Effects of Intracerebroventricular Injection of the Steroidal and Non-Steroidal Anti-Inflammatory Drugs on the Seizures during the Estrous Cycle in Rat.

Because of the mutual relationship between neural inflammation and seizure, this study aimed to determine the effects of intracerebroventricular (ICV) injection of the steroidal and non-steroidal anti-inflammatory drugs on pentylenetetrazol (PTZ)-induced seizures during the estrous cycle in rats. A total of 105 adult female Wistar rats were selected and divided into seven groups, including the control (saline), ketorolac tris salt (7.5, 15, and 30 µg), and methylprednisolone acetate (0.15, 0.3, and 0.6 µg), each with four subgroups (proestrus, estrus, metestrus, and diestrus) and three replicates (n=5). After a week of acclimatization, the estrous phase determination and synchronization were performed. Acute epilepsy was inspired by the intraperitoneal injection of 80 mg/kg of PTZ 30 min after the ICV injection of ketorolac and methylprednisolone acetate. The initiation time of myoclonic seizures (ITMS), the initiation time of tonic-clonic seizures (ITTS), seizure duration (SD), and mortality rate (MR) were measured for 30 min. Data were shown as mean±SD and analyzed using One-way ANOVA followed by Tukey-Kramer multiple comparison post hoc test (P<0.05). According to the results, ketorolac (15 and 30 µg) and methylprednisolone acetate (0.3 and 0.6 µg) significantly increased the ITTS and ITMS but decreased SD during the estrous cycle, compared to the control (P<0.05). Moreover, MR and SD were significantly decreased by ketorolac (7.5, 15, and 30 µg) and methylprednisolone (0.3 and 0.6 µg), compared to the control during the estrous cycle (P<0.05). Therefore, it seems that both ketorolac and methylprednisolone possess dose-dependent anticonvulsant effects that may decrease neural inflammation.

Central and Peripheral Effects of Lipopolysaccharide on Food Choice and Macronutrient Selection in Meat-Type Chick.

This report aimed to determine the effect of lipopolysaccharide (LPS) on food intake in broiler chicks with different rations. All birds received a starter diet until five days of age, but experimental diets were provided on days of injections. In experimental group one, chickens received an intracerebroventricular (ICV) injection of LPS (25, 50, and 100 ng) with a standard diet. In experimental group two, chickens received intraperitoneal (IP) injections of LPS (50, 100, and 200 µg) with a standard diet. In experimental group three, birds received ICV injections of saline and different diets. Accordingly, a standard diet without fat, a diet containing 20% higher nutrient energy than the standard, a diet containing 20% less nutrient energy than the standard, and a standard diet containing fat were offered to them to investigate the desire of chickens for the diets. Experimental groups four, five, and six were similar to experimental group three, except that the chickens received ICV injections of LPS. In experimental groups seven, eight, and nine, chickens received IP injections of LPS with different diets. Afterward, their cumulative food intake was measured until 180 min post-injection. According to the results, ICV and IP injections of LPS decreased food intake (P<0.05). However, the ICV injection of saline increased the desire of chickens for the standard diet with fat (P<0.05). The ICV injection of the LPS (50 and 100 ng) increased the appetite for a standard diet with nutrient energy 20% higher than the standard and a standard diet containing fat, at 120 and 180 min after the injection (P<0.05). In addition, IP injection of LPS (200 µg) significantly increased the desire for a standard diet with nutrient energy 20% higher than the standard and a standard diet containing fat (P<0.05). These results suggested the desire of chickens for different types of rations is affected by central or peripheral administration of the LPS.

The Effects of Melatonin Alone or in Combination with Zinc on Gonadotropin and Thyroid Hormones in Female Rats.

Thyroid and gonadotropin hormones play an essential role in the regulation of regulating various physiological functions. The effects of melatonin and zinc (Zn) on these hormones have already been investigated. The aim of the present study was to investigate the effect of melatonin with and without zinc on the levels of gonadotropin hormones and thyroid hormones (triiodothyronine (T3), thyroxine (T4) and thyroid-stimulating hormone (TSH)) in female rats. In general, 35 sexually mature female rats were randomly divided into five treatment groups, with each group comprising 7 rats, in a completely randomized design (CRD) during the research. The rats were treated daily with Zn and melatonin via gavage as follows T1 (control 1, basal diet), T2 (control 2, treatment with normal saline) and the other experimental groups, including T3, T4 and T5, were treated with Zn (40 ppm), melatonin (5 mg/kg) or a combination of Zn and melatonin at the same dose. The administration of the drugs was continued for 20 days (daily) . Plasma samples were then taken for the determination of LH, FFH, LH/FSH, estrogen, progesterone, T3, T4 and TSH levels. The results showed no significant differences in FSH and LH levels between treatments. Estrogen, progesterone and TSH levels were higher in the rats receiving 5 mg melatonin per day than in the other groups, but not statistically significant (P>0.05). However, T3 levels decreased significantly in the group receiving 40 mg/kg Zn compared to the other experiments. (P<0.05). The results showed no significant difference between the treatments in terms of T4 levels (P>0.05). In conclusion, no remarkable changes in other variables were observed in female rats receiving melatonin, Zn or a combination of melatonin and Zn, with the exception of T3.

