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Öğe 4-(3,4-dihydroxybenzoyloxymethyl)phenyl-O-beta-D-glucopyranoside effect in liver regeneration(F Hernandez, 2019) Fırat, Tülin; Söyler, Gizem; Töre, Fatma; Şit, Mustafa; Kıyan, Aysu; Özgen, Ufuk; Kükner, Aysel; Şit, MustafaFollowing an injury or resection, the mammalian liver has the capacity to regain its former volume and functioning by restoring itself. Studies have demonstrated that antioxidants play a role in hepatic regeneration. This study investigated the effect of 4-(3,4-dihydroxybenzoyloxymethyl)phenyl-O-beta-D-glucopyranoside (PG) obtained from Origanum micranthum on liver regeneration. Sixty Wistar Albino rats were used. In the sham-operated group, a midline abdominal laparotomy was performed without hepatectomy. In the partial hepatectomy (PHx) group, the median and left lateral lobes were removed. Rats in the PHx group received 20 mg/kg/day PG intraperitoneally before being sacrificed at 24, 48, and 72 hrs, and 7 days later. Liver tissues were collected for immunohistochemical analysis and electron microscopic evaluation. We found an increase in mitotic index, and the numbers of Ki-67 stained hepatocytes in all PHx early stage groups (24 hr, 48hr, 72 hr), but not in 7-day groups. The regeneration mediators eNOS, iNOS, TNF-alpha and NF-kappa B were shown to increase in PHx groups. This increase was more prominent dependening on time. In the PHx treatment (PHx+PG) groups, while eNOS was still high, iNOS, TNF-alpha and NF-kappa B had decreased. The apoptotic index was markedly high in the PHx groups; this was prevented by PG treatment. These findings were supported by the ultrastructural results. Our findings indicate that PG supports liver regeneration, hepatocyte proliferation, reduced liver damage, and inflammatory mediators following PHx.Öğe Activation of TRESK channels ameliorates pain and neurogenic inflammation in a nitroglycerin-induced migraine model in rats(Wiley, 2023) Torun, İbrahim Ethem; Kılınç, Yasemin Baranoğlu; Kılınç, Erkan; Töre, FatmaCloxyquin; Mast cell; Migraine; Neurogenic; Inflammation; TRESK Background Potassium ChannelsÖğe Anatomical and functional relationships between sensory nerves and mast cells(Bentham Science Publishers B.V., 2011) Töre, Fatma; Tuncel, NeşeMast cell and sensory nerve relationships fall into three categories: proximity, communication and a shared fate. Mast cells are found in all tissues of the human body, especially located closely to nerves. Mast-nerve membrane to membrane contact is a highly common configuration. This should be by design rather than by accident since such spatial distributions generally indicate a functional relationship. Mast cells associated to sensory nerves contain abundant neu-ropeptides and also a range of neuropeptide receptors enabling nerve to mast cell, mast cell to nerve and reciprocal communications which form the basis of neuroimmune interfacing. Wondering about the possible effects of this intimacy and communication potential on several physiological and pathophysiological events, specifically on diseases with low success rates of therapy and mysterious mechanisms, scientists have uncovered many aspects of mast-nerve interactions. In light of these studies, from a focal point between the nervous and immune systems, mast cells highlight the concept of collaboration as an indispensable building block of the neuroimmune system.Öğe The Comparison of Effects of Applications of Compound 48/80 and Mast Cell Mediator Suspension on Inflammation in Rats: A Methodological Study for Acute Inflammatory Pain(2019) Kılınç, Erkan; Dağıstan, Yaşar; Çetinkaya, Ayhan; Töre, FatmaObjective: Inflammation underlies the pathological basis of most diseases. Substance-P is a key mediator that participates in various inflammatory processes and painful conditions. Mast cells (MCs) have a key role in inflammatory processes via mediators released from their granules. The experimental models for the investigation of pathogenesis and treatment of inflammatory diseases represent merely certain characteristics of inflammatory cases, therefore, more comprehensive models are required. We aimed to compare effects of administrations of the compound-48/80 and mast cell mediator suspension (MCMS) obtained from peritoneal MCs on the inflammation in rats. Methods: Rats were divided into five groups (n=6): Intraperitoneally, Control group received 0.2 ml saline; C-48/80 group received 2 