|Year : 2015 | Volume
| Issue : 4 | Page : 144-150
Analgesic, antiepileptic, and behavioral study of Mimosa pudica (Linn.) on experimental rodents
Ganesh Patro1, Subrat Kumar Bhattamisra2, Bijay Kumar Mohanty3
1 School of Pharmaceutical Education and Research, Berhampur University, Berhampur, Odisha, India
2 Department of Pharmacology, Roland Institute of Pharmaceutical Sciences, Khallikote Autonomous College, Berhampur, Odisha, India; Department of Life Sciences, International Medical University, Bukit Jalil, Kuala Lumpur, Malaysia
3 Department of Botany and Biotechnology, Khallikote Autonomous College, Berhampur, Odisha, India
|Date of Web Publication||19-Oct-2015|
School of Pharmaceutical Education and Research, Berhampur University, Bhanja Bihar, Berhampur - 760 007, Odisha
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Objective: Mimosa pudica (M. pudica) Linn. (family: Mimosaceae) is a traditionally used folk medicine to treat various ailments including convulsion, alopecia, diarrhea, dysentery, insomnia, tumor, wound, snake bite, etc., Here, the study was aimed to evaluate the potential on antiepileptic, analgesic, and motor activities of M. pudica leaves on rodents. Materials and Methods: In an acute toxicity study, the extracts were administered in doses of 50-2,000 mg/kg/p.o. and behavioral changes were observed for up to 24 h. For a pharmacological study, the ethyl acetate extract of M. pudica (EAMP) leaves in doses of 100 mg/kg/day, 200 mg/kg/day, and 400 mg/kg/day were orally administered for consecutive 7 days to animals. The antiepileptic study was evaluated by inducing electric shock, pentylenetetrazole (PTZ), and isoniazid (INH) in mice, whereas the motor activity test was performed by using an actophotometer, rotarod test, and traction test in mice. The analgesic activity was done by hot-plate, tail flick, and acetic acid-induced writhing in rats. Statistical analysis was carried out by one-way analysis of variance (ANOVA) followed by Dunnett's test. Results: The EAMP showed dose-dependent analgesic activity by increasing the reaction time as compared to the vehicle control. Similarly, the motor performance was improved in dose-dependent manner as compared to standard. The doses (100 mg/kg/day, 200 mg/kg/day, 400 mg/kg/day) of the extract significantly (P < 0.01 and P < 0.001) reduced the duration of seizures induced by maximal electro shock (MES) and delayed the onset of tonic-clonic seizures produced by PTZ and INH. All the tested doses significantly prevented the latency and duration of convulsion against seizure inducers as compared to the vehicle controls. Conclusion: These results revealed that the EAMP possesses potent analgesic, antiepileptic, and motor activities on animals. This could be an effective treatment option for various motor or seizure disorders.
Keywords: Analgesic, antiepileptic, motor activity, Mimosa pudica (M. pudica)
|How to cite this article:|
Patro G, Bhattamisra SK, Mohanty BK. Analgesic, antiepileptic, and behavioral study of Mimosa pudica (Linn.) on experimental rodents. Int J Nutr Pharmacol Neurol Dis 2015;5:144-50
|How to cite this URL:|
Patro G, Bhattamisra SK, Mohanty BK. Analgesic, antiepileptic, and behavioral study of Mimosa pudica (Linn.) on experimental rodents. Int J Nutr Pharmacol Neurol Dis [serial online] 2015 [cited 2020 Jun 2];5:144-50. Available from: http://www.ijnpnd.com/text.asp?2015/5/4/144/167502
| Introduction|| |
Pain is an unpleasant sensory and emotional experience associated with tissue damage that results in warning signals and discomfort to the patient. It is a disabling accompaniment of various medical complicacies and its control is one of the most important therapeutic priorities. The drug of selection for pain management is either nonsteroidal anti-inflammatory drugs (NSAIDs) or corticosteroids. But these analgesics are associated with serious adverse effects, namely, ulceration, gastrointestinal bleeding, addictive potential, respiratory distress, drowsiness, nausea, and development of tolerance and dependence.