The Modulatory Role of Orexin 1 Receptor in Nucleus Accumbens (NAc) on Spatial Memory in Rats.

Neuropeptide orexin mainly exists in neurons within and around the lateral hypothalamus and exhibits high affinity to orexin 1 and 2 receptors (OX1R and OX2R, respectively). Orexinergic neurons send their axons to the nucleus accumbens (NAc), which expresses OX1Rs. Previous studies have shown the involvement of orexins and their role in learning and memory processes in the dorsal raphe nucleus and hippocampus. However, no study has examined the effects of orexins in the NAc on memory. The present study examined the effect of the post-training and pre-probe trial intra-NAc administration of SB-33486-A (OX1R antagonist, 12 µg/0.5µl) and TCS-OX2-29 (OX2R antagonist, 10 µg/0.5 µl) on the consolidation and retrieval of memory in the Morris Water Maze (MWM) task. In experiment 1, rats were trained in the MWM and, immediately after every training, received bilateral injections of dimethyl sulfoxide (DMSO) (control group), SB-334867-A (SB), and TCS-OX2-29 (TCS) into the NAc. Experiment 2 was similar to experiment 1, except that the rats received DMSO, SB, and TCS 15 min before the probe test. Probe and visible tests were performed after the last training, and the distance moved, escape latency, and velocity were recorded. In experiment 3, rats trained in experiments 1 and 2, immediately after the probe test, were given the trials for visuomotor coordination assessment on the visible platform. According to the results, the injection of SB increased the distance moved and escape latency in the treated groups, compared to the control group, in the consolidation phase of spatial memory (P<0.05) but not in its retrieval phase (P>0.05). However, TCS-OX2-29 had no effect. These results suggest that the inactivation of the NAc OX1Rs, but not OX2Rs, impairs the consolidation but not the retrieval of spatial memory in rats.

Interactions of Cholecystokinin and Glutamatergic Systems in Feeding Behavior of Neonatal Chickens.

This study aimed to assess the possible feeding behavior alterations by central interactions of cholecystokinin (CCK) and glutamatergic systems in neonatal chickens. In experiment 1, chickens received intracerebroventricular (ICV) administration of saline and CCK (CCK4; 0.25, 0.5, and 1 nmol). In experiment 2, birds were ICV injected with saline, CCK8s (0.25, 0.5, and 1 nmol). In experiment 3, chickens received the ICV injection of saline, CCK8s (1 nmol), MK-801 (15 nmol), and co-injection of the CCk8s+MK-801. Experiments 4-7 were performed similar to experiment 3, except for chickens that were injected with CNQX (390 nmol), AIDA (2 nmol), LY341495 (150 nmol), and UBP1112 (2 nmol) instead of MK-801. Subsequently, the total amount of the consumed food was determined. According to the results, the ICV administration of CCK4 (0.25, 0.5, and 1 nmol) could not affect the food intake in chickens (P>0.05). The ICV injection of the CCK8s (0.25, 0.5, and 1 nmol) led to a dose-dependent hypophagia (P<0.05). Moreover, hypophagia induced by CCK8s decreased by the co-injection of the CCK8s+MK-801 (P<0.05). These results showed that the hypophagic effects of the CCK on food intake can be mediated by NMDA glutamate receptors in layer-type chickens.

Central Phoenixin Protective Role on Pentylenetetrazol-Induced Seizures during Various Stages of the Estrous Cycle among Rats.

