The widespread availability of non-traditional dietary supplements and pharmacologically active substances via the Internet continues to introduce mechanisms for inadvertent toxidromes not commonly seen. Consumers are virtually unrestricted in their ability to acquire products purporting augmentation of normal physiology for the purposes of enhancement, recreation, and/or potential abuse. The safety profiles at standard or toxic doses remain largely unknown for many agents that can be purchased electronically. We report a case of mixed toxicity related to phenibut and fosaracetam, both of which are readily available for consumer purchase from online retailers. Written and verbal consent was obtained for this case presentation.
Aims: Implication of modified N-methyl-D-aspartate receptors (NMDAR) in synaptic plasticity and learning was investigated in normal and pathological conditions.
Study design: We studied the efficiency of synaptic plasticity, the development of the long-term potentiation/depression (LTP/LTD) in olfactory cortex slices, treated with antisense or sense oligodeoxynucleotides (aODNs and sODNs) to the GluN1 subunit of NMDAR.
Main outcome: aODNs induced the LTD development in slices after high-frequency tetanization. Contrariwise, in sliced treated with sODNs the enhanced LTP developed. Under conditions of severe anoxia (10 min), treatment of slices with aODNs and sODNs contributed to the preservation of synaptic activity which has been blocked in the control untreated slices. In practical implications such directed up- and down regulation of NMDAR might be useful in the readjustment of brain activity by the controlling balance of excitation/inhibition.
Aim:The work was to perform a comparative study of the neuroprotective and nootropic activities of two pharmaceutical substances, the HLDF-6 peptide and its amide form (HLDF-6-NH2).
Materials and Methods: We used in the study healthy adult male Wistar rats aged 180–200 days weighing 280–300 g. We modelled ischemic stroke in rats by chronical occlusion of carotid arteries. Solutions of the HLDF-6-NH2 and HLDF-6 peptides were administered intranasally. Cognitive functions we assessed with Novel object recognition test and Morris maze.
Results: The amide form of HLDF-6 peptide is more efficient: the neuroprotective activity of HLDF-6-NH2, evaluated by improvement of cognitive functions in animals, surpassed that of the native HLDF-6 peptide. A dose of 250 µg/kg of HLDF-6-NH2 peptide resulted in practically complete restoration of the disturbed functions. In the model of ischemic stroke, the amide form of the peptide significantly excelled the reference substance mexidol both in the effective dose and biological activity.
Conclusion: The results of study of the agent allow hoping for its success in further clinical investigation. In view of high demand for the agent and in case of successful clinical trials, it will surely become widely used in clinical practice in treatment of IS.
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