RESUMEN
This study was aimed at determining the role of the crustacean hyperglycemic hormone (CHH) in the physiological compensation to both saline and thermal stress, in the freshwater crayfish Cherax quadricarinatus. By determining the expression of the CHH gene in the eyestalk of juvenile crayfish, we found that maximal induction of CHH was induced at high salinity (10 g/L) and low temperature (20 °C). In order to investigate the role of CHH in the physiological compensation to such stressful conditions, recombinant CHH was supplied to stressed animals. CHH-injected crayfish showed increased hemolymphatic levels of glucose, in accordance with a significant utilization of glycogen reserves from the hepatopancreas. Furthermore, CHH administration allowed stressed animals to regulate hemolymphatic sodium and potassium at more constant levels than controls. Taken together, these results suggest a relevant role of CHH in increasing the energy available intended for processes involved in the physiological compensation of C. quadricarinatus to both saline and thermal stress.
Asunto(s)
Proteínas de Artrópodos/metabolismo , Astacoidea/metabolismo , Frío , Metabolismo Energético , Agua Dulce/química , Hormonas de Invertebrados/metabolismo , Proteínas del Tejido Nervioso/metabolismo , Salinidad , Tolerancia a la Sal , Estrés Fisiológico , Secuencia de Aminoácidos , Animales , Proteínas de Artrópodos/administración & dosificación , Proteínas de Artrópodos/genética , Astacoidea/genética , Clonación Molecular , Ecosistema , Metabolismo Energético/efectos de los fármacos , Glucosa/metabolismo , Glucógeno/metabolismo , Hemolinfa/metabolismo , Hepatopáncreas/metabolismo , Hormonas de Invertebrados/administración & dosificación , Hormonas de Invertebrados/genética , Datos de Secuencia Molecular , Proteínas del Tejido Nervioso/administración & dosificación , Proteínas del Tejido Nervioso/genética , Potasio/metabolismo , Proteínas Recombinantes/administración & dosificación , Transducción de Señal , Sodio/metabolismoRESUMEN
Protective autoimmunity (PA) is a physiological response to central nervous system trauma that has demonstrated to promote neuroprotection after spinal cord injury (SCI). To reach its beneficial effect, PA should be boosted by immunizing with neural constituents or neural-derived peptides such as A91. Immunizing with A91 has shown to promote neuroprotection after SCI and its use has proven to be feasible in a clinical setting. The broad applications of neural-derived peptides make it important to determine the main features of this anti-A91 response. For this purpose, adult Sprague-Dawley rats were subjected to a spinal cord contusion (SCC; moderate or severe) or a spinal cord transection (SCT; complete or incomplete). Immediately after injury, animals were immunized with PBS or A91. Motor recovery, T cell-specific response against A91 and the levels of IL-4, IFN-γ and brain-derived neurotrophic factor (BDNF) released by A91-specific T (T(A91)) cells were evaluated. Rats with moderate SCC, presented a better motor recovery after A91 immunization. Animals with moderate SCC or incomplete SCT showed significant T cell proliferation against A91 that was characterized chiefly by the predominant production of IL-4 and the release of BDNF. In contrast, immunization with A91 did not promote a better motor recovery in animals with severe SCC or complete SCT. In fact, T cell proliferation against A91 was diminished in these animals. The present results suggest that the effective development of PA and, consequently, the beneficial effects of immunizing with A91 significantly depend on the severity of SCI. This could mainly be attributed to the lack of T(A91) cells which predominantly showed to have a Th2 phenotype capable of producing BDNF, further promoting neuroprotection.
Asunto(s)
Autoinmunidad , Inmunización/métodos , Proteínas del Tejido Nervioso/farmacología , Traumatismos de la Médula Espinal/terapia , Animales , Proteínas del Tejido Nervioso/administración & dosificación , Proteínas del Tejido Nervioso/uso terapéutico , Fármacos Neuroprotectores , Péptidos/farmacología , Péptidos/uso terapéutico , Ratas , Ratas Sprague-Dawley , Recuperación de la Función , Traumatismos de la Médula Espinal/inmunología , Resultado del TratamientoRESUMEN
Multiple sclerosis (MS) is an autoimmune disease characterized by inflammatory immune response directed against myelin antigens of the central nervous system. In its murine model, EAE, Th17 cells play an important role in disease pathogenesis. These cells can induce blood-brain barrier disruption and CNS immune cells activation, due to the capacity to secrete high levels of IL-17 and IL-22 in an IL-6+TGF-ß dependent manner. Thus, using the oral tolerance model, by which 200 µg of MOG 35-55 is given orally to C57BL/6 mice prior to immunization, we showed that the percentage of Th17 cells as well as IL-17 secretion is reduced both in the periphery and also in the CNS of orally tolerated animals. Altogether, our data corroborates with the pathogenic role of IL-17 and IFN-γ in EAE, as its reduction after oral tolerance, leads to an overall reduction of pro-inflammatory cytokines, such as IL-1α, IL-6, IL-9, IL-12p70 and the chemokines MIP-1ß, RANTES, Eotaxin and KC in the CNS. It is noteworthy that this was associated to an increase in IL-10 levels. Thus, our data clearly show that disease suppression after oral tolerance induction, correlates with reduction in target organ inflammation, that may be caused by a reduced Th1/Th17 response.