mg/kg compound-48/80; MCMS group received 0.2 ml MCMS; Cr+C-48/80 group received 10 mg/kg cromolyn plus compound-48/80; Cr+MCMS group received cromolyn plus MCMS. Potent inflammatory markers, plasma substance-P levels, and number and degranulation of dural MCs were measured. Data were analyzed using one-way ANOVA followed by Dunnett’s post hoc test. Results: Compound-48/80 increased plasma substance-P levels (p<0.05) and dural MC-degranulation (p<0.001). Likewise, MCMS increased substance-P levels and dural MC-degranulation (p<0.001) as well as number of dural MCs (p<0.01). MC stabilizer cromolyn inhibited increases in the parameters induced by compound-48/80 and MCMS (p<0.01 and p<0.05, respectively). Conclusion: MCMS administration had greater impact to increase the plasma substance-P levels and number and degranulation of dural MCs than that of the compound-48/80 administration. The results demonstrate the potent inflammatory effect of MCMS treatment over the compund-48/80 administration. Administration of MCMS could be a useful tool to study inflammatory conditions.Öğe The comparison of the effects of application of compound 48/80 and autologous mast cell mediator suspension on plasma substance-P levels and dural mast cells in rats: a methodological study for acute Inflammatory Pain(Wiley, 2017) Kılınç, Erkan; Dağıstan, Yaşar; Çetinkaya, Ayhan; Töre, Fatma[No Abstract Available]Öğe Deneysel karaciğer hasarının akciğer dokusuna etkisi ve mast hücrelerinin rolü(Türkiye Klinikleri Tıp Bilimleri Dergisi, 2013) Fırat, Tülin; Ulaş, Nilüfer; Terzi, E. Hakan; Töre, Fatma; Kükner, AyselAmaç: Deneysel karaciğer hasarına bağlı oluşan akciğer dokusu ve mast hücre sayısındaki değişikliklerin ışık mikroskobik olarak incelenmesi. Gereç ve Yöntemler: Bu çalışmada yetişkin Wistar albino ratlar kullanıldı. Ratlar rastgele, her grupta 6 hayvan olmak üzere 3 gruba ayrıldı. Kontrol grubu, CCL4 grubu ve ligasyon grubu. CCL4 grubunda, CCl4 (1 mL/kg vücut ağırlığı, intraperitoneal), haftada 2 kez toplam 8 hafta uygulandı. Ligasyon grubu, ortak safra kanalı bağlanarak 3 hafta bekletildi. Karaciğer ve akciğer dokularından alınan örnekler hematoksilen-eozin ile boyandı. Akciğer kesitleri toluidin mavisi ile boyanarak parankim ve plevral mast hücreleri sayıldı. Bulgular: Kanal ligasyonu ve CCl4 uygulanan grupların akciğer dokularında interalveolar septum kalınlaşması, kapiller konjesyon, ödem, artmış inflamatuar hücreler ve degranüle mast hücresi tespit edildi. Ligasyon grubunda ise akciğer dokularında bu değişiklikler daha belirgindi. Parankimal ve plevral mast hücre sayısı ligasyon ve CCl4 grubunda kontrole göre anlamlı olarak artmıştı. Sonuç: Hepatopulmoner sendrom olarak tanımlanan karaciğer hasarının neden olduğu akciğer hasarına, artmış mast hücrelerinin aracılık edebileceği tespit edilmiştir.Öğe The effect of kisspeptin on spermatogenesis and apoptosis in rats(2017) Aytürk, Nilüfer; Fırat, Tülin; Kükner, Aysel; Özoğul, Candan; Töre, FatmaBackground/aim: To study the effect of kisspeptin, a gonadotropin release stimulator, on the testicular tissue of the rat. Materials and methods: Four groups were formed as follows: control, Kiss-10 50 nmol administration for 1 day, Kiss-10 administration for 13 days, and one last group kept for 7 days following Kiss-10 applied for 13 days. Testicular tissues were stained with hematoxylineosin, periodic acid Schiff, Masson trichrome staining, terminal deoxynucleotidyl transferased UTP nick-end labeling, and Ki-67 immune staining. Serum testosterone levels were determined. Results: Serum testosterone level increased following acute application, while it was reduced by chronic treatment. Spermatogenic cells as stained by Ki-67 and TUNEL increased in the treated groups compared to the controls. Following a 7-day rest after treatment, a decrease in testosterone levels and Ki-67–stained cell numbers and an increase in TUNEL-stained cells were observed. Leydig cells showed increased vacuolization in the Kiss-1 group. Leydig cell vacuolization continued in the Kiss (13) group and was reduced in the Kiss (13 + 7) group. Conclusion: Kiss-10 increased spermatogenic cell proliferation, while testosterone level and proliferation decreased and apoptosis increased during the waiting period.