Epilepsy is a disorder of the brain characterized by unpredictable and periodic occurrence of a transient alteration of behavior due to the disordered, synchronous, and rhythmic firing of populations of brain neurons. It became a major neurological disorder that affects up to 5% of the world population every year. Unfortunately, the drugs available in modern medicine not only fail to control the seizure activity in some patients but also quite frequently cause unwanted effects like neurotoxicity, aplastic anemia, hepatic failure, and sometimes expose to risk of drug interactions.
Thus, there is an unmet need for the searching of bioactive compounds from natural products, especially from medicinal plants for use as an alternative analgesic and antiepileptic with little or no side effects. Previous reports revealed that the plants containing saponins or flavonoids exhibit anticonvulsant activity.Mimosa pudica (M. pudica) (family: Mimosaceae) is locally known as lajwanti or chuimui in Hindi. The plant is native of Central America, Tanzania, South Asia, East Asia, and many Pacific islands. The roots and leaves of this plant were commonly used by tribal people for the treatment of headache, migraine, dysentery, fever, piles, insomnia, epilepsy, etc., The plant is used as bitter, astringent, acrid, cooling vulnerary, febrifuge, alexipharmic, diuretic, emetic and tonic. In traditional health-care systems, it has been used in the treatment of alopecia, diarrhea, constipation, leprosy, dysentery, insomnia, tumor, blood disorders, and various urogenital infections. Various medicinal and biological activities of this plant were reported, especially its antidiabetic, antihepatotoxic, antioxidant, antiasthmatic, aphrodisiac, sedative, and wound-healing activities. Phytochemical studies had revealed the presence of alkaloids, amino acid, flavonoid glycosides, sterols, terpenoids, tannins, and fatty acids., However, until today, there were no reports on the neurological behaviors on this plant. Hence, the present work was designed to evaluate the analgesic, antiepileptic, and behavioral study of ethyl acetate extract of M. pudica (EAMP) leaves on rodents.
| Materials and Methods|| |
The leaves of M. pudica were collected during the month of November from Ganjam district, Odisha, India. The plant material was authenticated by Dr. B. K. Mohanty (Professor), Department of Botany, K. K. Autonomous College, Berhampur, Ganjam, Odisha, and the plant specimen was deposited at plant herbarium for further reference.
Drugs and chemicals
Diclofenac sodium (Lupin limited, Mumbai, Maharashtra, India), pentylenetetrazole (PTZ) (Sigma Aldrich Chemical Co., Bengaluru, Karnataka, India.), isoniazid (INH) (S.D. Fine Chem. Ltd, India), and diazepam (Calmpose injection, Ranbaxy, Ranbaxy Laboratories Limited, Mumbai, India) were purchased. All the other chemicals used in this study were of analytical grade.
Preparation of the extract
The collected leaves of M. pudica were washed under running tap water and allowed to air-dry. The air-dried leaves were crushed to produce a moderately coarse powder. The powdered leaves (approximately 200 g) were defatted with petroleum ether [boiling point (B.P.) 40-60°C] and then packed in a Soxhlet apparatus for the extraction of ethyl acetate at room temperature. After 72 h of complete extraction, the solvent was removed by distillation and the concentrated extract was dried under reduced pressure at the temperature of 40°C in a rotary evaporator. A thick, semisolid, brown paste was obtained and stored in a desiccator at room temperature. The extractive yield was found to be 8.41%.
Adult Wistar albino rats (125-150 g) and Swiss albino mice (20-25 g) of either sex were obtained from Ghosh enterprises, Kolkata, West Bengal, India. They were randomly housed at an ambient temperature of 25 ± 1°C and 45-55% relative humidity in polypropylene cages with 12 h of light-dark cycle. The animals were allowed free access of standard food pellets (Rayans Biotechnologies Pvt. Ltd, Hyderabad, Telangana, India) and water ad libitum. All experimental protocols were approved and prior permission was obtained from the Institutional Animal Ethics Committee (IAEC) of Roland Institute of Pharmaceutical Sciences, Berhampur, Odisha, India, and the Committee for the Purposes of Control and Supervision of Experiments on Animal (CPCSEA).
