RESUMEN
Tonic immobility (TI) is an innate defensive response exhibited by prey when physical contact with a predator is prolonged and inescapable. This defensive response is able to activate analgesia mechanisms; this activation has adaptive value because, during an attack by a predator, the manifestation of recuperative behaviors can affect the appropriate behavioral defense strategy. Some studies have suggested that similar structures of the central nervous system can regulate the response of both TI and nociception. Thus, this study evaluated the effect of chemical lesion through the administration of ibotenic acid in restricted brain areas of the periaqueductal gray matter (PAG) in guinea pig on the TI response and nociception evaluated in the hot plate test before and after emission of TI. The data showed that an irreversible chemical lesion in the ventrolateral PAG reduced of the TI response as well as defensive antinociception. However, a lesion in the dorsal PAG blocked the defensive antinociception induced by TI but did not alter TI duration. In summary, one could hypothesize that the neural substrates responsible for defensive behavior and antinociception represent similar systems that are distinct in modulation. Thus, the ventrolateral PAG has been associated with the modulation of TI and the defensive antinociception induced by TI. In contrast, the integrity of the dorsal PAG should be necessary for defensive antinociception to occur but not to elicit TI behavior in guinea pigs.
Asunto(s)
Analgesia , Ácido Iboténico/farmacología , Pérdida de Tono Postural/fisiología , Sustancia Gris Periacueductal/fisiopatología , Animales , Cobayas , Ácido Iboténico/administración & dosificación , Masculino , Microinyecciones , Dimensión del Dolor , Sustancia Gris Periacueductal/efectos de los fármacosRESUMEN
Generalised tonic-clonic seizures, generated by abnormal neuronal hyper-activity, cause a significant and long-lasting increase in the nociceptive threshold. The pedunculopontine tegmental nucleus (PPTN) plays a crucial role in the regulation of seizures as well as the modulation of pain, but its role in postictal antinociceptive processes remains unclear. In the present study, we aimed to investigate the involvement of PPTN neurons in the postictal antinociception. Wistar rats had their tail-flick baseline recorded and were injected with ibotenic acid (1.0⯵g/0.2⯵L) into the PPTN, aiming to promote a local neurotoxic lesion. Five days after the neuronal damage, pentylenetetrazole (PTZ; 64â¯mg/kg) was intraperitoneally administered to induce tonic-clonic seizures. The tail-withdrawal latency was measured immediately after the seizures (0â¯min) and subsequently at 10-min intervals until 130â¯min after the seizures were induced pharmacologically. Ibotenic acid microinjected into the PPTN did not reduce the PTZ-induced seizure duration and severity, but it diminished the postictal antinociception from 0 to 130â¯min after the end of the PTZ-induced tonic-clonic seizures. These results suggest that the postictal antinociception depends on the PPTN neuronal cells integrity.
Asunto(s)
Analgesia , Ácido Iboténico/toxicidad , Núcleo Tegmental Pedunculopontino/fisiología , Convulsiones/fisiopatología , Animales , Ácido Iboténico/administración & dosificación , Masculino , Microinyecciones , Dimensión del Dolor , Pentilenotetrazol/farmacología , Ratas , Convulsiones/inducido químicamente , Factores de TiempoRESUMEN
The ability to react fast and efficiently in threatening situations is paramount for the survival of organisms and has been decisive in our evolutionary history. Defense mechanisms in primates rely on the fast recognition of potential predators and facial expressions of conspecifics. The neural circuitry responsible for the detection of threat is generally thought to be centered on the amygdala. Although it is a pivotal structure in the processing of emotional stimuli, the amygdala does not seem necessary for the early stages of this process. Here we show that bilateral neurotoxic lesions of the superior colliculus in infant capuchins monkeys impaired the recognition of a rubber-snake in a threat-reward conflict task. Lesioned monkeys were uninhibited by a snake in a food-reward retrieval task. Lack of inhibition in the task was observed over the course of 15 weeks. The long lasting recognition impairment of a natural predator observed here is similar to the tameness aspects of Kluver-Bucy syndrome, indicating an important role of this structure in threat recognition.
Asunto(s)
Conflicto Psicológico , Reacción de Fuga/fisiología , Conducta Alimentaria/fisiología , Inhibición Psicológica , Recompensa , Colículos Superiores/fisiopatología , Animales , Cebus , Modelos Animales de Enfermedad , Reacción de Fuga/efectos de los fármacos , Miedo/fisiología , Humanos , Ácido Iboténico/administración & dosificación , Ácido Iboténico/toxicidad , Instilación de Medicamentos , Síndrome de Kluver-Bucy , Neurotoxinas/administración & dosificación , Neurotoxinas/toxicidad , Reconocimiento Visual de Modelos , Tiempo de Reacción/fisiología , Serpientes , Colículos Superiores/efectos de los fármacos , Colículos Superiores/crecimiento & desarrolloRESUMEN
Medial prefrontal cortex (MPFC) damage causes profound behavioral and neuroendocrine alterations. However, many reports have been inconsistent regarding the direction of these effects. We hypothesized that the lesion recovery stage might be a key factor generating discrepancies. To examine changes over time following ibotenic acid lesion in the ventral part of the MPFC, behavioral and endocrine testing was conducted on the second and the fifth week after lesioning. On the second post-lesion week, bilaterally lesioned animals increased social interaction and swimming scores and their corticosterone response to restraint was exaggerated as compared with shams. On the fifth post-lesion week, social interaction and swimming scores were diminished in bilaterally lesioned animals; their basal plasma corticosterone was enhanced, while their corticosterone increase under restraint was blunted relative to shams. These results reveal that the emotional and endocrine responses to stress vary as a function of time following MPFC lesion, which may help to reconcile conflicting reports on effect direction. The role of the MPFC in anxiety, ability to cope with stress and adrenal regulation is also discussed.
