The arterial circle described by Willis, and the contribution of his predecessors / O círculo arterial descrito por Willis e a contribuição de seus predecessores

The description of arteries at the base of the human brain forming an 'arterial circle', named after Thomas Willis, has had a long history after the restoration of human dissection, partly due to the studies of many outstanding anatomists that preceded Willis. He provided, with the collaboration of Richard Lower and Christopher Wren, the first incontestable complete description, as recognized nowadays, accompanied by a superb illustration. Additionally, he presented an explanation for its meaning, indicating for the first time the functional significance of this structure, in health and disease. However, it should be recognized that the initial studies of the arteries of the base of the human brain by Willis' predecessors, as well as those from ancient times, despite their fragmentary descriptions, were certainly pivotal in paving the way for further and more detailed knowledge of this vascular formation.

A descrição das artérias da base do cérebro humano, formando um 'círculo arterial', designado com o nome de Thomas Willis, tem uma longa história após o restauro de dissecções humanas, em parte devido aos estudos de muitos anatomistas de renome que precederam Willis. Ele proveu, com a colaboração de Richard Lower e Christopher Wren, a primeira descrição completa e incontestável, assim como a reconhecida atualmente, acompanhada por uma ilustração soberba. Adicionalmente, apresentou uma explicação quanto ao seu significado, indicando pela primeira vez a importância funcional dessa estrutura, na saúde e na doença. Entretanto, deve ser reconhecido que os estudos iniciais das artérias da base do cérebro humano pelos predecessores de Willis, assim como os de tempos antigos, apesar de suas descrições fragmentárias, certamente foram fulcrais na pavimentação do caminho para o conhecimento mais avançado e detalhado dessa formação vascular.

Sound-sensitive neurons innervate the ventro-lateral protocerebrum of the heliothine moth brain.

Many noctuid moth species perceive ultrasound via tympanic ears that are located at the metathorax. Whereas the neural processing of auditory information is well studied at the peripheral and first synaptic level, little is known about the features characterizing higher order sound-sensitive neurons in the moth brain. During intracellular recordings from the lateral protocerebrum in the brain of three noctuid moth species, Heliothis virescens, Helicoverpa armigera and Helicoverpa assulta, we found an assembly of neurons responding to transient sound pulses of broad bandwidth. The majority of the auditory neurons ascended from the ventral cord and ramified densely within the anterior region of the ventro-lateral protocerebrum. The physiological and morphological characteristics of these auditory neurons were similar. We detected one additional sound-sensitive neuron, a brain interneuron with its soma positioned near the calyces of mushroom bodies and with numerous neuronal processes in the ventro-lateral protocerebrum. Mass-staining of ventral-cord neurons supported the assumption that the ventro-lateral region of the moth brain was the main target for the auditory projections ascending from the ventral cord.

Ablation of the sphenopalatine ganglion does not attenuate the infarct reducing effect of vagus nerve stimulation.

Electrical stimulation of the cervical vagus nerve reduces infarct size by approximately 50% after cerebral ischemia in rats. The mechanism of ischemic protection by vagus nerve stimulation (VNS) is not known. In this study, we investigated whether the infarct reducing effect of VNS was mediated by activation of the parasympathetic vasodilator fibers that originate from the sphenopalatine ganglion (SPG) and innervate the anterior cerebral circulation. We examined the effects of electrical stimulation of the cervical vagus nerve in two groups of rats: one with and one without SPG ablation. Electrical stimulation was initiated 30 min after induction of ischemia, and lasted for 1h. Measurement of infarct size 24h later revealed that the volume of ischemic damage was smaller in those animals that received VNS treatment (41.32±2.07% vs. 24.19±2.62% of the contralateral hemispheric volume, n=6 in both; p<0.05). SPG ablation did not abolish this effect; the reduction in infarct volume following VNS was 58% in SPG-damaged animals, 41% in SPG-intact animals (p>0.05). In both SPG-intact and SPG-damaged animals VNS treatment resulted in better motor outcome (p<0.05 vs. corresponding controls for both). Our findings show that VNS can protect the brain against acute ischemic injury, and that this effect is not mediated by SPG projections.