Caffeine has dose-dependent effects on mood, attention, and physiology. Behavioral effects of caffeine in humans have also been well documented. This article aimed to study the effect of different caffeine concentrations on behavior and motor activity of mice. The experiments was carried out using 24 male mice (25-30gm). Plus maze was used for screening of antianxiety effect of caffeine. While swimming maze was used to test antidepressant effect. Statistical analysis were performed using computer program SPSS (version 22). At dose of 100 mg/kg, caffeine acted as anxiolytic compound. Caffeine increased motor activity at dose of 25mg/kg and decreased motor activity at dose of 200mg/kg. At dose of 100mg/kg, caffeine acted as antidepressant. In conclusion, caffeine can act as stimulant, while in over dose it acts as depressant. Caffeine showed to have anxiolytic effect in certain doses. arabic 14 English 91
Sakina Salem Mohammed Saadawi, ٍSuhera Mehemed Abdulsalam Aburawi, SUMAYA ESEDEEG ABDALLAH BAAIO(4-2018)

مرض الاكتئاب هو عبارة عن اضطراب عقلى واسع الانتشار يصيب الملايين من الاشخاص حول العالم وهو احدالاسباب المهمة المؤدية للإعاقة في جميع أنحاء العالم و في أسوأ حالاته يمكن أن يؤدي إلى الانتحار, والوفاة المأساوية المرتبطة بفقدان نحو 850 ألف شخص سنويا. هناك العديد من النواقل العصبية التى لها دور معروف في آليات الاكتئاب, والعقاقير المضادة له. ان المونوامين (السيروتونين والدوبامين والنورادرينالين) من المعروف أنها لها دور واضح فى هذا الشأن ولكن دور حمض غاما امينوبيمتاريك ( الجابا ) لا يزال غير واضح بشكل جيد, كما انه هناك العديد من الدراسات المعملية و السريرية التى أظهرت نتائج متضاربة بشأن الدور الحاسم للجابا في الاكتئاب. لذلك تقرر دراسة إذا كان الجابا له دور مباشر في علاج الاكتئاب من خلال دراسة التأثير المضاد للاكتئاب للأدوية المختلفة التي تنشط نظام الجابا بآليات مختلفة فى نموذج الكآبة المعترف به وهو (اختبار سباحة اليأس السلوكى) و هذه الأدوية تشمل؛ ( الدايازيبام ) وهو مضاد للقلق يعمل كمحور ايجابى للجابا عندما يتحد مع مستقبلات البنزوديازيبين، ( البرازولام ) الذى يعمل كمعزز لمستقبل (الجابا أ) ولديه ثأثير مزدوج كمضا د للقلق والاكتئاب عندما يتحد مع مستقبلات البنزوديازيبين، ( الزولبيدم ) وهو عقار منوم يستعمل على نطاق واسع و يعمل على مستقبل (الجابا أ) ويظهر جادبية عالية الى ( مستقبل الجابا أ الفرعى ( الفا1)، مضاد الصرع ( فيغاباترين) وهو مثبط غير رجعى وذو انتقائية عالية لئنزيم (غاما امينوبيمتاريك اسيد ترانزامينيز)، وأخيرا كان من الضرورى أن نشمل فى دراستنا مضاد الاكتئاب القياسى (الأميبرامين) الذى يعمل بتثبيط إعادة امتصاص ( السيروتونين، والنورادرينالين) من قبل الخلايا العصبية نتائج الدراسة المتصلة بقياس مدّة السكون الحركى فى اختبار سباحة اليأس السلوكى بعد 60 دقيقة من اعطاء الدواء اظهرت أن كل الأدوية المختارة المنشطة لنظام الجابا بآليات مختلفة ماعدا الجرعة العالية من ( البرازولام) قد انتجت زيادة مهمة فى مدّة السكون الحركى (مفعول مسبب للاكتئاب). هذه النتائج تدل على أن الناقل العصبى المثبط (الجابا)، ربما يكون قد سبب المفعول المشابه للاكتئاب نتجية تأثيره المسبب لنقص توفر المونوامين فى مناطق معينة من الدماغ، وللذلك استنتاجنا أن الزيادة فىنشاط نظام الجابا بالآليات المختلفة لن ينتج عنه مفعول مضاد للاكتئاب. Abstract: Depression is a common mental disorder affecting many millions of people worldwide and among the leading causes of disability worldwide. At its worst, depression can lead to suicide, a tragic fatality associated with the loss of about 850,000 lives every year. Many neurotransmitters have been suggested to be involved in the mechanisms of depression and antidepressant drugs. The role of the monoamines (serotonin, noradrenaline and dopamine) is well recognized. On the other hand, the role of gamma aminobutyric acid (GABA) is still not well recognized and many of the animal and clinical studies are showing conflicting findings regarding a crucial role of GABA in the pathophysiology of depression. Therefore, it was decided to examine if GABA has a direct role in depression by studying the antidepressant effect of different drugs that enhance GABA system by different mechanism by using a will established model of animal depression (forced swim test-FST). The drugs included diazepam an anxiolytic which acts as positive allosteric modulator of GABA when it binds to benzodiazepine receptors; alprazolam that act as GABAA receptor agonist with reported anxiolytic-antidepressant