It is known that phoenixin-14 (PNX-14) has a mediatory role in reproduction; however, there is no report on the role of the PNX-14 on epilepsy. Therefore, this study aimed to investigate the antiepileptic effects of the PNX-14 on the pentylenetetrazol (PTZ)-induced epilepsy in the stages of the estrous cycle among rats. A total of 168 adult female Wistar rats were randomly divided into seven groups, including control (intracerebroventricular injection was performed with saline), PNX-14 (5 µg), PNX-14 (10 µg), bicuculline (competitive antagonist of GABAA receptors; 5 nmol)+PNX-14 (5 µg), bicuculline (BIC) (5 nmol)+PNX-14 (10 µg), saclofen (competitive antagonist of GABAB receptors; 2.5 µg)+PNX-14 (5 µg), and saclofen (2.5 µg)+PNX-14 (10 µg) in proestrus, estrus, metestrus, and diestrus. Afterward, the control and treatment groups were followed by intraperitoneal administration of 80 mg/kg PTZ. Initiation time of myoclonic seizures (ITMS), initiation time of tonic-clonic seizures (ITTS), seizure duration (SD), and mortality rate (MR) were monitored and recorded for 30 min. According to the results, PNX-14 alone significantly reduced the SD and seizure mortality in all phases of estrus (P<0.05). The injection of PNX-14 with BIC significantly reduced SD and seizure mortality in all estrus phases (P<0.05). PNX-14 alone increased both ITMS and ITTS in all phases of estrus (P<0.05). Furthermore, the injection of PNX-14 with BIC significantly reduced the effects of the PNX-14 on ITMS and ITTS in all estrus stages (P<0.05). These results showed that the antiepileptic activity of PNX-14 was probably mediated by GABAA receptors, and this effect was more prominent during the luteal phase than the follicular phase.

Correlation of Histamine Receptors and Adrenergic Receptor in Broilers Appetite.

The current study was conducted to investigate the interaction between the central adrenergic and histaminergic systems and the broiler chick's feed intake. In the first experiment, the intracerebroventricular (ICV) injection of solutions was conducted which included 10 nmol of prazosin (an α1-receptor antagonist), 300 nmol of histamine, co-injection of prazosin and histamine. Experiments two to five were conducted similarly the same as the first experiment, in which chickens were ICV injected with 13 nmol of yohimbine (an α2-receptor antagonist), 24 nmol of metoprolol (a ß1 adrenergic receptor antagonist), 5 nmol of ICI 118,551 (a ß2 adrenergic receptor antagonist), and 20 nmol of SR 59230R (a ß3 adrenergic receptor antagonist). The injected solutions in the sixth experiment included 300 nmol of noradrenaline, 250 nmol of α-FMH (an alpha fluoromethyl histidine), noradrenaline, and α-FMH. Seventh to ninth experiments were similar to the sixth experiment, except that the chickens were ICV injected with 300 nmol of chlorpheniramine (a histamine H1 receptors antagonist), 82 nmol of famotidine (a histamine H2 receptors antagonist), and 300 nmol of thioperamide (a histamine H3 receptors antagonist), rather than α-FMH. Afterward, the cumulative food intake was measured 120 min after injection. Based on the obtained results, both histamine ICV injection and noradrenaline injection reduced food intake (P<0.05). Moreover, co-injection of histamine and ICI 118,551 (P<0.05), and co-injection of noradrenaline and Chlorpheniramine reduced food intake (P<0.05). In addition, noradrenaline and Thioperamide co-injection improved hypophagic effect of noradrenaline in neonatal chicken (P<0.05). These findings suggested the effect of interconnection between adrenergic and histaminergic systems, which may be mediated by H1 and H3 histaminergic and ß2 adrenergic receptors, on the regulation of food intake in the neonatal broiler chicken.

Interaction of Central Glutamatergic and Histaminergic Systems on Food Intake Regulation in Layer Chickens.

This study purposed to discover the connection between the central glutamatergic and histaminergic systems on feeding behavior in layer chickens. In the first experiment, chicks obtained intracerebroventricular (ICV) injections of saline (control solution), α-FMH (250 nmol), glutamate (300 nmol), and α-FMH + glutamate. Experiments 2-6 were comparable to the first experiment, apart from the birds being injected with chlorpheniramine (histamine H1 receptor antagonist, 300 nmol), famotidine (histamine H2 receptor antagonist, 82 nmol), and thioperamide (histamine H3 receptor antagonist, 300 nmol) instead of α-FMH. In Experiment five, experimental groups were divided into (A) control solution, (B) MK-801 (N-methyl-D-aspartate receptor antagonist, 15 nmol), (C) histamine (300 nmol) and (D) MK-801 + histamine. Experiments 6-10 and Experiment five were similar apart from the ICV injections of CNQX (AMPA receptor antagonist, 360 nm), UBP-302 (Kainate receptor antagonist, 390 nm), AIDA (mGluR1 antagonist, 2 nmol), LY341495 (mGluR2 antagonist, 150 nmol), and UBP1112 (mGluR3 antagonist, 2 nmol) given instead of MK-801. Afterward, cumulative food intake was recorded at30, 60, and 120 minutes after the injection process. According to the results, ICV injection of glutamate considerably reduced food intake (p<0.05). Co-injection of α-FMH + glutamate and/or chlorpheniramine + glutamate reduced the hypophagic influence of glutamate (p<0.05), whereas thioperamide + glutamate augmented glutamate-induced hypophagia in neonatal chicks (p<0.05). Co-injection of MK-801 + histamine or UBP-302 + histamine reduced the hypophagic influence of the histamine (p<0.05), whereas LY341495 + histamine augmented the hypophagic influence of the histamine (p<0.05). Given the results, it is suggested that the effect of the connection between these systems on the process of food intake regulation is mediated by H1 and H3 histamines as well as NMDA, Kainate, and mGluR2 glutamate receptors in neonatal layer chickens.

