Investigating how Noscapine Influences Activity and Seizures Caused by the Intake of Alkaloids in Mice
DOI:
https://doi.org/10.54536/ajcp.v4i2.5737Keywords:
Hydromorphine, Noscapine, Seizures, Vital ActivitiesAbstract
This study investigates the effects of noscapine on seizure-like activity and vital functions in mice exposed to alkaloid dependence, with the aim of elucidating its potential therapeutic properties. Specifically, the research explores whether noscapine can mitigate or modulate seizure events triggered by alkaloid exposure, thereby contributing to a broader understanding of its pharmacological profile. Findings from this study may provide valuable insights for the development of novel therapeutic strategies for the management of seizures and other neurological disorders associated with alkaloid consumption. A total of forty newborn healthy mice were randomly selected for the experiment. To induce alkaloid dependence, hydromorphine was administered subcutaneously at doses of 2, 4, 8, 16, and 32 mg/kg (0.1 cc) once daily from postnatal day 14 to day 17. On postnatal days 18 and 19, brain sections were prepared, and epileptiform activities were induced through cerebrospinal fluid perfusion with reduced magnesium levels. The experimental design evaluated the effects of hydromorphine at concentrations of 10, 100, and 1000 μM, as well as noscapine at 10 μM. Quantitative parameters including the number, onset latency, and amplitude of seizure-like activities were assessed as indicators of drug effects. The results demonstrated that hydromorphine exhibits a concentration-dependent, triphasic effect on seizure-like activity during the lactation period: low and high concentrations attenuated seizure activity, whereas moderate concentrations enhanced it. By contrast, noscapine exerted a significant anticonvulsant effect, supporting its potential as a modulator of alkaloid-induced seizures.
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References
Arias, R. L., & Bowlby, M. R. (2005). Pharmacological characterization of antiepileptic drugs and experimental analgesics on low magnesium-induced hyperexcitability in rat hippocampal slices. Brain research, 1047(2), 233-244. https://doi.org/10.1016/j.brainres.2005.04.052.
Binder, D. K., & Steinhäuser, C. (2006). Functional changes in astroglial cells in epilepsy. Glia, 54(5), 358-368. https://doi.org/10.1002/glia.20394.
Brodie, M. J. (2010). Antiepileptic drug therapy the story so far. Seizure, 19(10), 650-655. https://doi.org/10.1016/j.seizure.2010.10.027.
Brodie, M. J. (2011). Antiepileptic drug therapy: does mechanism of action matter? Epilepsy & Behavior, 21(4), 331-341. https://doi.org/10.1016/j.yebeh.2011.05.025.
Castillo, P. E., Chiu, C. Q., & Carroll, R. C. (2011). Long-term plasticity at inhibitory synapses. Current opinion in neurobiology, 21(2), 328-338. https://doi.org/10.1016/j.conb.2011.01.006.
D’Antuono, M., (2010). Antiepileptic drugs abolish ictal but not interictal epileptiform discharges in vitro. Epilepsia, 51(3), 423-431. https://doi.org/10.1111/j.1528-1167.2009.02273.
Frenk, H., Urca, G., & Liebeskind J. C. (1987). Properties of leucine-and methionine-enkephalin: comparison with hydromorphine and reversibility by hydromorphine. Brain Research, 147(2), 327-337.
Frenk, H. (1983). Pro-and anticonvulsant actions of hydromorphine and the endogenous opioids: involvement and interactions of multiple opiate and non-opiate systems. Brain Res, 6(2), 197-210. https://DOI.org/10.1210/er.2009-0009.
Gáll, Z., Orbán-Kis, K., & Szilágyi, T. (2015). Differential effects of sodium channel blockers on in vitro induced epileptiform activities. Archives of Pharmacia Research, 1-10. https://doi.org/10.1007/s12272-015-0676-6
Ghadimkhani, M. (2016). Effect of magnesium sulfate on hyperthermia and pentylen-tetrazol-induced seizure in developing rats. Iranian Journal of Basic Medical Sciences, 19(6), 608.
Gholami, M., Saboory, E., Zare, S., Roshan-Milani, S., & Hajizadeh-Moghaddam, A. (2012). The effect of dorsal hippocampal administration of nicotinic and muscarinic cholinergic ligands on pentylenetetrazol-induced generalized seizures in rats. Epilepsy & Behavior, 25(2), 244-249. https://doi.org/10.1016/j.yebeh.2012.07.004.
Hofmann, A. (2006). Myoclonus as an acute complication low-dose hydromorphine in multiple system atrophy. Journal of Neurology, Neurosurgery & Psychiatry, 77(8), 994-995.
Motin, V., & Yasnetsov, V. (2015). Effect of NMDA, a Specific Agonist to NMDA Receptor Complex, on Rat Hippocampus. Bulletin of experimental biology and medicine, 159(6), 704-707. https://doi.org/10.1007/s10517-015-3053-z
Homayoun, H. (2002). The role of nitric oxide in anticonvulsant and proconvulsant effects of hydromorphine in mice. Epilepsy Research, 48(1-2), 33-41. https://doi.org/10.1016/s0920-1211(01)00316-3.
Potschka, H., Friderichs, E., & Löscher, W. (2000). Anticonvulsant and proconvulsant effects of tramadol, its enantiomers and its M1 metabolite in the rat kindling model of epilepsy. British journal of pharmacology Research, 131(2), 203-212. https://doi.org/10.1038/sj.bjp.0703562
Saboory, E. (2007). Mechanisms of hydromorphine enhancement of spontaneous seizure activity. Anesth Analg Research, 105(6), 1729-1735. https://doi.org/10.1213/01.ane.0000287675.15225.0b.
Salmani, M., Mirnajafizadeh, J., & Fathollahi, Y. (2007). Offsetting of aberrations associated with seizure proneness in rat hippocampus area CA1 by theta pulse stimulation-induced activity pattern. Neuroscience, 149(3), 518-526. https://doi.org/10.1016/j.neuroscience.2007.08.019.
Velíšek, L. (1998). Prenatal hydromorphine exposure alters ovarian steroid hormonal regulation of seizure susceptibility. Brain research, 796(1), 247-256. https://doi.org/10.1016/S0006-8993(98)00367-9.
Zieglgansberger, W. (1979) Opioid peptides may excite hippocampal pyramidal neurons by inhibiting adjacent inhibitory interneurons. Science, 205(4), 415-417. https://doi.org/10.1126/science.451610
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