Cholecystokinin (CCK), a peptide hormone found in the gut, is the most abundant peptide neurotransmitters in the brain, and its acute effects on the brain activity have been shown. In this study we aimed to evaluate the acute effects of CCK on short-term synaptic plasticity in the dentate gyrus (DG) of the rat hippocampus. Via stereotaxic surgery, the stimulating and the recording electrodes were placed in the perforant pathway and dentate gyrus, respectively and 30 min after intraperitoneal (i.p.) injection of CCK octapeptide sulfated (CCK-8S, 1.6 mg/kg), evoked responses were recorded after delivering of paired-pulse stimulations at 10 to 500 ms inter-stimulus intervals. With respect to the control group that received saline instead of CCK, in baseline responses, slope of field excitatory postsynaptic potential (fEPSP) 5 min and 10 min after injection of CCK-8S (p<0.05) and population spikes (PS)-amplitudes 5 min after injection of CCK-8S (p <0.05) were significantly increased. In paired pulse responses, PS amplitudes were increased in the CCK group, but these enhancements only were significant at inter-stimulus interval 40 ms (p<0.05). However fEPSP slopes were decreased at inter-stimulus intervals 70 ms (p <0.05), 120 ms (p <0.01), 150 ms (p <0.001) and 300 ms (p <0.001). The results showed that CCK-8S has a transient excitatory effects on baseline responses, but it inhibits paired pulse indices in acute. Therefore, in a short period of time, effect of CCK on the function of synapses is time dependent, and it has stimulatory or inhibitory effects at different time periods.

Background and purpose: Glial cells seem to play role in synaptic plasticity because they have the ability to release trophic factors and gliotransmitters and respond to neurotransmitters. They also play important role in synaptic space homeostasis. In this study, the role of hippocampal glial cells in baseline synaptic response and short term synaptic plasticity were investigated.Materials and methods: In this experimental study, flourocitrate, glia inhibitor (1nmol/0.5μl), was microinjected intrahippcampally for inhibition of hippocampal glial cells. Baseline synaptic response and short term synaptic plasticity were evaluated by field potential recording. fEPSP was recorded from CA1 following Schaffer collaterals stimulation. After Input/Output curve construction, short term synaptic plasticity was induced by paired pulse stimulations.Results: Inhibition of glial cells by flourocitrate microinjection in CA1 did not have any effect on baseline synaptic response (P>0.05). Flourocitrate increased paired pulse index (PPI, control: 62.80%±5.48; flourocitrate treated: 87.19%±12.11) at 20 ms inter pulse interval (P<0.05). But it did not affect PPI at 80 and 200 ms IPI (P>0.05).Conclusion: The results suggest that hippocampal glial cells functions did not influence the baseline synaptic response but affected short term synaptic plasticity in CA1 area of the hippocampus.

Background and purpose: Astrocytic connexins (Cxs) play roles in ion diffusion to the extracellular milieu and in release of ATP and gliotransmitters including glutamate. Connexin 43 (Cx43) is one of the most abundant Cxs in brain tissue, especially in the hippocampus, so, we investigated its role on CA1 baseline synaptic response and short term synaptic plasticity. Materials and methods: In this experimental study, bilateral intrahippocampal microinjection of TAT-Gap19, Cx43 blocker (1nmol/1μ l) was performed for inhibition of hippocampal astrocytic connexin 43. Baseline synaptic response and short term synaptic plasticity were evaluated by field potential recording. Results: According to two-way ANOVA, inhibition of hippocampal Cx43 did not have any effect on baseline synaptic response (P>0. 05). TAT-Gap19 decreased paired pulse index (PPI) at 20 and 80 ms inter pulse intervals (IPI, Unpaired t-test, P<0. 05), but it did not affect PPI at 200 ms IPI (P>0. 05). Conclusion: The results suggest that the function of hippocampal astrocytic Cx43 does not affect baseline synaptic response but affects short term synaptic plasticity in CA1 area of the hippocampus.

Background: Considering the increased activity of hypothalamic orexinergic neurons due to morphine administration, and its extensive projections to the hippocampus, it is probable that morphine effect on CA1 neuronal function is mediated by orexinergic system. So the effect of hippocampal orexin-1 receptors (OX1R) blockade on CA1 baseline synaptic response and short term synaptic plasticity was investigated.Materials and Methods: In this experimental study, animals received morphine 10 mg/kg/12h/ (SC) for 10 days. SB-334867-A, OX1R antagonist (0.5μg/0.5 ml), was microinjected intrahippcampally for OX1R inhibition before each morphine injection. Baseline synaptic response and short term synaptic plasticity were evaluated by field potential recording. fEPSP was recorded from CA1 following Schaffer collaterals stimulation. After Input/Output construction, short term synaptic plasticity was induced by paired pulse stimulations.Results: Chronic use of morphine did not affect the baseline synaptic response (p>0.05). SB- 334867-A microinjection in CA1 did not have any effect on baseline synaptic response in morphine dependent rats. Morphine increased paired pulse index (PPI) at 80 ms inter pulse interval (IPI, p<0.05). SB-334867-A pretreatment did not affect this morphine induced PPI change.Conclusion: The results suggest that orexin-1 receptors (OX1R) do not mediate the effect of morphine on baseline synaptic response and short term synaptic plasticity in CA1 area of the hippocampus.

Background. Glial cells release different gliotransmitters and response to neurotransmitters released from neurons. These cells especially astrocytes, having different transporters, play an important role in synaptic space homeostasis and synaptic plasticity. In this study, the role of hippocampal glial glutamate transporter (EAAT2) in baseline synaptic response and short term synaptic plasticity were investigated. Methods. In this experimental study, ceftriaxone, EAAT2 activator (0. 5mmol/0. 5μ, l), was microinjected intrahippcampally for activation of hippocampal glial glutamate transporter in male wistar rats. Baseline synaptic response and short term synaptic plasticity were evaluated by field potential recording. fEPSP was recorded from CA1 following Schaffer collaterals stimulation. After Input/Output curve construction, short term synaptic plasticity was induced by paired pulse stimulations. Results. Activation of EAAT2 by ceftriaxone microinjection in CA1 did not have any effect on baseline synaptic response (P> 0. 05, Two Way ANOVA). There was no significant difference in Paired Pulse Index at 20, 80, and 200 ms inter-pulse interval between ceftriaxone treated and control group (P> 0. 05, Two Way ANOVA). Conclusion. The results suggest that hippocampal glial glutamate transporter activation does not have effect on baseline synaptic response and short term synaptic plasticity in CA1 area of the hippocampus. Practical implications. Considering the role of glial cells in regulating the excitability of the nervous system as well as synaptic plasticity, correcting these features of the nervous system by manipulating glial cells can help the treatment or prevention of neurological diseases. In this study, the role of glial cells in the homeostasis of the glutamate in the synaptic space of the hippocampus was evaluated, through the stimulation of its uptake, on the basic synaptic activity and short-term synaptic plasticity.