Interconnection between Adrenergic and Dopaminergic Systems in Feeding Behavior in Neonatal Chicks.

Central dopaminergic (DAergic) and adrenergic systems have a prominent role in appetite regulation; however, their interaction(s) have not been studied in neonatal layer chickens.Therefore, the current study aimed to determine the interaction of central DAergic and noradrenergic systems in food intake regulation in neonatal layer chickens. In the first experiment, chickens received the intracerebroventricular (ICV) injection of a control solution, prazosin (i.e., &alpha;1 adrenergic receptor antagonist; 10 nmol), dopamine (DA; 40 nmol), and prazosin plus DA. The second to fifth experiments were similar to the first experiment except that the birds were injected with yohimbine (i.e., &alpha;2 receptor antagonist; 13 nmol), metoprolol (i.e., &beta;1 adrenergic receptor antagonist; 24 nmol), ICI 118,551 (i.e., &beta;2 adrenergic receptor antagonist; 5 nmol), and SR59230R (i.e., &beta;3 adrenergic receptor antagonist; 20 nmol) instead of prazosin. In the sixth experiment, the chickens received ICV injection with the control solution and noradrenaline (NA; 75, 150, and 300 nmol). In the seventh experiment, the birds were injected with the control solution, SCH23390 (i.e., D1 DAergic receptor antagonist; 5 nmol), NA (300 nmol), and SCH23390 plus NA In the eighth experiment, the control solution, AMI-193 (i.e., D2 DAergic receptor antagonist; 5 nmol), NA (300 nmol), and AMI-193 plus NA were injected. Then, cumulative food intake was recorded at 30, 60, and 120 min after the injection. According to the obtained results, the ICV injection of DA (40 nmol) significantly decreased food intake in comparison to that reported for the control group (p &lt;0.05). The co-injection of yohimbine plus DA significantly amplified DA-induced hypophagia in the neonatal chickens (p &lt;0.05). In addition, the co-administration of ICI 118,551 plus DA significantly inhibited the hypophagic effect of DA in the neonatal chickens (p &lt;0.05). Furthermore, NA (75, 150, and 300 nmol) significantly reduced food intake in a dose-dependent manner (p &lt;0.05). The co-injection of SCH23390 plus NA decreased the hypophagic effect of NA in the neonatal chickens, compared to that reported for the control group (p &lt;0.05). The co-injection of AMI-193 plus NA diminished NA-induced hypophagia, compared to that reported for the control group (p &lt;0.05). The aforementioned results suggested that there is an interconnection between central DAergic and noradrenergic systems through &alpha;2/&beta;2 adrenergic and D1/D2 DAergic receptors in food intake regulation in neonatal chicks.

Impact of the Central Histaminergic and Melanocortin Systems on Leptin-Induced Hypophagia in Neonatal Layer Chicken.

The present study aimed to assess the probable impact of the central histaminergic and melanocortin systems on leptin-induced hypophagia in neonatal layer chickens. In experiment 1, the chickens received intracerebroventricular (ICV) injections of the control solution, 250 nmol of α-FMH, 10 µg of leptin, and α-FMH+leptin. Experimental groups 2-8 were injected the same as experiment 1. Nonetheless, the chickens in experiments 2-8 received ICV injections of 300 nmol of chlorpheniramine (H1 receptor antagonist), 82 nmol of famotidine (H2 receptor antagonist), 300 nmol of thioperamide (H3 receptor antagonist), 0.5 nmol of SHU9119 (M3/M4 receptors antagonist), 0.5 nmol of MCL0020 (M4 receptor antagonist), 30 µg of astressin-B (CRF1/ CRF2 receptors antagonist), and 30 µg of astressin2-B (CRF2 receptor antagonist), instead of α-FMH, respectively. Food was provided for the birds immediately following the injection, and 30, 60, and 120 min after the injection, cumulative food intake (g) was measured. The findings pointed out that the ICV injection of leptin diminished food intake in neonatal chickens (P<0.05). The co-administration of M3/M4 receptor antagonist+leptin significantly decreased the hypophagic effect of leptin (P<0.05). A significant decrease was also detected in the hypophagic effect of leptin following the co-administration of the M4 receptor antagonist and leptin (P<0.05). Moreover, the co-injection of the antagonists of CRF1/CRF2 receptors and leptin significantly mitigated the hypophagic effect of leptin (P<0.05). The co-injection of CRF2 receptor antagonist and leptin led to a decrease in the hypophagic effect of leptin. As evidenced by the results of the current study the hypophagic effect of leptin is mediated by the receptors of H1, H3, M3/M4, and CRF1/CRF2 in neonatal layer chicken.

