Physiology and Pharmacology
Year:2006 | Volume:10 | Issue:3|Papers Count:13

Introduction: The protective and antisecretory effects of dopamine agonists on the stomach have been already reported, but the effect of bromocriptine (D2 dopamine agonist) on histamine stimulated gastric acid secretion (GAS) needs to be investigated.Methods: For gastric sampling, animals were anesthetized and a polyethylene tube was introduced into the stomach through esophagus. A cannula was also inserted into the pyloroduodenal junction and passed up into the stomach.Results: Our data showed that administration of bromocriptine (2 mg/kg), 60 minutes before histamine infusion, did not affect basal acid secretion but significantly reduced histamine-induced GAS (P<0.01). Also, simultaneous application of bromocriptine and histamine-infusion (0.8 mg/100g/h) had no effect on histamine-stimulated gastric acid secretion. The inhibitory effect of bromocriptine on GAS did not change by sulpiride, a D2 dopamine antagonist. Plasma glucose level was constant in our experimental conditions.Conclusion: Based on our data, we concluded that inhibitory effect of bromocriptine (2 mg/kg) on histamine stimulated acid output was probably mediated by non dopaminergic receptors or unknown subtypes of D2 receptors which are not sensitive to sulpiride.

Introduction: In this study the effect of Matricaria recutita extract on acute pain in the presence and absence of flumazenil (antagonist of benzodiazepine) and lesioned paragigantocellularis (PGi) nucleus was investigated.Method: Wistar male rats (250±20 g) were used. Animals were grouped randomly into intact, sham and bilateral lesion of PGi nucleus. Intact and lesioned animals, each divided into 4 subgroups which received saline, M. recutita hydro-alcoholic extract (25 mg/kg), flumazenil (1 mg/kg) and flumazenil + M. recutita. Hot plate test were used for pain thereshold evaluation.Results: Results showed that: In intact animals M. recutita induced analgesic effect but flumazenil had significant hyperalgesic effect. In these animals flumazenil prevented the analgesic effects of M. recutita. Lesion of PGi induced significant hyperalgesia. M. recutita in absence of PGi nucleus showed significant analgesic effect and flumazenil increased pain sensation and caused significant hyperalgesia. The analgesic effect of M. recutita attenuated by flumazenil in absence of PGi nucleus.Conclusion: It seems that PGi nucleus involves in pain modulation but analgesic effect of M. recutita that may be via the benzodiazepine-like activity of some its components does not interact with PGi nucleus.

Introduction: The functional effects of orexin-B on the calcium spikes and excitability of the neuronal soma membrane of garden snail, Helix aspersa were studied.Methods: Conventional intracellular recording, under the current clamp conditions was performed to examine the effects of orexin-B on the configuration and electrophysiological properties of calcium spikes.Results: Application of orexin-B (300 nM) led to a membrane depolarization and thereby the increase in excitability of neurons. It also decreased the duration and the amplitude of calcium spikes. On the other hand, orexin-B had a dual effect on the amplitude of afterhyper polarization (AHP) in a time dependent manner. The maximum reduction of the amplitude of AHP was recorded within 10 min of orexin-B exposure. However a maximum increase in AHP amplitude was observed later (15 min after exposure to orexin-B). Inactivation of G-proteins by pertussis toxin (100 nM) was used to test the involvement of Gi/Go in the orexin-B induced modulation of calcium channels. Pre-incubation of ganglia for 3-6 h with PTX blocked the depolarization effect of orexin-B on the resting membrane potential. Orexin-B on pretreated neuronal cells with PTX did not statistically change the calcium spike parameters, unless the peak amplitude of AHP increased remarkably.Conclusion: In conclusion, these data suggest that orexin-B (300 nM) may affect the membrane excitability and modulates the activity of calcium and calcium activated potassium channels in snail neurons.