Asunto(s)
Ansiedad/fisiopatología , Conducta Animal/fisiología , Lesiones Encefálicas/fisiopatología , Animales , Conducta Animal/efectos de los fármacos , Lesiones Encefálicas/inducido químicamente , Corticosterona/sangre , Lóbulo Frontal/efectos de los fármacos , Lóbulo Frontal/fisiopatología , Ácido Iboténico/administración & dosificación , Ácido Iboténico/farmacología , Inyecciones Intraventriculares , Masculino , Ratas , Ratas Wistar , Estrés Psicológico/fisiopatología , Natación , Factores de TiempoRESUMEN
We investigated the influence of ibotenic acid lesions of the medial hypothalamus (MH) on salt appetite and arterial blood pressure responses induced by angiotensinergic and adrenergic stimulation of the median preoptic nucleus (MnPO) of rats. Previous injection of the adrenergic agonists norepinephrine, clonidine, phenylephrine, and isoproterenol into the MnPO of sham MH-lesioned rats caused no change in the sodium intake induced by ANG II. ANG II injected into the MnPO of MH-lesioned rats increased sodium intake compared with sham-lesioned rats. Previous injection of clonidine and isoproterenol increased, whereas phenylephrine abolished the salt intake induced by ANG II into the MnPO of MH-lesioned rats. Previous injection of norepinephrine and clonidine into the MnPO of sham MH-lesioned rats caused no change in the mean arterial pressure (MAP) induced by ANG II. Under the same conditions, previous injection of phenylephrine increased, whereas isoproterenol reversed the increase in MAP induced by angiotensin II (ANG II). ANG II injected into the MnPO of MH-lesioned rats induce a decrease in MAP compared with sham-lesioned rats. Previous injection of phenylephrine or norepinephrine into the MnPO of MH-lesioned rats induced a negative MAP, whereas pretreatment with clonidine or isoproterenol increased the MAP produced by ANG II injected into the MnPO of sham- or MH-lesioned rats. These data show that ibotenic acid lesion of the MH increases the sodium intake and pressor responses induced by the concomitant angiotensinergic, alpha 2 and beta adrenergic activation of the MnPO, whereas alpha 1 activation may have opposite effects. MH involvement in excitatory and inhibitory mechanisms related to sodium intake and MAP control is suggested.
Asunto(s)
Presión Sanguínea/efectos de los fármacos , Ingestión de Alimentos/fisiología , Agonistas de Aminoácidos Excitadores/toxicidad , Hipotálamo Medio/fisiología , Ácido Iboténico/toxicidad , Área Preóptica/fisiología , Sodio en la Dieta , Agonistas Adrenérgicos/farmacología , Angiotensina II/farmacología , Animales , Agonistas de Aminoácidos Excitadores/administración & dosificación , Hipotálamo Medio/anatomía & histología , Hipotálamo Medio/efectos de los fármacos , Ácido Iboténico/administración & dosificación , Inyecciones , Masculino , Área Preóptica/anatomía & histología , Área Preóptica/efectos de los fármacos , RatasRESUMEN
Both the lesion of the parvocellular region of the PVN (FIG. 1) and the acute reduction of OT synthesis in that nucleus (FIG. 2) increase maternal aggression in rats. Previous work showed that ibotenic acid as well as the OT antisense in the PVN reduced the level of OT in the brainstem, but not in the pituitary. Therefore, the oxytocinergic parvocellular neurons of the PVN appear to exert an inhibitory effect on the aggressive behavior of the lactating female rat against an adult intruder. In a relationship of a different nature, mother-infant, a facilitatory effect of OT has been shown. Previous work showed a significant decrease of OT mRNA levels in the PVN of female rats during the first 10 days after delivery compared to late pregnancy, which is the inverse ratio of the natural temporal evolution of maternal aggressive behavior. Furthermore, in the present work, a functional decrease of OT mRNA was probably the effect of the antisense in the PVN. In conclusion, OT cells in the PVN appear to play different roles on maternal care and maternal aggression.
Asunto(s)
Agresión , Conducta Materna , Oligonucleótidos Antisentido/farmacología , Oxitocina/fisiología , Núcleo Hipotalámico Paraventricular/fisiología , Animales , Femenino , Ácido Iboténico/administración & dosificación , Ácido Iboténico/farmacología , Lactancia , Masculino , Microinyecciones , Oligodesoxirribonucleótidos/administración & dosificación , Oligodesoxirribonucleótidos/farmacología , Oligonucleótidos Antisentido/administración & dosificación , Oxitocina/biosíntesis , Núcleo Hipotalámico Paraventricular/efectos de los fármacos , Embarazo , RatasRESUMEN
We attempted to evaluate the effects of bilateral injection of ibotenic acid (IA) into the nucleus basalis magnocellularis (nbm) of rats as well as the potential recovery mediated by the infusion of nerve growth factor (NGF). The lesion caused an impairment of learning and memory processes. Also, a severe depletion of choline acetyl transferase activity was detected in cortical areas. After the NGF administration, a significant reversion of these functional changes was observed. Thus, IA-lesioned rats might serve as a model for the evaluation of neurotrophic factors actions on basal forebrain damaged neurons.