Acute toxicity study
The acute toxicity study of the extract was performed on albino rats according to the Organization for Economic and Cultural Development (OECD) guidelines - 425. The animals were fasted overnight prior to the experiment with free access to water. Doses of 50 mg/kg/p.o., 300 mg/kg/p.o., 500 mg/kg/p.o., and 2,000 mg/kg/p.o. of EAMP were administered to the animals and the behavioral changes were observed for up to 24 h.
Pharmacological investigation of EAMP
Assessment of analgesic activity
The animals were divided into five groups of six rats in each. Group I served as the control group and received vehicle only. Group II served as the standard group and received diclofenac sodium (5 mg/kg/p.o.). Groups III-V served as the test groups and were administered single doses of EAMP of 100 mg/kg/p.o., 200 mg/kg/p.o., and 400 mg/kg/p.o., respectively. The following tests were employed for the evaluation of analgesic activity after 1 h of administration of test extract and the animals were used once for each test:
This test is specifically used for the screening of centrally acting analgesics. Wistar rats were placed into an Eddy's hot-plate maintained at a temperature of 55°C surrounded by a Plexiglas cylinder to record the reaction time (s) for the licking of paw or jumping. A cutoff time of 15 s was used to avoid damage to the paw. The reaction time of the test groups was recorded at 30-min intervals for 150 min and compared with that of the control group.
Tail flick test 
This test is also used for the screening of centrally acting analgesic drugs. The rats were kept individually in a rat holder and the middle section of tail was placed on the nichrome wire of the analgesiometer. Then, 6-mA current was applied to the wire. Within a few seconds, the animal flicked the tail aside or tried to escape. The time when animal withdraw (flick) its tail from the hot wire was recorded as the reaction time (maximum 30 s). The reaction time of the test groups was recorded at 30-min intervals for 150 min and compared with that of the control group.
Acetic acid induced writhing test 
Thirty minutes after drug treatment, 0.7% solution of acetic acid (1 mL/kg) was injected intraperitoneally (i.p.). Then, each animal was placed in a transparent observation cage. The writhing activity consists of a contraction of the abdominal muscles together with a stretching of the hind limbs. The number of writhing in 60 min was recorded and the percentage of writhing inhibition was compared with that of the control group.
Assessment of antiepileptic activity
Swiss albino mice (25-30 g) were selected and divided into five groups of six animals each. Group I served as the vehicle control, group II served as the standard group that received diazepam (4 mg/kg/p.o.) once daily for 7 days, groups III-V served as the test groups that received EAMP doses of 100 mg/kg/p.o., 200 mg/kg/p.o., and 400 mg/kg/p.o., respectively, once daily for 7 days. The following tests were employed for the evaluation of antiepileptic activity and the animals were used once for each test:
Maximum electric shock (MES)-induced seizure model 
The electroshock was induced in animals by passing a current of 45 mA, 50 Hz for 0.2 s through electroconvulsiometer (INCO Instruments and Chemicals Pvt. Ltd., Ambala, Haryana, India.) using corneal electrodes. Under these conditions, all the vehicle-treated mice showed the characteristic extensor tonus. The standard drug and extract were administered before 1 h of the experiment. After shock treatment, the animals were closely observed for 2 min. Disappearance of the tonic hind limb extensor was used as the positive criterion. The onset and duration of tonic convulsion were calculated and compared with that of the control group.
PTZ-induced seizure model 
After 1 h of administration of test and standard drugs, the seizures were induced by the PTZ (75 mg/kg/i.p.). The animals were observed during the first 30 min with convulsions, i.e. latency as well as duration of the convulsions and percent of protection against the convulsions were calculated and were compared with those of the control group.