Introduction: Electrical low-frequency stimulation (LFS) has antiepileptic effect, but the role of different stimulation parameters on this effect has not been determined. In this study the effect of different LFS parameters (intensity, pulse duration and train duration) on piriform-cortex kindled seizures was investigated.Methods: Seizure was produced in animals using kindling model of epilepsy. Then, the effect of LFS on seizure severity was investigated.Results: Different patterns of LFS (1 Hz) applied immediately before kindling stimulation in fully kindled animals, had no significant effect on seizure parameters. In the second experiment, effect of LFS (1 Hz) on inter-seizure interval was investigated. Data showed that daily stimulation of animals for 15 min with LFS for one week after the last kindling stimulation reduced significantly stage 5 seizure duration. Application of the same LFS protocols for three days and two weeks had no significant effect on seizure parameters. In the third experiment, effect of LFS (1 Hz) on kindling rate was investigated.Results: showed that when LFS was delivered daily after each kindling stimulation it could decrease after discharge duration in various days during kindling and delayed the appearance of seizure stages 1 and 2 significantly.Conclusion: It may be concluded that LFS has antiepileptic effects on kindling acquisition and inter-seizure interval in kindled animals and that the characteristics of LFS protocol (intensity, pulse duration and train duration) have an essential role on these effects.

Introduction: Effective perception of fear signals is crucial for organism survival. When threated, the organism indicates defensive behaviors. Methods: Elevated plus-maze has high efficiency for measurement of fear behavior and is widly used for fear behavior determination. Increase in two parameters; percent of openarm entries (%OAE) and percent of time spent in the open-arm (%OAT) in the elevated plus- maze were considered as the indexes of fear reduction effect. In this study, the effect of testosterone and naloxone on fear behavior of gonadectomized rats (GDX) was investigated. Also, the interaction of testosterone with naloxone was investigated. Results: Subcutaneous (SC) injections of different doses of testosterone (100,200, 300, 450 mg/rat) increased the %OAE and %OAT in a dose dependent manner. Maximum response was obtained by 450  mg/rat dose of testosterone (P<0.001).SC injections of opioid receptors antagonist, naloxone 1,2.5,5, 7.5 mg / kg reduced %OAE and %OAT (P<0.01).Conclusion: It may be concluded that testosterone decreases fear behavior and naloxone increased fear behavior. Also the results indicate that there is an interaction between testosteone and naloxone (P<0.001).

Introduction: Neuropeptide Y (NPY) is the most abundant peptide present in mammals' brains. The majority of NPY-producing neurons are in acute and Para ventricular nuclei of hypothalamus which affect hypophysiotrapic factors secretion. In this study we investigated the effect of intravenous injections of various doses of NPY on thyroxin (T4) and triiodothyronine (T3) serum concentrations.Methods: Sixteen adult male sannan goats were assigned to four treatment groups. Treatments were included daily injections of 0, 10, 20 and 40  mg NPY per kg body weight named C, L, M and H, respectively. The duration of experiments was 13 consecutive days divided into three intervals; pre-treatment (days 1-3), treatment (days 4-10) and posttreatment (days 11-14). Blood collections were being done throughout the experiment at 09:00 via jugular vein and injections were in treatment interval via carotid artery at 08:00. Blood samples were centrifuged and the sera were harvested and used for hormone assay via radioimmunoassay.Results: Results showed that treatment H caused 11-fold increase in T4 concentrations and 4-fold increase in T3 concentrations ones versus treatment C (P<0.001). Treatment M also increased T4 and T3 significantly (P<0.001). The effect of treatment L on T4 concentrations was significantly incremental (P<0.001) but it has no effect on T3 concentrations (P=0.877). The stimulatory effect of NPY on thyroid hormones was transient because in post-treatment interval, T4 and T3 concentrations in treatments L, M and H tended to decline but were yet significantly higher versus treatment C.Conclusion: Previous studies in rodents demonstrated inhibitory effect of NPY on thyroid hormones but in present study completely stimulatory and dose-dependent effects of NPY on these hormones secretion in goat were observed. Thus, we suggest the stimulatory effect of NPY on thyrotrophic axis in ruminants. This discrepancy can be due to different methodology and difference in neuroendocrine framework controlling thyrotrop axis of ruminants with rodents.

Introduction: Compounds which are used to treat organophosphate (OP) poisoning are not able to fully alleviate long lasting effects. They are mainly used to antagonize cholinergic effects of Ops. However, non-cholinergic effects, such as interference with different neurotransmitter systems, especially GABA release and uptake, are recently attracting more attentions. We have tried to investigate any potential interaction between paraoxon and GABA uptake.Methods: We used cerebellar synaptosomes. Cerebellum of 250-280 g Wistar rats were rapidly dissected out, homogenized, centrifuged, and incubated with 0.01 m M [3H] GABA in the presence of different doses of paraoxon for 10 minutes at 37 oC. At the end of the incubation period, synaptosomes were layered in chambers of superfusion system. In order to assay the amounts of [3H] GABA taken up, radioactivity was measured using a b-counter.Results: Our findings reveal that mean GABA uptake was 111.42, 95.37, 71.6, 73.53 and 75 percent of the control values in the presence of different concentrations of paraoxon (0.01, 0.1, 1, 10 and 100m M) respectively. GABA uptake was significantly reduced at doses 1, 10 and 100m M (p<0.05).Conclusion: It seems that paraoxon at higher doses may interfere with GABA uptake by cerebellar synaptosomes.