Role of Dopaminergic and Cannabinoidergic Receptors on Ghrelin-Induced Hypophagia in 5-Day-Old Broiler Chicken.

The present study aimed to identify the role of dopaminergic and cannabinoidergic systems in the ghrelin-induced hypophagia among meat-type chickens. In the first experiment, intracerebroventricular (ICV) injection was applied to birds with control solution, D1 receptor antagonist (5 nmol), ghrelin (6 nmol), and D1 receptor antagonist plus ghrelin. The second to sixth experiments were similar to the first one, with the difference that D2 receptor antagonist (5 nmol), D3 receptor antagonist (6.4 nmol), D4 receptor antagonist (6 nmol), the precursor of dopamine (125 nmol), and 6-hydroxy dopamine (150 nmol) instead of D1 antagonist were injected into the broiler chickens. In experiment 7, control solution and different levels of ghrelin antagonists (5, 10, and 20 nmol) were injected. In experiment 8, the chickens were ICV injected with control solution, ghrelin antagonist (10 nmol), dopamine (40 nmol), and ghrelin antagonist plus dopamine. In experiments 9 and 10, CB1 and CB2 receptors antagonist (6.25µg and 5µg) were co-injected with ghrelin (6 nmol), respectively, measuring the food intake for 120 min after the injection. It was observed that ghrelin ICV injection considerably reduced food intake, whereas ghrelin antagonist increased food intake, depending on the dose (P<0.05). In addition, ghrelin-induced hypophagia was significantly attenuated by D1 receptor antagonist and 6-hydroxy dopamine (P<0.05), while the dopamine precursor considerably elevated the ghrelin-induced food intake (P<0.05). The dopamine-induced feeding behavior was diminished by the co-administration of [D-Lys-3]-GHRP-6 (10 nmol)+dopamine (40 nmol) (P<0.05). In addition, CB1 receptor antagonists enhanced the ghrelin influence on food intake (P<0.05). The results implied that the hypophagic impact of ghrelin was probably mediated by D1 and CB1 receptors within neonatal broilers.

ß2 adrenergic receptors and leptin interplay to decrease food intake in chicken.

1. The present study was designed to examine the effects of intracerebroventricular (ICV) injection of different α and [Formula: see text] adrenergic receptor antagonists on leptin-induced hypophagia in broiler chickens.2. The study consisted of six experiments. In all experiments, chickens were deprived of feed for 3 h prior to the ICV injections and thereafter were returned immediately to the individual cages and cumulative feed intake, based on the percentage of body weight, was measured at 30, 60 and 120 min post-injection.3. In experiment 1, leptin (2.5, 5 or 10 µg) were injected in birds. In experiment 2, groups received either control solution, prazosin (10 nmol), leptin (10 µg) or a co-injection of prazosin (10 nmol) and leptin (10 µg). The other experiments were conducted as experiment 2, but instead of prazosine (10 nmol), yohimbine (13 nmol) was used in experiment 3, metoprolol (24 nmol) in experiment 4, ICI 118,551 (5 nmol) in experiment 5 and SR 59230R (5 nmol) in experiment 6 were injected either in a group or in combination with leptin (10 µg).4. The results of this study revealed a dose-dependent hypophagic effect of leptin and, in experiment 5, ICV co-injection of ICI118, 551 (5 nmol) and leptin (10 µg) significantly attenuated this effect (P˂0.5). These results suggest that the hypophagic effect of leptin is probably mediated by ß2 adrenergic receptors in chickens.

Interaction of the dopaminergic and Nociceptin/Orphanin FQ on central feed intake regulation in chicken.

