IS THERE TREATMENT EFFECT OF VINPOCETINE ON AUTONOMIC DYSFUNCTION IN RATS WITH ALZHEIMER
Alzheimer'sÂ diseaseÂ (AD) shows less autonomic dysfunction. There was lack ofÂ responseÂ or prolongation of its latency in skinÂ sympatheticÂ response. Vinpocetine is a classic inhibitor of PDE1 activity. Vinpocetine treatment has been shown to enhance performance on cognitive tests in humans. The efficacy of the use of vinpocetine in clinical trials has been controversial. A comparison of multiple studies evaluating vinpocetine use in Alzheimer'sÂ diseaseÂ AD was recently conducted. Objective: Our first aim was to assess dysautonomia inÂ rat with Alzheimer'sÂ diseaseÂ AD electrophysiologically, usingÂ sympatheticÂ skinÂ responseÂ (SSR) test. The second aim in this study, evaluate of the effect of vinpocetine treatment on Alzheimer autonomic dysfunction and attention deficiency.
Method: Rats were dividedÂ intoÂ four groups: Sham group (GroupÂ C, i.p. saline), Alzheimer group (GroupÂ A),Â Vinpocetine group (Group V, 5mg/kg, every other day, i.p.), Alzheimer+ Vinpocetine group (Group AV). Alzheimer'sÂ diseaseÂ was induced in old maleÂ ratsÂ by AlCl3 (40 mg/kg i.p.) and D-Galactose (90 mg/kg) daily for 6 weeks. Then Skin Conductance Level (SCL), which is a sympathetic skin response parameter, was measured as tonic (no-stimuli period, 2 min) and phasic SSR (simultaneouslyÂ with 15 auditory stimuli, 10 min). TonicÂ SSR is useful to investigate general states of arousal and alertness, while phasic SSR is useful to study multifaceted attentional processes (related to novelty, intensity). Results: SCL was difference among groups (tonic: F=21.47, pâ‰¤0.000; phasic: F=9.86, pâ‰¤0.000). Skin conductance level (SCL) was statistically lower in Group A than Group C (pâ‰¤0.005) and Group V (pâ‰¤0.000). SCL of Group V was statistically higher then Group C (pâ‰¤0.04), Group A (pâ‰¤0.000) and Group AV (pâ‰¤0.000). SCL of Group AV was lower than Group C's (pâ‰¤0.01). Conclusion: There were no statistically difference between Group A and Group AV. We concluded that autonomic disturbances accompaniedÂ Alzheimer'sÂ diseaseÂ and vinpocetine treatment couldn't ameliorate this disturbance.
Keywords: Autonomic dysfunction, Dysautonomia, Inhibitor, Skin conductance level, SympatheticÂ skinÂ response Â
Zhang X, Yin W, Shi X, Li Y. Curcumin activates Wnt/Î²-catenin signaling pathway through inhibiting the activity of GSK-3Î² in APPswe transfected SY5Y cells. European Journal of Pharmaceutical Sciences.2011;42(5):540â€“546
PanRui, Qiu Sheng, Lu Da-xiang, Dong Jun. Curcumin improves learning and memory ability and its neuroprotective mechanism in mice. ChinMed J 2008; 121(9): 832-839.
Paradowski B, BiliÅ„ska M, Koszewicz M, Pokryszko A. Evaluation of cardiovascular and sudomotor functions in Alzheimer's disease. Pol MerkurLekarsk. 1999;7(40):180-184.
Zakrzewska-Pniewska B, Gawel M, Szmidt-Salkowska E, Kepczynska K, Nojszewska M. Clinical and functional assessment of dysautonomia and its correlation in Alzheimer's disease.Am J AlzheimersDisOther Demen 2012; 27(8): 592-599.
Dolu N, Keloglan S, Bitiktas S, Cug S. The effects of the enriched environment on sympathetic skin response in pentylenetetrazol-kindled rats.Biomed Environ Sci 2013; 26(5): 394-397.
Edelberg R. Electrical activity of the skin: It smeasurement and uses in psychophysiology. In: Greenfield, N.S.,Sternbach, R.S. (Eds), Handbook of Psychophysiology. New York: Holt, Rinehartand Winston, 1967:367â€“418.
Andor T, Gerlach AL, Rist F. Superior perception of phasicphysiological arousal and the detrimental consequences of the conviction to be aroused on worrying and metacognitions in GAD. J AbnormPsychol 2008;117:193â€“205.
Dawson ME, Schell AM, Filion DL, Berntson GG. The Electrodermal System. Handbook of Psychophysiology. Third edition. New York: Cambridge UniversityPress; 2007. p. 159â€“81.
Naccache L, Dehaene S, Cohen L, Habert MO, GuichartGomez E, Galanaud D. Effortless control: executive attention and conscious feeling of mental effort are dissociable. Neuropsychologia 2005; 43:1318â€“1328.
Bradley MM, Codispoti M, Cuthbert BN, Lang PJ. Emotion and motivation I: defensive and appetitive reactions in picture processing. Emotion 2001;1:276-298.
Strauman TJ. Self-discrepancies in clinical depression and social phobia: cognitive structures that underlie emotional disorders? J AbnormPsychol 1989;98:14â€“22.
Wang SJ1, Liao KK, Fuh JL, Lin KN, Wu ZA, Liu CY, Liu HC. Cardiovascular autonomic functions in Alzheimer's disease. Age Ageing 1994;23(5):400-4.
Filgueiras CC, Krahe TE, Medina AE. Phosphodiesterase type 1 inhibition improves learning in rats exposed to alcohol during the third trimester equivalent of human gestation.NeurosciLett 2010; 473: 202â€“207.
Medina AE, Krahe TE, Ramoa AS. Restoration of neuronalplasticityby a phosphodiesterase type 1 inhibitor in a model of fetal alcohol exposure. J Neurosci 2006; 26(3):1057-1060.
Deshmukh R, Sharma V, Mehan S, Sharma N, Bedi KL. Amelioration of intra cerebroventricular streptozotocin induced cognitive dysfunction and oxidative stress by vinpocetine â€“ a PDE1 inhibitor. Eur J Pharmacol 2009; 620: 49â€“56.
Szatmari SZ, Whitehouse PJ. Vinpocetine for cognitive impairment and dementia. Cochrane Database SystRev 2003; 1: CD003119.
Bereczki D, Fekete I. Vinpocetine for acute ischaemic stroke. Cochrane Database SystRev 2009; 23: CD000480.
Medina AE. The rapeuticutility of phosphodiesterase type I inhibitors in neurological conditions. Frontiers in Neuroscience 2011; 5: 1-5.
GaÃ¡l L, MolnÃ¡r P. Effect of vinpocetine on noradrenergic neurons in rat locus coeruleus. Eur J Pharmacol 1990; 187(3): 537-539.
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