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    Evaluation of Antidepressant Potential of Agmatine in Diabetes Induce Depression in Rats

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    This document proposes a study to evaluate the antidepressant potential of agmatine in diabetes-induced depression in rats. The study would involve inducing depression in diabetic rats using streptozotocin and assessing the effects of agmatine treatment using tests like the forced swim test and tail suspension test. If agmatine shows antidepressant effects, it could provide a novel treatment option for depression comorbid with diabetes. The document provides background on the link between diabetes and depression, and the potential roles of insulin and monoamine neurotransmitters in this link. It also summarizes previous research demonstrating antidepressant effects of insulin in diabetic rats and the various neuroprotective effects of agmatine that provide rationale for investigating its effects on diabetes-induced

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    Evaluation of Antidepressant Potential of Agmatine in Diabetes Induce Depression in Rats

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    niku
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    This document proposes a study to evaluate the antidepressant potential of agmatine in diabetes-induced depression in rats. The study would involve inducing depression in diabetic rats using streptozotocin and assessing the effects of agmatine treatment using tests like the forced swim test and tail suspension test. If agmatine shows antidepressant effects, it could provide a novel treatment option for depression comorbid with diabetes. The document provides background on the link between diabetes and depression, and the potential roles of insulin and monoamine neurotransmitters in this link. It also summarizes previous research demonstrating antidepressant effects of insulin in diabetic rats and the various neuroprotective effects of agmatine that provide rationale for investigating its effects on diabetes-induced

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    This document proposes a study to evaluate the antidepressant potential of agmatine in diabetes-induced depression in rats. The study would involve inducing depression in diabetic rats using streptozotocin and assessing the effects of agmatine treatment using tests like the forced swim test and tail suspension test. If agmatine shows antidepressant effects, it could provide a novel treatment option for depression comorbid with diabetes. The document provides background on the link between diabetes and depression, and the potential roles of insulin and monoamine neurotransmitters in this link. It also summarizes previous research demonstrating antidepressant effects of insulin in diabetic rats and the various neuroprotective effects of agmatine that provide rationale for investigating its effects on diabetes-induced

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    © All Rights Reserved
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    Download as doc, pdf, or txt
    30 views6 pages

    Evaluation of Antidepressant Potential of Agmatine in Diabetes Induce Depression in Rats

    Uploaded by

    niku
    This document proposes a study to evaluate the antidepressant potential of agmatine in diabetes-induced depression in rats. The study would involve inducing depression in diabetic rats using streptozotocin and assessing the effects of agmatine treatment using tests like the forced swim test and tail suspension test. If agmatine shows antidepressant effects, it could provide a novel treatment option for depression comorbid with diabetes. The document provides background on the link between diabetes and depression, and the potential roles of insulin and monoamine neurotransmitters in this link. It also summarizes previous research demonstrating antidepressant effects of insulin in diabetic rats and the various neuroprotective effects of agmatine that provide rationale for investigating its effects on diabetes-induced

    Copyright:

    © All Rights Reserved
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    of 6

    SYNOPSIS

    For approval of topic of the thesis to be submitted in the partial


    fulfillment of the requirement for the degree of Master of
    Pharmacy in Pharmacology

    Evaluation of antidepressant potential of


    agmatine in diabetes induce depression in rats

    By
    Nitin P. Nimje
    B.Pharm

    Guide
    Mr. B. G. Taksande
    M.Pharm

    SMT.KISHORITAI BHOYAR COLLEGE OF PHARMACY,


    New Kamptee, Nagpur, Maharashtra, 441002 (India)
    2013-2014
    Rashtrasant Tukadoji Maharaj Nagpur University, Nagpur.
    Introduction:-

    Diabetes is a chronic metabolic disorder characterized by


    hyperglycemia
    as a result of impaired insulin regulatory mechanism, which
    often results in neuropsychological complications such as
    depression.
    Studies have reported the prevalence rates of depression of 24
    30% in
    diabetic individuals with significantly increased risk of morbidity
    and mortality. Pharmacological reports manifest that the altered
    physiological processes such as elevated glucose oxidation,
    insulin
    deficiency and/or sensitivity and adaptive neurocellular responses
    as a
    consequence of diabetes may cause depression.
    The monoamine serotonin is a well established neurotransmitter
    involved in the pathophysiology of depression. The classic
    monoamine
    hypothesis states that monoamine imbalance or more specifically
    neurotransmitter deficiency in certain areas in the brain
    develops depression
    Insulin as a peptide hormone and neuromodulator has been
    known
    to have diverse functions in the brain. Previous studies have
    demonstrated
    the role of insulin in improving cognitive functions including
    learning and memory and in attenuating the neuronal damage
    associated
    with neurodegenerative diseases. Literary data give evidence that
    the administration of insulin causes a sequential increase in the
    concentration of tryptophan(a serotonin precursor) and serotonin
    in the rat brain. In addition, a growing body of evidence suggests
    the activity of insulin in depression comorbid with diabetes.
    Behavioral studies have shown that treatment with insulin
    produces antidepressant effects in streptozotocin (STZ) induced
    diabetes such as a decreased duration of immobility in rat tail
    suspension