1. The aim of the current study was to determine the effects of the central dopaminergic system on N/OFQ-induced feed intake in 3-h feed-deprived neonatal broilers. 2. In experiment 1, chicken received intracerebroventricular (ICV) injections of a control solution, SCH 23 390 (D1 receptors antagonist, 5 nmol), N/OFQ (16 nmol) or their combination (SCH23 390 + N/OFQ). In experiment 2, a control solution, AMI-193 (D2 receptors antagonist, 5 nmol), N/OFQ (16 nmol) or their combination (AMI-193 + N/OFQ) were ICV injected into chickens. In experiment 3, birds received ICV injections of a control solution, NGB2904 (D3 receptors antagonist, 6.4 nmol), N/OFQ (16 nmol) and co-injection of NGB2904 + N/OFQ. In experiment 4, ICV injections of the control solution, L-741,742 (D4 receptors antagonist, 6 nmol), N/OFQ (16 nmol) or their combination (L-741,742 + N/OFQ) were applied to broilers. In experiment 5, birds were ICV injected with control solution, L-DOPA (dopamine precursor, 125 nmol), N/OFQ (16 nmol) and L-DOPA + N/OFQ. Cumulative feed intake was recorded until 120 min after injection. 3. According to the results, ICV injection of N/OFQ significantly increased feed intake (P < 0.05). Co-injection of N/OFQ and D1 receptor antagonist (SCH 23390) amplified hyperphagic effect of N/OFQ (P < 0.05). The N/OFQ-induced feed intake was increased by the D2 receptor antagonist (P < 0.05). The hyperphagic effect of N/PFQ was weakened by co-injection of L-DOPA + N/OFQ (P < 0.05). 4. These results suggested that an interaction exists between dopamine and N/OFQ via D1 and D2 receptors on central feed intake in neonatal broiler chickens.

Interaction of neuropeptide Y receptors (NPY1, NPY2 and NPY5) with somatostatin on somatostatin-induced feeding behaviour in neonatal chicken.

1. The present study was conducted to investigate whether brain somatostatin increases feed intake in neonatal chickens. The mediating role of neuropeptide Y receptors on feed intake induced by somatostatin was investigated. 2. In this study, seven experiments were designed, each with four treatment groups (n = 44 in each experiment). In Experiment 1, chicks received control solution and 0.5, 1 and 2 nmol of somatostatin through intracerebroventricular (ICV) injection. In experiments 2, 3 and 4, chickens were ICV injected with control solution and 1.25, 2.5 and 5 µg of B5063 (NPY1 receptor antagonist), SF22 (NPY2 receptor antagonist) and SML0891 (NPY5 receptor antagonist), respectively. In experiment 5, 6 and 7 chickens received ICV injection of B5063, SF22, SML0891, with a co-injection of + somatostatin, control solution and somatostatin. The cumulative feed intake was measured until 120 min post injection. 3. Somatostatin significantly increased feed intake in FD3 chicks. Both B5063 and SML0891 dose-dependently decreased feed intake compared with the control group, while SF22 led to a dose-dependent increase in feed intake. In addition, the hyperphagic effect of somatostatin significantly decreased with co-injection of B560 plus somatostatin (p < 0.05), but SF22 and SML0891 had no effect on feed intake induced by somatostatin in chicks (p > 0.05). 4. Based on the results of this study, it is likely that somatostatin increased feed intake and NPY1 receptor acts as a mediator in hyperphagic effect of somatostatin in neonatal chicks.

Consequence of dopamine D2 receptor blockade on the hyperphagic effect induced by cannabinoid CB1 and CB2 receptors in layers.

1. Endocannabinoids (ECBs) and their receptors play a regulatory function on several physiological processes such as feed-intake behaviour, mainly in the brain. This study was carried out in order to investigate the effects of the dopaminergic D1 and D2 receptors on CB1/CB2 ECB receptor-induced hyperphagia in 3-h feed-deprived neonatal layer chickens. 2. A total of 8 experiments were designed to explore the interplay of these two modulatory systems on feed intake in neonatal chickens. In Experiment 1, chickens were intracerebroventricular (ICV) injected with control solution, l-DOPA (levo-dihydroxyphenylalanine as precursor of dopamine; 125 nmol), 2-AG (2-arachidonoylglycerol as CB1 receptor agonist; 2 µg) and co-administration of l-DOPA (125 nmol) plus 2-AG (2 µg). Experiments 2-4 were similar to Experiment 1 except birds were injected with either 6-OHDA (6-hydroxydopamine as dopamine synthesis inhibitor; 150 nmol), SCH23390 (D1 receptor antagonist; 5 nmol) and AMI-193 (D2 receptor antagonist; 5 nmol) instead of l-DOPA, respectively. Additionally, Experiments 5-8 followed the previous ones using the same dose of l-DOPA, 6-OHDA and dopamine antagonists except that birds were injected with CB65 (CB2 receptor agonist; 5 µg) instead of 2-AG. Coadministrations were at the same dose for each experiment. Cumulative feed intakes were measured until 120 min after each injection. 3. ICV administration of 6-OHDA and AMI-193 significantly attenuated 2-AG-induced hyperphagia. Interestingly, the hyperphagic effect of CB65 was significantly attenuated by administration of l-DOPA, whereas the administration of 6-OHDA and AMI-193 together amplified the hyperphagic effect of CB65. 4. It was concluded that cannabinoid-induced feeding behaviour is probably modulated by dopamine receptors in neonatal layer-type chickens. It seems that their interaction may be mediated by the D2-dopamine receptor.

