P.5.c. Dementia and neurological disorders − Neurological disorders (basic) S647 Exocytosis, endocytosis, intracellular pH and plasma membrane potential were monitored. In our previous investigation we have shown that moderate concentration of KB inhibits endocytosis and did not change exocytosis in synaptosomes [1]. Methods: Exocytosis and endocytosis were measured using acridine orange fluorescent dye according to Zoccarato et al. [2]. Intracellular pH was measured with 2 ′ ,7 ′ -bis(2-carboxyethyl)- 5(6)-carboxyfluorescein (BCECF) fluorescent dye according to Nachshen and Drapeau [3]. Plasma membrane potential was measured with 3,3 ′ -dipropylthiadicarbocyanine iodide [DiSC3(5)] fluorescent dye according to Waseem and Fedorovich [4]. Statistical significance was evaluated using one-tailed Student’s t-test. Results: We have shown that even high concentration KB did not change exocytosis, but endocytosis was significantly (P  0.01) inhibited down to 30.2±5.5% from control. This is the more pronounced reduction of endocytosis as compared to that reported for moderate concentration of KB [1]. Also ratio between endocytosis/exocytosis was reduced down to 25.7±6.1%. It is suggested that compensatory endocytsis in conditions of endocytosis not able to compensate synaptic vesicles depletion. We found that pHi in synaptosomes in normal glucose- containing medium is 7.03±0.01. These results are close to those reported by other researchers [3]. Replacing of glucose by mod- erate concentration of KB or additions of high KB concentration does not change pHi. Withdrawing of glucose or replacing of glucose by pyruvate was also not effective. In our previous investigation we have shown that replacing of glucose by moderate concentrations of KB did not change plasma membrane potential [1]. However, we found that additional KB in glucose-containing incubation medium increase of DiSC3(5) fluorescence what reported plasma membrane depolarization. Po- tentially it can provoke neurotransmitter release with following excitotoxic-like brain damages. Conclusion: Strong inhibiting of endocytosis must lead to fast depletion of synaptic vesicles in neurons. Together with depolarization of presynaptic endings it can provoke synaptic failure in case of high KB concentration which is accompanied by hypoglycemic coma. Intracellular acidification does not contribute to pathogenesis of ketoacidosis at least on synaptic level. References [1] Hrynevich, S.V., Waseem, T.V., Hebert, A., Pellerin, L., Fe- dorovich, S.V., 2016. b-hydroxybutirate supports synaptic vesicle cy- cling but reduces endocytosis and exocytosis in rat brain synaptosomes. Neurochem. Int. 93, 73−81. [2] Zoccarato, F., Cavallini, L., Alexandre, A., 1999. The pH-sensitive dye acridine orange as a tool to monitor exocytosis/ endocytosis in synaptosomes. J. Neurochem. 72, 625–633. [3] Nachshen, D.A., Drapeau, P., 1988. The regulation of cytosolic pH in isolated presynaptic nerve terminals from rat brain. J. Gen. Physiol. 91, 289–303. [4] Waseem, T.V., Fedorovich, S.V., 2010. Presynaptic glycine receptors in- fluence plasma membrane potential and glutamate release. Neurochem. Res. 35, 1188–1195. P.5.c.003 Methyl jasmonate attenuated lipopolysaccharide-induced memory dysfunction through inhibition of neuroinflammatory markers and beta-amyloid generation in mice S. Umukoro 1° , A.T. Eduviere 2 1 University of Ibadan, Pharmacology and Therapeutics, Ibadan, Nigeria; 2 Afe Babalola University, Pharmacology and Therapeutics, Ado-Ekiti, Nigeria Background: Neuroinflammation plays a central role in the eti- ology and progression of Alzheimer’s disease (AD), a neurode- generative disorder, characterized by a gradual loss of memory functions. AD is a debilitating disorder, which imposes untold sufferings on the patients and their relatives, thus of a major public health concern. Actylcholinesterase inhibitors currently used for AD, only provide symptomatic relief as cure remains elusive. Thus, it has been proposed that agents that could reduce inflammatory processes in AD brains might be of benefit for the treatment of the disease. Methyl jasmonate (MJ) is a bioactive compound, which has been reported to exhibit anti-amnesic and anti-inflammatory activities in experimental models [1,2] and [3]. In this study, we further examine its effects on neuroinflammatory markers and beta-amyloid generation in lipopolysaccharide (LPS)- induced memory deficits in mice. Methods: Male Swiss mice (8-weeks old, n = 6) were given intraperitoneal administration of LPS (250 mg/kg) alone or in combination with MJ (10−40 mg/kg, i.p.) or vehicle once daily for 7 consecutive days prior to assessment of memory function using Y-maze test. Thereafter, the animals were sacrificed un- der ether anesthesia and the brains were harvested and stored for biochemical and immunohistochemical analysis. The levels of biomarkers of neuroinflammation: prostaglandin E2 (PGE2), tumor necrosis factor a (TNFa) and interleukin 1b (IL1b) were estimated in the brain tissue homogenates using ELISA kits ac- cording to the manufacturer’s instructions. Expressions of positive cells of cyclooxygenase-2 (COX2), inducible nitric oxide synthase (iNOS), nuclear factor kappa B (NF-úB) and amyloid-beta (Ab) in the prefrontal cortex were also assessed using immunohisto- chemistry technique. Statistical significance was ascertained by repeated ANOVA at p < 0.05. The experimental procedures were approved by the University of Ibadan Animal Care and Use Research Ethics Committee (UI-ACUREC/App/2015/030) and performed in accordance with the NIH Guideline for the Care and Use of Laboratory Animals. Results: LPS (250 mg/kg) significantly (p = 0.0002) decreased the level of alternation behavior in comparison with vehicle, suggesting impairment of memory function. MJ (10, 20 and 40 mg/kg) significantly (p = 0.0002) reversed LPS-induced mem- ory deficit in mice. The increased brain levels of PGE2, TNFa and IL1b in LPS-treated mice were significantly (p < 0.05) reduced by MJ, which indicate anti-neuroinflammatory activity. MJ (10, 20 and 40 mg/kg) also suppressed LPS-induced increases in the expressions of positive cells of COX2, iNOS and NFúB, which further suggest anti-neuroinflammation. Also, MJ (10, 20 and 40 mg/kg, i.p) significantly (p < 0.05) attenuated the expressions of amyloid beta positive cells evoked by LPS ((250 mg/kg), i.p.), suggesting anti-amyloidogenesis-like effect. Conclusion: Our present data showed that methyl jasmonate attenuated lipopolysaccharide-induced memory dysfunction via mechanisms related to inhibition of pro-inflammatory mediators and beta-amyloid generation in mice. These findings further