INH-induced seizure model 
After 1 h of administration of test and standard drugs, the seizures were induced by INH (300 mg/kg/s.c.). The mice were placed in an isolated perplex chamber and were observed for the next 120 min for convulsion latency and rate of mortality after 30 min and 24 h of INH treatment. The percentage of convulsion inhibition was calculated and was compared with that of the control group.
Assessment of behavioral changes
The mice were grouped into five groups of six mice each. Group I served as the control, group II received diazepam (4 mg/kg i.p.), and groups III-V received single doses of EAMP of 100 mg/kg/p.o., 200 mg/kg/p.o., and 400 mg/kg/p.o., respectively.
Locomotor test ,
The locomotor activity of the animals was monitored by placing them individually in an actophotometer (INCO, Ambala Pvt. Ltd., India) for 5 min in a square closed field arena (30 cm × 30 cm × 30 cm) equipped with six photocells in the outer wall. The locomotor activity for each animal of the tested groups was recorded and was compared with that of the control group.
Rotarod test ,
The effect on motor coordination was assessed using a rotarod apparatus (INCO, Ambala, India). Prior to the experiment, the animals were trained in the rotarod. Each animal was placed after 60 min of drug administration on the rotating rod at a speed of 25 rpm. The fall of time was recorded for each tested group and was compared with that of the control group.
Traction test 
The test was conducted 1 h prior to obtaining EAMP and 30 min after the injection of diazepam (4 mg/kg i.p.). Forepaws of a mouse were placed on a 15-cm long twisted wire rigidly supported and 20 cm above the table top. Normal mice grasped the wire with forepaws and when allowed to hang free, placed at least one hind foot on the wire within 5 s. Inability to put up at least one hind foot was considered failure to the traction.
The values were expressed in mean ± standard error of the mean (SEM). Statistical analysis was done by one-way analysis of variance (ANOVA) followed by Dunnett's multiple comparison (test vs control). P < 0.05 and P < 0.01 were considered as significant.
| Results|| |
Acute toxicity study
No mortality and sign of toxicity were observed at the dose of 2,000 mg/kg/p.o. in case of albino rats.
Effect of EAMP on analgesic activity
Analgesic activity was evaluated by acetic acid-induced writhing, hot-plate, and tail flick models. It can be substituted as INCO Instruments and Chemicals Pvt. Ltd., Ambala, Haryana, India. In both the models of hot-plate and tail flick, the reaction time was increased in EAMP at 100 mg/kg, 200 mg/kg and 400 mg/kg as well as the standard and showed significant analgesic activity at P < 0.01 and P < 0.05 as compared with control [Table 1] and [Table 2]. All the doses of EAMP followed dose-dependent inhibition against pain inducers. Again, the EAMP at 400 mg/kg showed a closer resemblance of analgesic potential as compared with the standard group in the hot-plate model. Similarly, in the acetic acid-induced writhing model, the writhing response was significantly reduced by EAMP doses of 100 mg/kg, 200 mg/kg, and 400 mg/kg at P < 0.01 as compared with the control [Table 3]. At EAMP doses of 100 mg/kg, 200 mg/kg, and 400 mg/kg, the treated group showed 20.18%, 33.42%, and 43.46% of writhing inhibition, respectively, while the standard (diclofenac sodium) group showed 52.01% of writhing inhibition against acetic acid.
Effect of EAMP on antiepileptic activity
Seizures were produced in mice by inducing electric shock, PTZ, and INH. In electric shock and PTZ-induced seizure model, the onset and duration of convulsion were measured [Table 4] and [Table 5] and the percentages of inhibition of convulsions were compared with those of the control [Figure 1]. Swiss mice pretreated with EAMP doses of 100 mg/kg/p.o., 200 mg/kg/p.o., and 400 mg/kg/p.o. exhibited delayed onset time of convulsion as well as decreased duration of convulsion when compared with the control group. Swiss mice pretreated with EAMP at doses of 100 mg/kg, 200 mg/kg, and 400 mg/kg were provided significant (P < 0.01) protection from convulsions induced by the electroshock method in a dose-dependent manner. Animals pretreated with EAMP exhibited significant antiepileptic activity and closer resemblance in percentage inhibition of convulsions at the dose of 400 mg/kg when compared to diazepam-treated animals. In the INH-induced seizure model, all the three doses of EAMP showed significant (P < 0.01) reduction in convulsion latency in a dose-dependent manner as compared with the control group. EAMP at doses of 200 mg/kg and 400 mg/kg was able to complete protection (100%) against mortality while EAMP at 100 mg/kg was not able to complete protection against mortality, i.e. 81% as compared to the control group [Table 6].