Serotonin-induced hypophagia is mediated via α2 and ß2 adrenergic receptors in neonatal layer-type chickens.

1. Serotoninergic and adrenergic systems play crucial roles in feed intake regulation in avians but there is no report on possible interactions among them. So, in this study, 5 experiments were designed to evaluate the interaction of central serotonergic and adrenergic systems on food intake regulation in 3 h food deprived (FD3) neonatal layer-type chickens. 2. In Experiment 1, chickens received intracerebroventricular (ICV) injection of control solution, serotonin (56.74 nmol), prazosin (α1 receptor antagonist, 10 nmol) and co-injection of serotonin plus prazosin. In Experiment 2, control solution, serotonin (56.74 nmol), yohimbine (α2 receptor antagonist, 13 nmol) and co-injection of serotonin plus yohimbine were used. In Experiment 3, the birds received control solution, serotonin (56.74 nmol), metoprolol (ß1 receptor antagonist, 24 nmol) and co-injection of serotonin plus metoprolol. In Experiment 4, injections were control solution, serotonin (56.74 nmol), ICI 118.551 (ß2 receptor antagonist, 5 nmol) and serotonin plus ICI 118.551. In Experiment 5, control solution, serotonin (56.74 nmol), SR59230R (ß3 receptor antagonist, 20 nmol) and co-administration of serotonin and SR59230R were injected. In all experiments the cumulative food intake was measured until 120 min post injection. 3. The results showed that ICV injection of serotonin alone decreased food intake in chickens. A combined injection of serotonin plus ICI 118.551 significantly attenuated serotonin-induced hypophagia. Also, co-administration of serotonin and yohimbine significantly amplified the hypophagic effect of serotonin. However, prazosin, metoprolol and SR59230R had no effect on serotonin-induced hypophagia in chickens. 4. These results suggest that serotonin-induced feeding behaviour is probably mediated via α2 and ß2 adrenergic receptors in neonatal layer-type chicken.

D1- and D2-like dopamine receptors within the nucleus accumbens contribute to stress-induced analgesia in formalin-related pain behaviours in rats.

BACKGROUND: Stressful experiences can produce analgesia, termed stress-induced analgesia (SIA). Meanwhile, it has been widely established that the mesolimbic dopamine pathway and nucleus accumbens (NAc) have a profound role in pain modulation. In this study, we examined the role of accumbal dopamine receptors in antinociception caused by forced swim stress (FSS) in order to understand more about the function of these receptors within the NAc in FSS-induced analgesia. METHOD: Stereotaxic surgery was unilaterally performed on adult male Wistar rats weighing 230-250 g (some on the left and some on the right side of the midline). Two supergroups were microinjected into the NAc with a D1-like dopamine receptor antagonist, SCH-23390, at doses of 0.25, 1 and 4 µg/0.5 µl saline per rat or Sulpiride as a D2-like dopamine receptor antagonist at the same doses [0.25, 1 and 4 µg/0.5 µl dimethyl sulfoxide (DMSO) per rat]; while their controls just received intra-accumbal saline or DMSO at 0.5 µl, respectively. The formalin test was performed after rats were subjected to FSS (6 min, 25 ± 1 °C) to assess pain-related behaviours. RESULTS: The results demonstrated that intra-accumbal infusions of SCH-23390 and Sulpiride dose-dependently reduced FSS-induced antinociception in both phases of the formalin test. However, the percentage decrease in area under the curve (AUC) values calculated for treatment groups compared to formalin-control group was more significant in the late phase than the early phase. CONCLUSION: Our findings suggest that D1- and D2-like dopamine receptors in the NAc are involved in stress-induced antinociceptive behaviours in the formalin test as an animal model of persistent inflammatory pain. WHAT DOES THIS STUDY ADD: Forced swim stress (FSS) induces the antinociception in both phases of formalin test. Blockade of accumbal dopamine receptors attenuate the antinociception induced by FSS. Stress-induced analgesia is dose-dependently reduced by dopamine receptor antagonists in both phases, although it is more prominent during the late phase.

Central histaminergic system interplay with suppressive effects of immune challenge on food intake in chicken.

