Introduction: Chronic morphine exposure can cause addiction and affect synaptic plasticity, but the underlying neural mechanisms of this phenomenon remain unknown. Herein we used electrophysiologic approaches in hippocampal CA1 area to examine the effect of chronic morphine administration on short-term plasticity. Methods: Experiments were carried out on hippocampal slices taken from either control animals or animals made dependent via oral chronic morphine administration. Population spikes (PSs) were recorded from stratum pyramidale of CA1 following stimulation the Schaffer collateral afferents. For examining the short-term synaptic plasticity, paired pulse stimulations with inter pulse interval (IPI) of 10, 20, 80, and 200 ms were applied and paired pulse index (PPI) was calculated.Results: Chronic morphine exposure had no effect on the baseline response. A significant increase in PPI was observed in dependent slices at 80 ms IPI as compared to the control ones. There was no significant difference in baseline response between control and dependent slices when we used long term morphine, naloxone, and both. However, long term morphine administration caused significant difference in PPI at IPI of 20 ms. This effect was eliminated in the presence of naloxone.Conclusion: These findings suggest that morphine dependence could affect short-term plasticity in hippocampal CA1 area and increase the hippocampus network excitability.

Kindling epileptigenesis was induced by repeated administrations of the chemical convulsant pentylenetetrazol (PTZ).The progressive nature of the chemical kindling was demonstrated by a detailed description of the behavioral sings in the course of the kindling acquistion. The Changes of Paired-Pulse Index (PPI) were primariliy investigated with extracellular recording in stratum pyramidale following stimulation of Schaffer collaterals in the CA1 region of hippocampus of the PTZ-Kindled and the control rats. The results were as follow:(1) in most of the kindled rats the first stimulus evoked a double population spike at moderate and high stimulus .intensities:(2) 40-100 hours after the kindling no significant difference was observed between the control and the kindled rats, and (3) 30-33 days after the kindling PPI was increased in the kindled rats at IPI of 10 and 20 ms with low and moderate stimulus intensities as compared with the control ones. It seems that an increase in PPI may be resulted from an enhancement of excitatory synaptic transmission and/or an increase in intrinsic excitability of pyramidal neurons of hippocampal CAI.

Introduction: The Basolateral Amygdala (BLA) substantially affects neuronal transmission and synaptic plasticity processes through the dentate gyrus. Orexin neuropeptides play different roles in the sleep/wakefulness cycle, feeding, learning, and memory. The present study aimed to investigate the function of the orexin receptors of the BLA in the hippocampal local interneuron circuits. Methods: For this, the region’, s paired-pulse responses from the Dentate Gyrus (DG) were recorded. Within the procedure, SB-334867-A (12μ, g/0. 5μ, L) and TCS-OX2-29 (10μ, g/0. 5μ, L (orexin 1 & 2 receptors antagonists, respectively), were administered into both sides of the BLA areas of the rat brain. Dimethyl Sulfoxide (DMSO) was used as the solvent in the control animals with a volume of 0. 5μ, L. Results: Our data indicated that the Paired-pulse (PP) responses were not affected by the inactivation of the orexin receptors of the BLA. Conclusion: Due to not observing any significant changes in the short form of synaptic plasticity, after inactivation of the orexin system of the BLA, we hypothesize that the orexinergic fibers to the basolateral part of the amygdala influence the long-term synaptic efficacy,however, the primary processing of information in short-term plasticity model is not affected by the same system. The elementary processing of the data by the amygdala might happen through the action of other neurotransmitter systems.