    test (TST) and rat forced swim test (FST). Furthermore,


    insulin increases reward behavior in STZ diabetic mice subjected
    to an
    intracranial self stimulation testing paradigm. While insulin
    deficiency
    leads to depression like symptoms in STZ-diabetic rats.
    However, the neurochemical mechanism underlying these effects
    is
    poorly understood.
    Agmatine is a polycationic amine synthesized via decarboxylation
    of L-arginine by argininedecarboxylase(ADC) and is defined as a
    neuromodulator. In mammalian brains agmatine is expressed in
    some regions like as hypothalamus, hippocampus, cortex, locus
    ceruleus, Raphe nucleus and forebrain. Agmatine has been
    reported to have some neuroprotective effects against MPTP
    neurotoxicity, spinal cord ischemia, restraint-induced structural
    changes in the brain,LPS and scopolamine induced memory
    impairment. Additionally it is known to exert antidepressant,
    anxiolytic, anti-tumor cell proliferative and anticonvulsive effects.

    Objective:
    To study the influence of intra-hippocampal agmatine on ketamine induced
    memory impairment in rats and involvement of 2-adrenergic receptors in it.
    Plan of work:
    1. Induction of schizophrenia in rats by chronic ketamine administration and
    assessment of memory in inhibitory avoidance

    2. Dose dependant effect of agmatine and 2-adrenergic receptors ligand on


    memory of ketamine treated rats
    3. Influence of 2-adrenergic receptors ligands on the action of agmatine in
    ketamine treated rats

    Material and method:Animal:- Adult male Sprague-Dawley rats(240-260 g) will be group housed in
    acrylic cages (24x17x12 cm) under ambient room temperature (25+ 2 c ) And
    relative humidity (50 + 5%),maintained at 12:12 h dark-light cycle (lights on at
    07:00 h).Food and water will be available ad libitum. The experimental procedure
    will be performed as per the protocol approved by Institutional Animal and Ethical
    Committee according to the guidelines of CPCSEA. Every possible effort will be
    made to reduce the suffering of animals in all the experimental design.
    Drugs:- Agmatine Sulphate, Clonidine, Yohimbine, Ketamine
    Induction of Schizophrenia:-Schizophrenia in rats will be induced by injections
    of ketamine:- Ketamine is NMDA antagonist, and its chronic administration will
    lead to psychosis in rodents. Rat will be injected with ketamine (30 mg/kg I.P)
    twice daily for 7 days.
    Assessment of memory:-Apparatus: Inhibitory Avoidance Apparatus
    Training :- Rats will be allowed to habituate in experimental room for 30 min prior
    to experiments. All experiments groups will be first habituated to apparatus. Each
    animal will be gently placed in light compartment for 10 sec, after which the
    guillotine door will be lifted and the latency with which animal crosses to the dark
    compartment will be recorded. Animals that wait more than 60 sec to cross to other
    side will be eliminated from the experiment. Once animal crosses with all four
    paws to dark compartment, the door will be closed and rat will be taken from the
    dark compartment into the cage. The Habituation trail will be repeated after 30 min
    and will be followed after same interval by acquisition trail during which the
    guillotine door will be closed and foot shock (50 Hz, 1.5 sec, 2.5 mA) will be
    delivered immediately after the rat has entered the dark compartment. After 10 sec,

    rat will be removed from apparatus and place temporarily into the home cages
    (zarrindes et al., 2002).
    Testing (retention test):-Twenty four hours after training, retention test will be
    performed to determine step through latency. Each animal will be placed in the
    light compartment for 10 sec, door will be opened, and the step through latency
    will be measured for entering into dark compartment. The test session ends when
    the animal remains in the light compartment for 300 sec. During this session no
    electric shock will be applied.
    Possible outcome
    This study may provide novel therapeutic options for treatment of memory
    impairment associated with schizophrenia and could also project agmatine in the
    treatment of schizophrenia and associated complications.
    Reference
    [1] Ali S, Stone MA, Peters JL, Davies MJ, Khunti K. The prevalence
    of comorbid depression
    in adults with type 2 diabetes: a systematic review and meta
    analysis. Diabet
    Med 2006;23:116573.
    [2] Goldney RD, Phillips PJ, Fisher LJ,Wilson DH. Diabetes,
    depression, and quality of life
    a population study. Diabetes Care 2004;27:106670.
    [3] Roy T, Lloyd CE. Epidemiology of depression and diabetes: a
    systematic review.
    J Affect Disord 2012;142:S8S21.
    [4] Park M, KatonWJ,Wolf FM. Depression and risk ofmortality in
    individualswith diabetes:
    a meta-analysis and systematic review. Gen Hosp Psychiatry
    2013;35:21725.
    [5] Talbot F, Nouwen A. A review of the relationship between
    depression and diabetes
    in adults: is there a link? Diabetes Care 2000;23:155662.
    [6] Egede LE, Nietert PJ, Zheng D. Depression and all-cause and
    coronary heart disease
    mortality among adults with and without diabetes. Diabetes Care
    2005;28:133945.

    Student
    Mr. Abhinav Bawiskar
    Chopde

    Guide
    Dr.

    C.

    T.

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