RESUMEN
Posterior thalamic pulvinar nuclei have been implicated in different aspects of spatial attention, but their exact role in humans remain unclear. Most neuropsychological studies of attention deficits after pulvinar lesion have concerned single patients or small samples. Here we examined a group of 13 patients with focal damage to posterior thalamus on a visual search task with faces, allowing us to test several hypotheses concerning pulvinar function in controlling attention to visually salient or emotionally significant stimuli. Our results identified two subgroups of thalamic patients with distinct patterns of attentional responsiveness to emotional and colour features in face targets. One group with lesions located in anterior and ventral portions of thalamus showed intact performance, with a normal facilitation of visual search for faces with emotional (fearful or happy) expressions on both side of space, similar to healthy controls. By contrast, a second group showed a slower and poorer detection of face targets, most severe for neutral faces, but with a paradoxically enhanced facilitation by both colour and emotional features. This second group had lesions centred on the pulvinar, involving mainly the dorso-medial sectors in patients showing enhanced effects of colour features, but extending to more dorso-lateral sectors in those with enhanced effects of emotional features. These findings reveal that pulvinar nuclei are not critical for orienting attention to emotionally or visually salient features, but instead provide new evidence in support of previous hypotheses suggesting an important role in controlling attention in visual scenes with distracting information.
Asunto(s)
Emociones , Expresión Facial , Desempeño Psicomotor , Pulvinar/lesiones , Percepción Visual/fisiología , Adulto , Anciano , Anciano de 80 o más Años , Atención , Percepción de Color , Femenino , Humanos , Imagen por Resonancia Magnética , Masculino , Persona de Mediana Edad , Trastornos de la Percepción , Estimulación Luminosa , Núcleos Talámicos Posteriores/diagnóstico por imagen , Núcleos Talámicos Posteriores/lesiones , Núcleos Talámicos Posteriores/patología , Pulvinar/diagnóstico por imagen , Pulvinar/patología , Tiempo de Reacción , Percepción Social , Campos Visuales , Adulto JovenRESUMEN
The lateral nucleus of the amygdala (LA) is a site of convergence for auditory (conditioned stimulus) and foot-shock (unconditioned stimulus) inputs during fear conditioning. The auditory pathways to LA are well characterized, but less is known about the pathways through which foot shock is transmitted. Anatomical tracing and physiological recording studies suggest that the posterior intralaminar thalamic nucleus, which projects to LA, receives both auditory and somatosensory inputs. In the present study we examined the expression of the immediate-early gene c-fos in the LA in rats in response to foot-shock stimulation. We then determined the effects of posterior intralaminar thalamic lesions on foot-shock-induced c-Fos expression in the LA. Foot-shock stimulation led to an increase in the density of c-Fos-positive cells in all LA subnuclei in comparison to controls exposed to the conditioning box but not shocked. However, some differences among the dorsolateral, ventrolateral and ventromedial subnuclei were observed. The ventrolateral subnucleus showed a homogeneous activation throughout its antero-posterior extension. In contrast, only the rostral aspect of the ventromedial subnucleus and the central aspect of the dorsolateral subnucleus showed a significant increment in c-Fos expression. The density of c-Fos-labeled cells in all LA subnuclei was also increased in animals placed in the box in comparison to untreated animals. Unilateral electrolytic lesions of the posterior intralaminar thalamic nucleus and the medial division of the medial geniculate body reduced foot-shock-induced c-Fos activation in the LA ipsilateral to the lesion. The number of c-Fos labeled cells on the lesioned side was reduced to the levels observed in the animals exposed only to the box. These results indicate that the LA is involved in processing information about the foot-shock unconditioned stimulus and receives this kind of somatosensory information from the posterior intralaminar thalamic nucleus and the medial division of the medial geniculate body.
Asunto(s)
Amígdala del Cerebelo/metabolismo , Condicionamiento Psicológico/fisiología , Electrochoque , Regulación de la Expresión Génica/efectos de la radiación , Núcleos Talámicos Posteriores/fisiología , Proteínas Proto-Oncogénicas c-fos/metabolismo , Animales , Conducta Animal , Mapeo Encefálico , Recuento de Células/métodos , Pie/inervación , Lateralidad Funcional , Masculino , Vías Nerviosas/fisiología , Núcleos Talámicos Posteriores/lesiones , Proteínas Proto-Oncogénicas c-fos/genética , Ratas , Ratas Sprague-DawleyRESUMEN
In the rodent somatosensory system, stimulus information received by the whiskers is relayed to the barrel cortex via two parallel pathways, the lemniscal pathway and the paralemniscal pathway. The lemniscal pathway includes the principal trigeminal nucleus (Pr5) and the ventral posteromedial thalamic nucleus (VPm). The paralemniscal pathway includes the spinal trigeminal subnucleus interpolaris (Sp5i) and the medial division of posterior thalamic nucleus (POm). The purpose of this study was to investigate the roles of those pathways in perceptions of the direction of the single-whisker stimulation in the rat. Rats were trained to perform a go/no-go task that required the discrimination of forward or backward stimulation applied to their single whisker. When a selective lesion was made in VPm or Pr5, error rate for the task performance increased significantly. In contrast, when a selective lesion was made in POm or Sp5i, we found no significant change in performance. These results suggest that the lemniscal pathway plays more important roles in a discrimination of stimulus direction applied to the single whisker.
Asunto(s)
Vías Aferentes/lesiones , Discriminación en Psicología/fisiología , Trastornos de la Percepción/etiología , Vibrisas/inervación , Vías Aferentes/fisiología , Animales , Conducta Animal , Potenciales Evocados/fisiología , Masculino , Modelos Neurológicos , Estimulación Física/métodos , Núcleos Talámicos Posteriores/lesiones , Núcleos Talámicos Posteriores/fisiología , Ratas , Ratas Wistar , Tiempo de Reacción/fisiología , Núcleo Espinal del Trigémino/lesiones , Núcleo Espinal del Trigémino/fisiologíaRESUMEN
Zebra finches utilize neural circuits in both cerebral hemispheres to produce their learned songs. Although direct reciprocal connections do not exist between song control nuclei across hemispheres, premotor activity in these nuclei during singing is precisely and continuously coordinated between the hemispheres. We hypothesized that this interhemispheric coordination is mediated by bilateral feedback projections from medullary and midbrain song control nuclei to the thalamic song control nucleus uvaeformis (Uva). Consistent with our hypothesis, bilateral lesions of Uva severely impaired singing. This impairment was long-lasting, as it persisted for at least 35 days after the lesions. Unilateral lesions of Uva on either side also resulted in an immediate singing impairment. However, song recovered substantially after less than 15 days, suggesting a possible compensation by the unlesioned side. Although the acoustic structure of individual syllables recovered fully after unilateral lesioning, subtle changes in the sequencing of syllables were observed after song recovery, suggesting that the lesion led to an alteration in the functioning of the remaining song control network. These results demonstrate that the adult songbird brain can adjust to damage to certain parts of the song control network and recover from their associated singing deficits. The well-identified and localized central neural pathways mediating birdsong production provide an advantageous model system to analyze systematically the sensorimotor contexts and the specific sites and mechanisms for behavioral recovery following partial damage to a behavior-producing neural circuit.