The aim of the current study was to investigate the interaction of the lipopolysaccharide (LPS) and histaminergic systems on appetite regulation in broilers. Effects of intracerebroventricular (ICV) injection of α-fluoromethylhistidine (α-FMH, histidine decarboxylase inhibitor), chlorpheniramine (histamine H1 receptor antagonist), famotidine (histamine H2 receptor antagonist) and thioperamide (histamine H3 receptor antagonist) on LPS-induced hypophagia in broilers were studied. A total of 128 broilers were randomly allocated into 4 experiments (4 groups and 8 replications in each experiment). A cannula was surgically implanted into the lateral ventricle. In Experiment 1, broilers were ICV injected with LPS (20 ng) prior to α-FMH (250 nmol). In Experiment 2, chickens were ICV injected with LPS followed by chlorpheniramine (300 nmol). In Experiment 3, broilers were ICV injected with famotidine (82 nmol) after LPS (20 ng). In Experiment 4, ICV injection of LPS was followed by thioperamide (300 nmol). Then, cumulative food intake was recorded until 4 h post-injection. According to the results, LPS significantly decreased food intake. Chlorpheniramine significantly amplified food intake, and LPS-induced hypophagia was lessened by injection of chlorpheniramine. α-FMH, famotidine and thioperamide had no effect on LPS-induced hypophagia. These results suggest that there is an interaction between central LPS and the histaminergic system where LPS-induced hypophagia is mediated by H1 histamine receptors in 3 h food-deprived broilers.

Lipopolysaccharide and histaminergic systems interact to mediate food intake in broilers.

1. The aim of the current study was to investigate the interaction of the lipopolysaccharide and histaminergic systems on appetite regulation in broilers. The effects of intracerebroventricular (ICV) injection of α-fluoromethylhistidine (α-FMH, histidine decarboxylase inhibitor), chlorpheniramine (histamine H1 receptor antagonist), famotidine (histamine H2 receptor antagonist) and thioperamide (histamine H3 receptor antagonist) on lipopolysaccharide (LPS)-induced hypophagia in broilers were studied. 2. A total of 128 broilers were randomly allocated into 4 experiments (4 groups and 8 replications in each experiment). A cannula was surgically implanted into the lateral ventricle. In Experiment 1, broilers were ICV injected with LPS (20 ng) prior to α-FMH (250 nmol). In Experiment 2, chickens were ICV injected with LPS followed by chlorpheniramine (300 nmol). In Experiment 3, broilers were ICV injected with famotidine (82 nmol) after LPS (20 ng). In Experiment 4, ICV injection of LPS was followed by thioperamide (300 nmol). The cumulative food intake was recorded until 4 h post injection. 3. LPS decreased food intake; chlorpheniramine amplified food intake and LPS-induced hypophagia was lessened by injection of chlorpheniramine. α-FMH, famotidine and thioperamide had no effect on LPS-induced hypophagia. 4. The results suggest that there is an interaction between central LPS and the histaminergic system where LPS-induced hypophagia is presumably mediated by H1 histamine receptors in 3 h food-deprived broilers.

Endocannabinoid and nitric oxide interaction mediates food intake in neonatal chicken.

The aim of the current study was to investigate the interaction of the nitric oxide and cannabinoidergic systems on feeding behaviour in neonatal chicken. A total of 6 experiments were designed to evaluate the interaction between cannabinoidergic and nitrergic systems on food intake in 3-h food-deprived (FD3) neonatal chickens. In Experiment 1, chickens received intracerebroventricular (ICV) injections of saline, 2-arachidonoylglycerol (2-AG) (a CB1 receptor agonist, 2 µg), l-arginine (nitric oxide precursor, 200 nmol) and co-administration of 2-AG + l-arginine. In Experiment 2, ICV injection of saline, 2-AG (2 µg), l-NAME (a nitric oxide synthesis inhibitor, 100 nmol) and their combination (2-AG + l-NAME) were applied to the birds. In Experiment 3, injections were saline, CB65 (a CB2 receptor agonist, 1.25 µg), l-arginine (200 nmol) and CB65 + l-arginine. In Experiment 4, birds received ICV injection of saline, CB65 (1.25 µg), l-NAME (100 nmol) and CB65 + l-NAME. In Experiment 5, chickens were ICV injected with saline, l-arginine (800 nmol), SR141716A (a selective CB1 receptor antagonist, 6.25 µg) and l-arginine + SR141716A. In Experiment 6, birds were injected with saline, l-arginine (800 nmol), AM630 (a selective CB2 receptor antagonist, 5 µg) and l-arginine + AM630. Cumulative food intake was recorded until 2-h post injection. ICV injection of CB1 and CB2 receptor agonists increased food intake. Co-injection of 2-AG + l-NAME increased the hyperphagic effects of CB1 receptors. CB2 receptor-induced food intake was not affected by co-administration of CB65 + l-NAME. l-Arginine decreased food intake and this effect was amplified by co-injection of l-arginine + SR141716A. However; CB2 receptor antagonists had no effect on l-arginine-induced hypophagia. The results suggest that there is an interaction between endogenous nitric oxide and the cannabinoidergic system on feeding behaviour which is mediated via CB1 receptors in the neonatal chicken.