Öğe The effect of thymoquinone on the calcitonin gene-related peptide release and dural mast cell degranulation induced by compound-48/80(Wiley, 2019) Kılınç, Erkan; Töre, Fatma[No Abstract Available]Öğe Effects of probiotic bacteria on central neuronal activation in experimental colitis(AVES, 2022) Şengül, Neriman; Töre, Fatma; Işık, Sevil; Aslım, Belma; Uçar, Gülberk; Fırat, TülinBackground: Brain-gut axis dysregulation is observed in inflammatory bowel disease. However, the effect of altered gut flora on neuro-immunomodulation and its role in the pathogenesis of inflammatory bowel disease are unknown. The aims of this study are to determine (i) whether colitis modifies the expression of c-fos, a marker of general neuronal activation in the brain and (ii) whether this activation could be modulated by probiotic bacteria. Methods: In this study, 28 Sprague-Dawley rats were divided into 4 groups: colitis-probiotic group, non-colitis-fed-control group receiving probiotic Lactobacillus delbrueckii subsp. Bulgaricus B3 strain for 7 days, colitis group, and sham group receiving only sodium chloride. Colitis was induced by intracolonic administration of trinitrobenzene sulfonic acid-ethanol. The expression of c-fos was detected by immunohistochemistry in the brain tissue. Cytokines and inflammatory mediators were analyzed in the plasma. Histological scores and oxidative status were analyzed in the colon samples. Results: The inflammatory response was accompanied by increased levels of cytokines, lipid peroxidation activities, c-fos expression in the medial nucleus of the amygdala, and decreased levels of antioxidant enzymes in the colitis (P < .001). Probiotic treatment reversed those effects. Also, histopathologic scores were significantly lower in the probiotic-treated groups compared to the colitis group (P = .035). In contrast, the expression of c-fos was significantly increased in the paraventricular nucleus of hypothalamus in the probiotic-treated rats (P <.001). Conclusion: Colitis and intestinal inflammation are associated with the activation of neurons in the limbic system creating stress-like effects in the brain. Probiotics diversely modulate limbic response and hypothalamic axis activity in addition to protective effects in inflammation.Öğe The effects of reactive oxygen species and TRPA1 receptors on nociceptive firing and calcitonin gene-related peptide release in rat meninges(Wiley-Blackwell, 2016) Kılınç, Erkan; Töre, Fatma; Giniatullin, Rashid[No Abstract Available]Öğe The effects of vasoactive intestinal peptide on dura mater nitric oxide levels and vessel-contraction responses in sympathectomized rats(Humana Press Inc, 2010) Töre, Fatma; Korkmaz, Orhan Tansel; Doğrukol-Ak, Dilek; Tunçel, NeşeNitric oxide (NO) and neurogenic inflammation in dura mater due to nociceptor activation has been implicated for pathophysiology of primary headache disorders. Development of migraine has also been observed in patients treated with ganglion blockage for sympathetic reflex dystrophy. Vasoactive intestinal peptide (VIP) is an antioxidant, anti-inflammatory, and neuroprotective neuropeptide. This study is intended to investigate the effects of VIP on dura mater NO levels and vessel-contraction responses in sympathectomized rats. In the experiments, 30 male rats in five groups were used. Group 1 sympathectomized: under anesthesia, superior cervical sympathetic ganglion was removed via incision at the center line in the neck area. Group 2 sympathectomized + VIP: postoperative VIP of 25 ng/kg/day (0.2 ml) intraperitoneally administered to the rats exposed to the same operations for 5 days. Group 3 sham: ganglia and nerves were exposed but not dissected. Group 4 control: no treatment was done. Group 5 VIP: only VIP was administered for 5 days. Sympathectomy induced a significant increase in dura mater NO levels and VIP decreased NO to control levels and increased the norepinephrine vessel-contraction responses of sympathectomized rats. VIP is an efficient NO modulator in superior cervical ganglionectomized rats.