|Figure 1: Effect of EAMP on percentage of convulsion inhibition in mice. Values were represented as mean ± SEM of six animals in each group and compared with the control group|
Click here to view
Effect of EAMP on behavioral study of mice
The EAMP significantly (P < 0.01) decreased the locomotor activity in mice at all three doses as compared with the control group and followed dose-dependent relationship with locomotor effect. In rotarod test, the fall of time was decreased significantly at P< 0.01 and the muscle relaxant activity was followed in dose-dependent manner as compared with control. Similarly in traction test, the holding time of mice was significantly decreased (P< 0.01) in EAMP-treated and standard group as compared to control group, which strongly indicates muscle relaxant activity by decline of motor coordination [Table 7].
| Discussion|| |
Epilepsy is a chronic neurological disorder characterized by episodic attack of convulsive seizures, sensory disturbance, abnormal behavior, and loss of consciousness resulting in brain dysfunction or an abnormal discharge of cerebral neurons. It is a major health problem in the developing countries due to higher prevalence, lack of awareness, cultural and social stigma, and nonavailability of proper diagnostic or treatment facilities. In this study, the EAMP was evaluated for antiepileptic activity by three animal models involving GABA neurotransmission, i.e. MES-, PTZ-, and INH-induced convulsions in mice. The MES test is used primarily as an indication for compounds that are effective in grand mal epilepsy that is evoked by electric stimuli. PTZ-induced convulsion is generally used for petitmal epilepsy due to GABA antagonist action. It has been indicated that PTZ-induced seizures can be prevented by drugs that reduce T-type Ca + currents and also by drugs that enhance GABA receptor-mediated inhibitory neurotransmission. INH is a GABA synthesis inhibitor that produces seizure by precipitating convulsion.
GABA is known to be an important inhibitory neurotransmitter in the brain, whereas glutamate is the excitatory neurotransmitter. GABA acts on the GABA receptors and glutamate acts through the NMDA (N-methyl-D-aspartate) and non-NMDA receptors. Activation of these receptors modifies various voltage gated including Na +, K +, Ca 2+, and Cl - ion channels and excites or inhibits the neuron. Abnormalities in the GABA system have been found in neurological and psychiatric diseases such as Huntington's disease, anxiety, panic attacks, schizophrenia, and epilepsy. One major factor in an epileptic patient is decreased function of the GABA synapses.
The present investigation revealed that EAMP significantly inhibited the convulsions induced by MES, PTZ, and INH. Previous phytochemical investigations of EAMP revealed the presence of flavonoids, tannins, terpenoids, coumarins, alkaloids, steroids, phenols, and saponins. It is also found that many flavonoids can act as benzodiazepine-like molecules in the central nervous system and modulate GABA generated chloride currents in animal models of anxiety, sedation, and convulsion. Flavonoids, sterols, and terpenoids have been implicated in various pharmacological actions on the central nervous system including anticonvulsant and anxiolytic activities. Flavonoids and sterols have been involved in central inhibitory and neuromodulatory effects., The plants containing saponins or flavonoids exhibit anticonvulsant activity. Some alkaloids, monoterpenes, and flavonoids also have protective effects against PTZ-, picrotoxin-, and NMDA-induced convulsions.
The EAMP extract also increased the threshold of seizures and offered protection in the MES test. The drugs that inhibit PTZ-induced convulsions and raise the threshold for production of MES-induced seizures are generally effective against absence of seizures. The EAMP possess antiepileptic action that is due to the presence of the above phytoconstituents that facilitates GABA transmission.
