic plasticity and provide preclinical confirmation of the cognitive improvement seen with memantine in the treatment of demented patients.
Dopaminergic modulation of LTP induction in the dentate gyrus of intact brain
D1/D5 receptor activation appears to modulate LTP induction in vivo, and is associated with the induction of dentate gyrus LTP in anesthetized rats.
Induction of tyrosine hydroxylase in the rat substantia nigra by local injection of forskolin
It is confirmed that, in vivo, TH induction is cAMP‐dependent and demonstrate that the TH‐gene activity is not strictly coupled to the activity of dopaminergic cells in the SN.
D1/D5 receptor agonists induce a protein synthesis-dependent late potentiation in the CA1 region of the hippocampus.
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  • Biology, Chemistry
    Proceedings of the National Academy of Sciences of the United States of America
  • 1995
The results suggest that the D1/D5 receptor may be involved in the late, protein synthesis-dependent component of LTP in the hippocampal CA1 region, either as an ancillary component or as a mediator directly contributing to the late phase.