effect when it binds to benzodiazepine receptors; zolpidem which is a widely used hypnotic agent acting at the GABAA receptor and displays a high affinity to 1-GABAA receptor; the antiepileptic vigabatrin which is an irreversible and highly selective inhibitor of γ-aminobutyric acid transaminase; and finally imipramine was included as a standard antidepressant drug which acts by inhibiting the re-uptake of the neurotransmitters noradrenaline and serotonin. The results related to the measurement of the duration of immobility during FST after 60 min of drugs treatment showed that there was a tendency for all drugs (except for the high dose of alprazolam) to prolong the duration of immobility in dose dependent manner i.e. a depressant like action. These findings suggest that the neurotransmitter GABA might have produced a depressant like action by decreasing the availability of monoamines at certain brain areas. It was concluded therefore that increasing central GABAergic activity by different mechanisms will not result in an antidepressant activity.
نجوى أحمد الزحاف (2009)

Paracetamol is one of the most widely used drug as antipyretic and analgesic for mild to moderate pain. Currently, paracetamol is the first-line choice for pain management and antipyresis. Ion channels are pore-forming proteins that allow the flow of ions across membranes and involved in many cellular processes; drugs acting on ion channels have long been used for the treatment of many diseases. Objective: To estimate the effect of voltage gated ion channel blockers on analgesic activity of Paracetamol and explore the interaction between ion channel blockers and paracetamol on pain behaviour. Materials and Methods: Male albino mice were used. The central antinociceptive activity was determined by hot plate test and formalin test (Phase I; neuropathic pain). Antiinflammatory activity was determined by formalin test (Phase II). Intraperitoneal injection was adopted. Five groups of mice were used. Group 1; control group (1% T80), group 2; treated with (200mg/kg) paracetamol, group 3; treated with different drugs of ion channel blockers, group 4; received standard drugs, Aspirin (200mg/kg) for formalin test (phase II) or tramadol (5mg/kg) for hot plate test and formalin test (phase I), group 5; received combined treatment of ion channel blockers and paracetamol. Results: Pain produced by noxious stimuli (heat and formalin) was significantly reduced by acute administration of paracetamol. Inflammation pain produced by formalin injection was significantly decreased by acute administration of paracetamol. Acute administration of nifedipine showed significant decrease in nociception and inflammation pain. Combined treatment of nifedipine and paracetamol produced antinociceptive and anti-inflammatory activity but less than the additive effect. Verapamil has no analgesic effect in the two models, and did not change the affect of paracetamol analgesic activity when administered together. Phenytoin produces significant decrease in nociceptive pain using hot plate but not in formalin test (Phase I), and produce significant decrease in inflammatory pain (Phase II). The combined treatment of phenytoin and paracetamol showed analgesic activity less than the additive effect. 4-Aminopyridine produces significant antinociceptive and anti-inflammatory activity. The combined administration of 4-aminopyridine and paracetamol showed analgesic activity, which is less than the additive effect using formalin test, while paracetamol analgesic activity is potentiated by 4-aminopyridine using hot plate test. Conclusion: Paracetamol has antinociception and anti-inflammatory activity on pain model used (Hot plate test and Formalin test). Ion channel blockers produce antinociception and anti-inflammatory activity. Verapamil has no effect on nociception or inflammation pain and no effect on paracetamol analgesic activity. Nifedipine, phenytoin and 4-aminopyridine interact with paracetamol producing less additive analgesic effect, except 4-aminopyridine in thermal stimuli (Hot plate) is more sensitive compared to chemical stimuli (formalin test – phase I), where potentiates paracetamol action.
هناء مدحت الزقلعي (2014)