Asunto(s)
Alérgenos/administración & dosificación , Encefalomielitis Autoinmune Experimental/inmunología , Encefalomielitis Autoinmune Experimental/patología , Tolerancia Inmunológica , Interleucina-17/antagonistas & inhibidores , Depleción Linfocítica , Proteínas del Tejido Nervioso/administración & dosificación , Linfocitos T Colaboradores-Inductores/inmunología , Administración Oral , Alérgenos/inmunología , Secuencia de Aminoácidos , Animales , Encefalomielitis Autoinmune Experimental/terapia , Glicoproteínas/administración & dosificación , Glicoproteínas/inmunología , Glicoproteínas/uso terapéutico , Inmunosupresores/administración & dosificación , Inmunosupresores/inmunología , Inmunosupresores/uso terapéutico , Inflamación/inmunología , Inflamación/patología , Inflamación/terapia , Interleucina-17/metabolismo , Depleción Linfocítica/métodos , Masculino , Ratones , Ratones Endogámicos C57BL , Datos de Secuencia Molecular , Glicoproteína Mielina-Oligodendrócito , Proteínas del Tejido Nervioso/inmunología , Fragmentos de Péptidos/administración & dosificación , Fragmentos de Péptidos/inmunología , Fragmentos de Péptidos/uso terapéutico , Linfocitos T Colaboradores-Inductores/patologíaRESUMEN
It is known that the sleep-waking cycle is modulated by several molecules that may also regulate food intake, among them several neuropeptides. The cocaine-and-amphetamine-regulated transcript has been studied in relation to food ingestion, but it seems to have several other functions that may include sleep regulation. In this context, we studied the effect of the intracerebroventricular administration of the cocaine-and-amphetamine-regulated transcript (0.15, 0.3, 0.6, 0.9nmol) on the sleep-waking cycle (12-h recordings), as well as its effect on food intake in rats. Additionally, we analyzed the neuronal activity as measured by c-Fos expression induced by the cocaine-and-amphetamine-regulated transcript in neurons of nuclei involved in the regulation of sleep and feeding behavior. Our main finding is that 0.3nmol of the cocaine-and-amphetamine-regulated transcript increases rapid-eye-movement sleep. In addition, our results further support that this neuropeptide triggers satiety; c-Fos expression suggested that the cocaine-and-amphetamine-regulated transcript activates specific hypothalamic nuclei without affecting other brain structures known to be involved in sleep regulation. These data further support the notion that a few neuropeptides are involved in the regulation of both the sleep-waking and the hunger-satiety cycles.
Asunto(s)
Proteínas del Tejido Nervioso/farmacología , Neurotransmisores/farmacología , Sueño REM/efectos de los fármacos , Animales , Peso Corporal , Ingestión de Alimentos/efectos de los fármacos , Conducta Alimentaria/efectos de los fármacos , Humanos , Masculino , Proteínas del Tejido Nervioso/administración & dosificación , Neurotransmisores/administración & dosificación , Proteínas Proto-Oncogénicas c-fos/metabolismo , Ratas , Ratas Wistar , Sueño REM/fisiologíaRESUMEN
The present study was performed to evaluate the effect of 3 rdV injection on water intake of brain natriuretic peptide (BNP), which is structurally different from the atrial natriuretic peptide. VNP was recently isolated from porcine brain and appears to have a different precursor than the family of atrial natriuretic peptides. Central administration of BNP 3rdV decreased water intake. At a dose of 2.0 mmol/rat, BNP partially inhibited dehyfration-induced water intake and completely blocked the stimulatory effect of 478 pmol/rat angiotension II in rats
Asunto(s)
Ratas , Animales , Masculino , Angiotensina II/farmacología , Deshidratación/complicaciones , Ingestión de Líquidos , Proteínas del Tejido Nervioso/administración & dosificaciónRESUMEN
The present study was performed to evaluate the effect of 3rdV injection on water intake of brain natriuretic peptide (BNP), which is structurally different from the atrial natriuretic peptide. BNP was recently isolated from porcine brain and appears to have a different precursor than the family of atrial natriuretic peptides. Central administration of BNP 3rdV decreased water intake. At a dose of 2.0 nmol/rat, BNP partially inhibited dehydration-induced water intake and completely blocked the stimulatory effect of 478 pmol/rat angiotensin II in rats.