The present investigation revealed that EAMP produced motor impairment and decreased spontaneous locomotor activity at anticonvulsant dose. Presence of high flavonoid content in EAMP may be responsible for anticonvulsant activity in mice. Various chemical constituents of plant origin, such as terpenoids and flavonoids, are reported to have muscle relaxant properties.
Pain sensation is elicited by triggering localized inflammatory response, resulting in the release of free arachidonic acid from the tissue phospholipids via cyclooxygenase (COX) and prostaglandin biosynthesis. The acetic acid-induced writhing has been associated with increased level of prostaglandin E2 (PGE2) and PGF2α in peritoneal fluids as well as lipoxygenase products. The increase in prostaglandin level within the peritoneal cavity enhances inflammatory pain by increasing capillary permeability. The acetic acid-induced writhing method was found effective to evaluate peripherally active analgesics. The agent reducing the number of writhing will render analgesic effect preferably by the inhibition of prostaglandin synthesis, a peripheral mechanism of pain inhibition. The significant pain reduction of EAMP might be due to the presence of analgesic principles acting through the prostaglandin pathways. The hot-plate and tail immersion tests measure the complex response to a noninflammatory acute nociceptive input and they are the models normally used for studying central nociceptive activity. Therefore, the EAMP must have a central activity. Again, narcotic analgesics inhibit both peripheral and central mechanisms of pain while NSAIDs inhibit only peripheral pain. The analgesic effect of EAMP in three models suggests that they have been acting analgesic property through central and peripheral mechanisms.
In conclusion, the EAMP possesses both central and peripheral analgesic properties with antiepileptic activity by GABA facilitatory action. Again, the plant possesses muscle relaxant activity and decreased locomotor activity. However, further studies are needed to evaluate the precise mechanism (s) involved in GABA activity, active principles, and the safety profile of the plant as a medicinal remedy for neurological disorders.
We are very grateful to the Principal and the Management of the Roland Institute of Pharmaceutical Sciences, Berhampur, Odisha, India for providing necessary research facility to carry out a part of this work. This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Rang HP, Dale MM, Ritter JM, Moore PK. Pharmacology. Edinburgh, New York: Churchill Livingstone; 2003. p. 556-7.
McNamara JO. Drugs effective in the therapy of the epilepsies: In: Hardman JG, Limbird LE, Gilman AG, editors. Goodman and Gillman's the Pharmacological Basis of Therapeutics. New York: McGraw-Hill; 2001. p. 521-39.
Govindu S, Adikay S. Evaluation of antiepileptic activity of chloroform extract of Acalypha fruticosa
in mice. Ph cog. Res 2014;6:108-12.
Aldenkamp AP. Cognitive side effects of antiepileptic drugs. Neuropsychol Childhood Epilep 2006;50:257-67.
Joseph B, George J, Mohan J. Pharmacology and Traditional Uses of Mimosa pudica
. Int J Pharma Sci Drug Res 2013;5:41-4.
Merlin FF, Narsimhan D. Plant names and uses as indicators of knowledge patterns. Indian J Tradit Know 2009;8:645-8.
Joy PP, Thomas J, Mathew S, Skaria BP. Medicinal plants. TropHort 2001;2:449-632.
Vaidyaratanm PS. Indian Medicinal Plants Database. 1st
ed. Kottakkal II, Orient Longman: Arya Vidyashala; 2001. p. 36-7.
Chatterjee A, Prakash SC. The Treatise of Indian Medicinal Plants, Publications and Information Directorate. Vol. 2. New Delhi: CSIR; 2000. p. 65-6.
Sivarajan VV, Balachandran I. Ayurvedic drugs and their plant sources. New Delhi: Oxford and IBH Publishing Co. Pvt. Ltd.; 2002. p. 271-2.
Tamilarasi T, Ananthi T. Phytochemical analysis and anti-microbial activity of Mimosa pudica
Linn. Res J Chem Sci 2012;2:72-4.
