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Lacidipine attenuates reserpine-induced depression-like behavior and oxido-nitrosative stress in mice.

Abstract

Depression is a serious medical illness displaying high lifetime prevalence, early-age onset that adversely affects socio-economic status. The bidirectional association between oxidative stress and calcium-signaling adversely affects the monoaminergic neuron functions that instigate the pathogenesis of depression. The present study investigates the effect of lacidipine (LCD), L-type Ca2+-channel blocker, on reserpine-induced depression in mice. Separate groups of mice (Swiss albino, 18-25 g) were administered lacidipine (0.3, 1 and 3 mg/kg, i.p.) daily for 14 days and reserpine (5 mg/kg, i.p.) was injected on day 14. Rectal temperature, catalepsy, and tail-suspension test (TST) were performed 18 h and ptosis scores at 60, 120, 240, 360 min post-reserpine treatment. Whole-brain TBARS, GSH, nitrite, and superoxide dismutase (SOD) and catalase activities were estimated. Reserpine elevated the catalepsy, ptosis, hypothermia, and immobility period in TST owing to the marked increase in oxidative-nitrosative stress in the brain of mice. LCD attenuated the reserpine triggered the rise in catalepsy, ptosis scores, hypothermia, and immobility period in mice. LCD pretreatment attenuated the increase in TBARS and nitrite levels, and the decline of GSH, SOD, and catalase activities in the brain of reserpine injected mice. Bay-K8644 (0.5 mg/kg, i.p.), Ca2+-channel agonist, attenuated these effects of LCD (3 mg/kg) in reserpine-treated mice. It can be inferred that lacidipine (Ca2+ channel antagonist) attenuates depression-like symptoms in reserpine-treated mice. Furthermore, the abrogation of antidepressant-like effects of LCD by Bay-K8644 revealed that modulation of Ca2+-channels might present a potential strategy in the management of depression.

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  • Authors+Show Affiliations

    ,

    I. K. Gujral Punjab Technical University, Kapurthala, Punjab, 144603, India. Department of Pharmacology, ASBASJSM College of Pharmacy, Bela (Ropar), Punjab, 140111, India.

    Department of Pharmacology, ASBASJSM College of Pharmacy, Bela (Ropar), Punjab, 140111, India. nitindsp@rediffmail.com.

    Source

    Pub Type(s)

    Journal Article

    Language

    eng

    PubMed ID

    31187187

    Citation

    Khurana, Kunal, and Nitin Bansal. "Lacidipine Attenuates Reserpine-induced Depression-like Behavior and Oxido-nitrosative Stress in Mice." Naunyn-Schmiedeberg's Archives of Pharmacology, 2019.
    Khurana K, Bansal N. Lacidipine attenuates reserpine-induced depression-like behavior and oxido-nitrosative stress in mice. Naunyn Schmiedebergs Arch Pharmacol. 2019.
    Khurana, K., & Bansal, N. (2019). Lacidipine attenuates reserpine-induced depression-like behavior and oxido-nitrosative stress in mice. Naunyn-Schmiedeberg's Archives of Pharmacology, doi:10.1007/s00210-019-01667-6.
    Khurana K, Bansal N. Lacidipine Attenuates Reserpine-induced Depression-like Behavior and Oxido-nitrosative Stress in Mice. Naunyn Schmiedebergs Arch Pharmacol. 2019 Jun 11; PubMed PMID: 31187187.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Lacidipine attenuates reserpine-induced depression-like behavior and oxido-nitrosative stress in mice. AU - Khurana,Kunal, AU - Bansal,Nitin, Y1 - 2019/06/11/ PY - 2019/01/20/received PY - 2019/05/16/accepted PY - 2019/6/13/entrez KW - Calcium channel KW - Depression KW - Lacidipine KW - Oxidative stress KW - Reserpine JF - Naunyn-Schmiedeberg's archives of pharmacology JO - Naunyn Schmiedebergs Arch. Pharmacol. N2 - Depression is a serious medical illness displaying high lifetime prevalence, early-age onset that adversely affects socio-economic status. The bidirectional association between oxidative stress and calcium-signaling adversely affects the monoaminergic neuron functions that instigate the pathogenesis of depression. The present study investigates the effect of lacidipine (LCD), L-type Ca2+-channel blocker, on reserpine-induced depression in mice. Separate groups of mice (Swiss albino, 18-25 g) were administered lacidipine (0.3, 1 and 3 mg/kg, i.p.) daily for 14 days and reserpine (5 mg/kg, i.p.) was injected on day 14. Rectal temperature, catalepsy, and tail-suspension test (TST) were performed 18 h and ptosis scores at 60, 120, 240, 360 min post-reserpine treatment. Whole-brain TBARS, GSH, nitrite, and superoxide dismutase (SOD) and catalase activities were estimated. Reserpine elevated the catalepsy, ptosis, hypothermia, and immobility period in TST owing to the marked increase in oxidative-nitrosative stress in the brain of mice. LCD attenuated the reserpine triggered the rise in catalepsy, ptosis scores, hypothermia, and immobility period in mice. LCD pretreatment attenuated the increase in TBARS and nitrite levels, and the decline of GSH, SOD, and catalase activities in the brain of reserpine injected mice. Bay-K8644 (0.5 mg/kg, i.p.), Ca2+-channel agonist, attenuated these effects of LCD (3 mg/kg) in reserpine-treated mice. It can be inferred that lacidipine (Ca2+ channel antagonist) attenuates depression-like symptoms in reserpine-treated mice. Furthermore, the abrogation of antidepressant-like effects of LCD by Bay-K8644 revealed that modulation of Ca2+-channels might present a potential strategy in the management of depression. SN - 1432-1912 UR - https://www.unboundmedicine.com/medline/citation/31187187/Lacidipine_attenuates_reserpine-induced_depression-like_behavior_and_oxido-nitrosative_stress_in_mice L2 - https://dx.doi.org/10.1007/s00210-019-01667-6 DB - PRIME DP - Unbound Medicine ER -