Öğe The effects of vasoactive intestinal peptide on duramater mast cells and C-FOS activity of trigeminal nucleus at sympathectomized rats(Humana Press Inc, 2012) Töre, Fatma; Kılınç, Erkan; Fırat, Tülin; Kükner, Aysel; Tuncel, NeşeÖğe The effects of vasoactive intestinal peptide on duramater nitric oxide levels and vessel-contraction responses at sympathectomized rats(Churchill Livingstone, 2009) Töre, Fatma; Korkmaz, Orhan Tansel; Doğrukol-Ak, Dilek; Tunçel, NeşeNitric oxide (NO) and neurogenic inflammation in dura mater due to nociceptor activation has been implicated for pathophysiology of primary headache disorders. Development of migraine has also been observed in patients treated with ganglion blockage for sympathetic reflex dystrophy. Vasoactive intestinal peptide (VIP) is an antioxidant, antiinflammatory, and neuroprotective neuropeptide. This study is intended to investigate the effects of VIP on dura mater NO levels and vessel-contraction responses in sympathectomized rats. In the experiments, 30 male rats in five groups were used. Group 1 sympathectomized: under anesthesia, superior cervical sympathetic ganglion was removed via incision at the center line in the neck area. Group 2 sympathectomized+ VIP: postoperative VIP of 25 ng/kg/day (0.2 ml) intraperitoneally administered to the rats exposed to the same operations for 5 days. Group 3 sham: ganglia and nerves were exposed but not dissected. Group 4 control: no treatment was done. Group 5 VIP: only VIP was administered for 5 days. Sympathectomy induced a significant increase in dura mater NO levels and VIP decreased NO to control levels and increased the norepinephrine vesselcontraction responses of sympathectomized rats. VIP is an efficient NO modulator in superior cervical ganglionectomized rats.Öğe From adipose tissue protein secretion to adipopharmacology of disease(2007) Töre, Fatma; Tonchev A.B.; Fiore M.; Tunçel N.; Atanassova P.An extensive research in the last few years has identified about hundred adipose tissue-secreted proteins, named adipokines or adipocytokines. However, our knowledge of the structures and molecules involved in the intracellular secretory pathway (synthesis, translocation, folding, targeting, sorting, storage, and exocytosis) of adipokines is at present limited. Relatively more is known about insulin-responsive trafficking of glucose transporters (GLUTs). Adipokines have multiple biological functions beyond lipid and carbohydrate metabolism, whereas GLUT4 is the major glucose transporter of adipocytes and skeletal muscles. Adipokines play an important role in the pathogenesis of a wide variety of diseases, and dysregulation of GLUT4 transport is implicated in insulin resistance and related disorders. Conceptually, adipobiology of disease has emerged as a novel field of studies in basic and clinical medicine. Here we present a state-of-the-science on some aspects of these studies with a special reference to the intracellular secretory pathway, focusing on adiponectin, GLUT4, and nerve growth factor (NGF), and suggesting that each step of this pathway may be a potential drug target. Given the beneficial effects of adiponectin, NGF and GLUT4 on various metabolic, vascular and inflammatory processes, a hypothesis of metabotrophic factor deficit in the pathogenesis of adipose-linked diseases is discussed. Adipopharmacological evaluation of this hypothesis may provide novel targets for drug development. © 2007 Bentham Science Publishers Ltd.Öğe Mast cell activation alleviates pentylenetetrazole-induced epileptic seizures via serotonin in rats(KARGER, 2021) Kılınç, Erkan; Torun, İbrahim Ethem; Çetinkaya, Ayhan; Töre, FatmaMast cell activation alleviates pentylenetetrazole-induced epileptic seizures via serotonin in ratsÖğe Mast cell activation ameliorates pentylenetetrazole-induced seizures in rats: the potential role for serotonin(Blackwell Publishing Ltd, 2021) Kılınç, Erkan; Torun, İbrahim Ethem; Çetinkaya, Ayhan; Töre, FatmaNeuroinflammation plays a key role in the pathogenesis of epilepsy, but the underlying mechanisms are not well understood. Mast cells are multifunctional immune cells that are also activated by stress. The effects of activated mast cells on epileptogenesis are not yet known. This study investigated the effects and mechanisms of compound 48/80-stimulated mast cell activation on pentylenetetrazole-induced epileptic seizures in rats. Male Wistar rats were separated into seven groups (n = 12). Group-1(NS+PTZ) received intraperitoneal saline solution, while groups 2(C-48/80+PTZ-1), 3(C-48/80+PTZ-2), and 4(C-48/80+PTZ-3) received compound-48/80 at doses of 0.5, 1, and 2 mg/kg, respectively, 30 min before 45 mg/kg pentylenetetrazole administration. Similarly, Group-5(Cr+C-48/80+PTZ) received 10 mg/kg cromolyn plus 2 mg/kg compound-48/80 before pentylenetetrazole, and Group-6(MC Dep+C-48/80+PTZ) was exposed to a mast cell-depletion process, and then received 2 mg/kg compound-48/80. Group-7(5-HT+PTZ) received 10 mg/kg serotonin. Seizure stages were evaluated using Racine's