Introduction: The differences among dorsal and ventral hippocampal neural circuits affect synaptic plasticity. In this study, we aim to compare the occurrence of short-term plasticity in the field excitatory postsynaptic potential (fEPSP) in dorsal and ventral hippocampal CA1 areas following kindled seizures. Methods: Animals (male C57 B6/J mice, 12 weeks of age) were kindled by intraperitoneal injections of pentylenetetrazole (PTZ), and fEPSPs were recorded from dorsal and ventral hippocampal slices. Short-term plasticity was evaluated by measuring fEPSP-slope and fEPSP-area following paired-pulse stimulation delivered at three inter-pulse intervals (20, 80, and 160 ms). Results: In control slices, the fEPSP-slope was greater in the ventral hippocampus compared to the dorsal hippocampus, but there was no difference in the fEPSP-area between the two regions. In hippocampal slices, the fEPSP-slope was similar in the dorsal and ventral regions, but the fEPSP-area was greater in the ventral region compared to the dorsal region. In addition, the fEPSP-area was greater in the kindled group than in the control group only in the ventral hippocampus. PTZ-induced kindled slices showed impaired short-term facilitation, and the paired-pulse index decreased only in the dorsal hippocampus. Kindling had no significant effect on the paired-pulse ratio in the ventral hippocampus. Conclusion: The seizure occurrence affects the neural activity of the hippocampus in a region-dependent manner. Although kindling increases the fEPSP area in the ventral hippocampus of mice, kindling-induced changes in short-term synaptic plasticity are significant only in the dorsal hippocampus. The difference in the responses of dorsal and ventral poles should be considered in future studies.

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.

Introduction: The primary somatosensory cortex has an important role in nociceptive sensory-discriminative processing. Altered peripheral inputs produced by deafferentation or by long-term changes in levels of afferent stimulation can result in plasticity of cortex. Capsaicin-induced depletion of C-fiber afferents results in plasticity of the somatosensory system. Plasticity includes short-term and long-term changes in synaptic strength. We studied the interaction between paired-pulse facilitation, as one form of short-term plasticity, with long-term potentiation (LTP) in the neocortex of normal and C-fiber depleted freely moving rat.Methods: Neonatally capsaicin-treated rats and their controls were allowed to mature until they reached a weight between 250 and 300g. Then animals were anesthetized with ketamine and xylazine. For recording and stimulation, twisted teflon-coated stainless steel wires were implanted into somatosensory cortex or corpus callusom. In experiments for LTP induction, after two weeks of recovery period, 30 high frequency pulse trains were delivered once per day for 12 days. Paired-pulse ratio (PPR) was monitored before and after the induction of LTP in capsaicin-treated and control rats.Results: Paired-pulse stimulation affected all field potential components at intervals<200 ms. The largest changes occurred at intervals between 20- 30 ms. C-fiber depletion postponed the development of LTP, whereas it had no effect on PPR.Discussion: This finding provides further evidence that the expression of this form of LTP is postsynaptic. Furthermore, these results suggest that the effect of C-fiber depletion on cortical LTP is also postsynaptic and, therefore, is not caused by a decrease in neurotransmitter release.

The effect of cysteamine, a somatostatin depletor, on synaptic plasticity induced by tetanic and paired-pulse stimulation was investigated in rat hippocampal CA1. For this purpose, hippocampal slices from saline (1ml/Kg, s.c.) and cysteamine (200 mg/Kg, s.c.)-treated and intact rats were used. Population spikes were recorded following Schaffer collateral stimulation: To induce LTP, primed burst titanic stimulation was used. Paired-pulse stimulation at IPIs of 10, 20, 60, 120, 240, 360, and 480 ms were used and then EPI and PPI of CA1 were calculated. The results showed that the amplitude of population spike (PSA) increased 5, 15, 30, and 60 min after tetanic stimulation and 60 min after primed bursts, PSA increased at all stimulus intensities for all groups. In cysteamine-treated group, the magnitude of LTP was decreased as compared to intact and saline-treated groups. In the latter group, the magnitude of LTP increased as compared to intact and cysteaminetreated group. At IPI of 10ms, mean value of EPI was greater than 1 for intact group and less than 1 for saline- and cysteamine-treated groups. In cysteamine-treated group, the mean value of EPI was significantly less than intact group. At IPIs from 20 to 480 ms, mean value of EPI was greater than or equal to 1 for all of the groups and no s'ign ificant difference was observed among them. At IPI of 10 ms, mean value of PPI was greater than 1 in intact group and less than 1 in saline- and cysteamine-treated groups. In these groups,mean value of PPI was significantly less than intact group. At IPI of 20 ms, mean value of PPI was greater than 1 in intact and saline-treated group and less than 1 in cysteamine-treated group. In the latter group, the mean value of PPI was significantly less than saline-treated and intact groups. At IPIs of 60-680 ms, mean value of PPI was greater than 1 in all of the groups with no significant difference among them.It is concluded that cysteamine can alter susceptibility of hippocampal CA1 for synaptic plasticity induced by tetanic and paired-pulse paradigms.