Introduction: We previously shown that microinjection of glutamate into the hDB of rat elicited cardiovascular depressive responses. Microinjection of AP5 (an NMDA receptor antagonist, 2.5 mM, 50 nl) and CNQX (an AMPA receptor antagonist, 1 mM, 50 nl) caused no significant changes in the blood pressure and heart rate. Microinjection of bicuculline (BMI: a GABAA receptor antagonist, 1 mM, 50 nl) resulted in the increased blood pressure and heart rate. In this study we investigated the possible interaction of GAB Aergic and glutaminergic systems by coinjection of the antagonists of both systems.Methods: Experiments were performed on 27 urethane anesthetized rats. Drugs were microinjected into the hDB using micropipettes. The arterial pressure and heart rate were continuously recorded and repeated measures ANOVA was used for data analysis.Results: Our results showed that co injection of 50 nl of BMI (1mM) and AP5 (2.5 mM) significantly (P < 0. 01) decreased the presser effects of BMI. Also, coinjection of 50 nl of BMI (1 mM) and CNQX (1 mM) significantly (P < 0.01) decreased the presser effects of BMI. Microinjection of the doses of BMI and two glutamate receptor antagonists produced the same results.Conclusion: These findings suggest that the cardiovascular effects of the blockade of GABAergic system depend on the activation of local NMDA and AMPA receptors. A possible explanation for the results is that, GABAergic system tonically inhibits the glutaminergic neurons.

Introduction: Phonophoresis is the use of ultrasound to enhancing cellular drug delivery through the skin. In this study the effect of clobethasole and hydrocortisone ointments phonophoresis on pain, knee osteoarthritis and some other symptoms was studied.Methods: An experimental single blind randomized clinical trial (RCT) was used. An available sampling technique was used for selection of patients. Sixty subjects with osteoarthritis knee (tibiofemoral) joints were randomly assigned to six groups: 1-Ultrasound with acoustic gel. 2- Placebo ultrasound with hydrocortisone. 3- Placebo ultrasound with clobetasole. 4- Hydrocortisone phonophoresis. 5- Clobetasole phonophoresis. 6- Placebo ultrasound with acoustic gel. All of the patients received treatments for ten sessions. Pain level was determined by visual analog scale (VAS) at the beginning, day 6 and follow up day (11th session). Edema and knee range of motion (ROM) were measured at the beginning, day 4, day 7 and follow up day. 20 meters walking test time was measured at the beginning and follow up day. Wilcoxon and Friedman statistical tests were used to analyze data.Results: At the end of treatment sessions; groups 1, 4, 5 showed a significant decrease in pain and edema and an increase in knee ROM and 20 meters walking test time (P < 0.05). Additionally, there was a significant difference in improvement rates between group 5 and groups 1 and 4.Conclusion: This study showed that both hydrocortisone and clobetasole phonophoresis were more effective than ultrasound and acoustic gel on osteoarthritis pain of knee joint. Clobetasole has a faster effect than other treatments.

Introduction: Oxytocin is a active neuropeptide of central nervous system. In this study the effects of naloxone (opioid receptor antagonist) and yohimbine (a-2 adrenergic receptor antagonist) on analgesic effect of oxytocin applied into the locus coeruleus (LC) nucleus were investigated.Methods: Adult male Wistar rats were used. Animals divided into different groups receiving saline, oxytocin (3 nmol / 2ml), naloxone (3 nmol / 2ml) + oxytocin, yohimbine (3 nmol / 2ml) + oxytocin, and naloxone + yohimbine + oxytocin. Hot-plate and tail-flick tests were used to evaluate pain threshold.Results: Data showed that the injection of oxytocin into the LC nucleus increases the response time to thermal stimulations in both tail flick and hot plate tests. Injection of naloxone and yohimbine either separately and or in combination inhibite the antinociception effect of oxytocin.Conclusion: It seems that oxytocin induces its inhibitory effect on acute pain via LC nucleus. This effect is probably mediated by the combination of opioid and a-2 adrenergic systems.