scale. Compound-48/80 at 2 mg/kg induced anticonvulsive effects against pentylenetetrazole-induced seizures by extending onset-times of both myoclonic-jerk and generalized tonic–clonic seizures (p = 0.0001), and by shortening the duration of generalized tonic–clonic seizure (p = 0.008). These effects were reversed by cromolyn (p = 0.0001). These effects were not observed in mast cell-depleted rats. Similarly to compound 48/80, serotonin also exhibited anticonvulsive effects against seizures (p < 0.05). Compound 48/80 acts as an anticonvulsant by activating mast cells in a dose-dependent manner. The anticonvulsive effects of mast cell activation may be mediated by serotonin. Mast cell activation may therefore provide protective activity against seizures under appropriate circumstances.Öğe Mast cell degranulation mediates compound 48/80-induced meningeal vasodilatation underlying migraine pain(Marmara Univ, Inst Health Sciences, 2018) Kılınç, Erkan; Dağıstan, Yaşar; Töre, FatmaObjective: The cranial dura mater contains plenty of mast cells and is principally supplied by the middle meningeal artery which has a key role in the generation of headaches. Neurogenic inflammation caused by perivascular nerve activation and dural vasodilation is held responsible for migraine pain. Dural mast cells contribute neurogenic inflammation and migraine via vasoactive and proinflammatory mediators in their secretory granules. In the present study, it was aimed to investigate vasoactive effect of mast cell degranulating agent compound 48/80 induced dural mast cell degranulation on the middle meningeal artery and its anterior and posterior branches. Methods: Isolated skulls obtained from male Wistar rats were divided into 2 halves. The skull cavities with intact the dura mater were applied synthetic interstitial fluid for control group or mast cell degranulating agent compound 48/80 (10 mu g/ml) in synthetic interstitial fluid for treated group at 37 degrees C for 15 min. Diameters of middle meningeal artery and its anterior and posterior branches were measured and mast cells were counted from whole-mount preparations of meningeal dura mater. Results: While compound 48/80 induced massive degranulation of dural mast cells (P<0.01), it did not change the number of mast cells in the dura mater. Moreover, compound 48/80 increased diameter of middle meningeal artery (P<0.01) and its anterior (P<0.05) and posterior (P<0.01) branches, respectively compared to synthetic interstitial fluid treatment. Conclusion: Dural mast cell degranulation causes dilatation of middle meningeal artery which is involved in the pathophysiology of migraine, therefore testing of mast cell stabilizing agents in vivo models of migraine pain may promise hope for the next big things in the treatment of migraine headaches.Öğe Mast Cell Degranulation Mediates Compound 48/80-Induced Meningeal Vasodilatation Underlying Migraine Pain(2018) Kılınç, Erkan; Dagistan, Yaşar; Töre, FatmaObjective: The cranial dura mater contains plenty of mast cells and is principallysupplied by the middle meningeal artery which has a key role in the generation ofheadaches. Neurogenic inflammation caused by perivascular nerve activation anddural vasodilation is held responsible for migraine pain. Dural mast cells contributeneurogenic inflammation and migraine via vasoactive and proinflammatory mediatorsin their secretory granules. In the present study, it was aimed to investigate vasoactiveeffect of mast cell degranulating agent compound 48/80 induced dural mast celldegranulation on the middle meningeal artery and its anterior and posterior branches.Methods: Isolated skulls obtained from male Wistar rats were divided into 2 halves.The skull cavities with intact the dura mater were applied synthetic interstitial fluidfor control group or mast cell degranulating agent compound 48/80 (10 µg/ml) insynthetic interstitial fluid for treated group at 37 oC for 15 min. Diameters of middlemeningeal artery and its anterior and posterior branches were measured and mastcells were counted from whole-mount preparations of meningeal dura mater.Results: While compound 48/80 induced massive degranulation of dural mast cells(P<0.01), it did not change the number of mast cells in the dura mater. Moreover,compound 48/80 increased diameter of middle meningeal artery (P<0.01) andits anterior (P<0.05) and posterior (P<0.01) branches, respectively compared tosynthetic interstitial fluid treatment.Conclusion: Dural mast cell degranulation causes dilatation of middle meningealartery which is involved in the pathophysiology of migraine, therefore testing of mastcell stabilizing agents in vivo models of migraine pain may promise hope for the nextbig things in the treatment of migraine headaches.