Hafsa A, Sakshi S, Anurag M, Rajiv G. Mimosa pudica
L. (Laajvanti): An overview. Pharmacogn Rev 2012;6:115-24.
OECD Guidelines for testing of chemicals. Acute oral toxicity-Up and Down procedure. 2001;425:1-26.
Kulkarni SK. Handbook of Experimental Pharmacology. 3rd
ed. New Delhi: Vallabh Prakashan; 2005. p. 125-8.
Ghosh MN. Fundamentals of Experimental Pharmacology. 2nd
ed. Calcutta: Calcutta Scientific Book Agency; 1984. p. 120-2.
Salawu OA, Chindo BA, Tijani AY, Adzu B. Analgesic, anti-inflammatory, antipyretic and antiplasmodial effects of the methanol extract of Crossopteryx febrifuga
. J Med Plants Res 2008;2:213-8.
Vogel GH. Drug Discovery and Evaluation; Pharmacological Assays. Germany: Springer; 1997. p. 487.
Sivaraman D, Muralidaran P. CNS depressant and antiepileptic activities of the methanol extract of the leaves of Ipomoea aquatica
Forsk. Eur J Chem 2010;7:1555-61.
Madhu A, Keerthi PH, Jaideep S, Shivalinge GK. Antiepileptic activity of aqueous root extracts of Hemidesmus indicus
in rats. Arch Pharm Sci Res 2009;1:43-7.
Bhattamisra SK, Singh PN, Singh SK. Behavioural characterization of Marsilea minuta
in rodents. Indian J Nat Prod 2006;22:3-7.
Achliya GS, Wadodkar SG, Dorle AK. Evaluation of CNS activity of Bramhi Ghrita. Indian J Pharmacol 2005;37:33-6.
Kulkarni SK. Handbook of Experimental Pharmacology. In: Jain MK, editor. 3rd
ed. Delhi: Vallabh Prakashan; 2002; p. 122-3,131-2.
Hosseinzadeh H, Nassiri-Asl M. Anticonvulsant, sedative and muscle relaxant effects of carbenoxolone in mice. BMC Pharmacol 2003;3:3.
Jerome E, Timothy AP. A Comprehensive Textbook. 2nd
ed. Philadelphia: Lippincott Williams and Wilkins; 1997. p. 1-7.
Aguirre-Hernandez E, Rosas-Acevedo H, Soto-Hernandez M, Martinez AL, Moreno J, Gonzalez-Trujano ME. Bioactivity guided isolation of beta-sitosterol and some fatty acids as active compounds in the anxiolytic and sedative effects of Tilia americana
var. mexicana. Planta Med 2007;73:1148-55.
Rocha FF, Lapa AJ, De Lima TC. Evaluation of the Anxiolytic-like effects of Cecropia glazioui
Sneth in mice. Pharmacol Biochem Behav 2002;71:183-90.
De S, Dey YN, Gaidhani S, Ota S. Effects of the petroleum ether extract of Amorphophallus paeoniifolius on experimentally induced convulsion in mice. Int J Nutr Pharmacol Neurol Dis 2012;2:132-4.
Bhandari PR. Potential role of Nigella sativa (black cumin) in epilepsy. Int J Nutr Pharmacol Neurol Dis 2014;4:188-9.
Sinoriya P, Irchhaiya R, Sharma B, Sahu G, Kumar S. Anticonvulsant and muscle relaxant activity of the ethanolic extract of stems of Dendrophthoe falcata
(Linn. F.) in mice. Indian J Pharmacol 2011;43:710-3.
Sikka P, Kaushik S, Kapoor S, Saini M, Saxena KK. Evaluation of antinociceptive/analgesic activity of SSRIs (fluoxetine and escitalopram) and atypical antidepressants (venlafaxine and mirtazapine): An experimental study. Int J Nutr Pharmacol Neurol Dis 2012;2:223-8.
Sabina EP, Chandel S, Rasool MK. Evaluation of analgesic, antipyretic and ulcerogenic effect of Withaferin A. Int J Integrative Bio 2009;6:52-6.
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]