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The collective efforts of Australasian neuroscientists over the past 50 years to forge a binational presence are reviewed in this article. The events in the 1970s leading to the formation of an informal Australian Neurosciences Society are discussed in the context of the international emergence of neuroscience as an interdisciplinary science. Thereafter, the establishment in 1980 of the Australian Neuroscience Society, subsequently renamed as the Australasian Neuroscience Society (ANS), is described. The achievements of ANS—including its active role in developing national, regional, and global cooperation to promote neuroscience—are chronicled over successive decades, followed by a discussion of the future challenges facing the society and its associated neuroscience institutions. [ABSTRACT FROM AUTHOR]

In patients with high thoracic spinal lesions that remove most of the central drive to splanchnic preganglionic neurons, visceral or nociceptive stimuli below the lesion can provoke large increases in blood pressure (autonomic dysreflexia). We have examined the effects of [T.sub.4] spinal transection on isometric contractions of mesenteric arteries isolated from spinalized rats. Nerve-evoked contractions involved synergistic roles for norepinephrine and ATP. At 7 wk after spinal transection, responses to perivascular stimulation at 1-5 Hz were enhanced five-fold, whereas the [[alpha].sub.1]-adrenoceptor antagonist prazosin (10 nM) produced a twofold larger reduction in contraction (to 20 pulses at 10 Hz) than in unoperated controls. In contrast, the reduction in nerve-evoked contractions by the P2-purinoceptor antagonist suramin (0.1 mM) and the responses to the P2-purinoceptor agonist [alpha],[beta]-methylene ATP or to high [K.sup.+] concentration did not greatly differ between groups, indicating that arteries from spinalized rats were not generally hyperreactive. Sensitivity to the [[alpha].sub.1]-adrenoceptor agonist phenylephrine was enhanced in arteries from spinalized rats, and the difference from controls was abolished by the norepinephrine uptake blocker desmethylimipramine. Sensitivity to the [[alpha].sub.1]-adrenoceptor agonist methoxamine, which is not a substrate for the neuronal norepinephrine transporter, was similar among the groups. Thus the increased neurally evoked response after spinal transection appeared to be due to a reduction in neuronal uptake of released norepinephrine, a mechanism that did not explain the enhanced response of tail arteries after spinal transection that we previously reported. The findings provide further support for potentiated neurovascular responses contributing to the genesis of autonomic dysreflexia. neurovascular transmission; vascular reactivity; spinal cord injury; sympathetic nerve; autonomic dysreflexia

An experiment conducted with rats revealed that noradrinergic axons sprout around the dorsal root ganglia as a result of peripheral nerve injury. These axons developed unique connections with nearby sensory neurons, an event which could account for the discharge observed after nerve damage. This form of contralateral sprouting is unique because the axons chose to target axotomized neurons.

The sympathetic nervous system forms part of the autonomic nervous system, which is responsible for the regulation of all tissue and organ functions except those of the skeletal muscle fibers. Results from early studies on the system have created a purely neuroendocrine view of its functions. However, studies using various neuroscientific techniques and analyzing the system from a molecular, cellular and integrative perspective have established the existence of specialized characteristics of its functional pathways. These findings reveal the inadequacy of a purely neuroendocrine concept of the system.