Öğe Mast cells: Target and source of neuropeptides(Bentham Science Publ Ltd, 2009) Töre, Fatma; Tuncel, NeşeMast cells, originating from bone marrow pluripotential cells are generally populated near to strategic locations of mammalian body. They store a wide variety of biologically active molecules in their granules and also can de novo synthesize an additional spectrum of mediators, depending on their microenvironment, phenotype and status. Mast cells have numerous receptors that can trigger a wide spectrum of cellular responses, some of them which can be preprogrammed against specific pathogens. Mast cells secrete mediators, go under total degranulation, or degranulate only some of the specific granules with required content according to the environmental conditions, pathogens or signaling molecules binding to their receptors. Mast cells are functionally multi faceted cells. A single cell can behave such as an immune cell, an endocrine cell and even as a sensorial neuron. In this context, mast cells can significantly influence inflammation, tissue remodeling, host defense and homeostasis. Specifically the mast cells proximal to nerve fibers, contain, secrete and respond to, several neuropeptides, suggesting many potential functions for mast cells in health and disease. Mast cells are target cells for neuropeptides and, they have distinct profiles of responsiveness to these molecules. This extends the flexibility of neurogenic signaling pathways via reciprocity. Those neuropeptides have direct and indirect effects on mast cells such as inducing or suppression of degranulation, triggering, modulation or amplification of mediator content and release. The exploration of interactions of mast cells and neurons is a promising field of study which may bring treatments to several diseases. Since mast cells seem to form the major link between neurons and inflammation via neuropeptides, mast cell and mast cell mediator connection may lead to a better understanding of the autocrine, paracrine, and neuro-immune-endocrine systems in physiology and physiopathology. Therefore, mast cell manipulator drug designs, capable of granular content modulation, with effects on, selective mediator release, activity and, ablation of mast cells, would be very beneficial for the treatment of various diseases that mast cells may be involved in.Öğe Passage of VIP/PACAP/secretin family across the blood-brain barrier: therapeutic effects(Bentham Science Publ Ltd, 2004) Doğrukol-Ak, Dilek; Töre, Fatma; Tuncel, NeşeIn recent years, VIP/PACAP/secretin family has special interest. Family members are vasoactive intestinal peptide (VIP), pituitary adenylate cyclase-activating polypeptide (PACAP), secretin, glucagon, glucagon like peptide-1 (GLP(1)), GLP(2), gastric inhibitory peptide (GIP), growth hormone releasing hormone (GHRH or GRF), and peptide histidine methionine (PHM). Most of the family members present both in central nervous system (CNS) and ill various peripheral tissues. The family members that are released into blood from periphery, especially gut, circulate the brain and they can cross the blood brain barrier. Oil the other hand, some of the members of this family that present in the brain, call cross from brain to blood and reach the peripheral tat-gets. VIP, secretin, GLP(1), and PACAP 27 are transported into the brain by transmembrane diffusion, a non-saturable mechanism. However, uptake of PACAP 38 into the brain is saturable mechanism. While there is no report for the passage of GIP, GLP(2) and PHM, there is only one report that shows, glucagon and GHRH can cross the BBB. The passage of VIP/PACAP/secretin family members opens up new horizon for understanding of CNS effects of peripherally administrated peptides. There is much hope that those peptides may prove to be useful in the treatment of serious neurological diseases such as Alzheimer's disease, amyotropic lateral sclerosis, Parkinson's disease, AIDS related neuropathy, diabetic neuropathy, autism, stroke and nerve injury. Their benefits ill various pathophysiologic conditions undoubtly motivate the development of a novel drug design for future therapeutics.
