Cartesian representation of stimulus direction: parallel processing by two sets of giant interneurons in the cockroach.

The cockroach Periplaneta americana responds to wind puffs by turning away, both on the ground and when flying. While on the ground, the ventral giant interneurons (ventrals) encode the wind direction and specify turn direction, whereas while flying the dorsal giant interneurons (dorsals) appear to do so. We report here on responses of these cells to controlled wind stimuli of different directions. Using improved methods of wind stimulation and of positioning the animal revealed important principles of organization not previously observed. All six cells of largest axonal diameter on each side respond preferentially to ipsilateral winds. One of these cells, previously thought to respond non-directionally (giant interneuron 2), was found to have a restricted directional response (Fig. 3). The organization of directional coding among the ventral giant interneurons is nearly identical to that among the dorsals (Fig. 2). Each group contains, on each side, one cell that responds primarily to wind from the ipsilateral front, another primarily in the ipsilateral rear, and a third responding more broadly to ipsilateral front and rear. These results are discussed in terms of the mechanisms of directional localization by the assembly of giant interneurons.

[Traumatic asphyxia].

Traumatic asphyxia is a commonly used designation of a syndrome related to severe compressive trauma to the thorax. It is characterized by cranial cyanosis, subconjunctival hemorrhage, vascular engorgement of the head, mucosal petechiae, hemoptysis, esophageal and rectal hemorrhage, hematuria, and varying degrees of cerebral dysfunction. By 1985 approximately 210 cases had been reported world-wide. We present an illustrative case in a 24-year-old man.

Somatostatin-like immunoreactivity in a subpopulation of nerve terminals in frog sympathetic ganglia.

A somatostatin-like substance was observed specifically in a subset of B-type nerve terminals in frog paravertebral ganglia. The middle ganglia (4th and 5th) of the sympathetic chain contained the highest proportions of somatostatin-positive terminals, with decreasing proportions in more caudal or rostral ganglia. Intracellular recordings from the 6th ganglion demonstrated that it contained both B and C neurons. Although prolonged depolarizing potentials were observed in B and C neurons after bursts of stimuli in C-type preganglionic axons, no slow potentials were observed after stimulating somatostatin-positive B-type axons. In addition, no effects of exogenously applied somatostatin were observed on the membrane potentials of B neurons. The present results are compared to a growing list of autonomic systems where peptidergic transmitters appear to have only subtle or no acute electrical consequences on postsynaptic neurons.

The efferent role of sensory axons in nerve-evoked contractions of bullfrog bladder.

The neural input to the frog bladder was characterized in vitro. The nerve-evoked bladder contraction consists primarily of an early parasympathetic cholinergic component and a later, longer-lasting non-adrenergic non-cholinergic component. This slow non-adrenergic non-cholinergic contraction is not only resistant to cholinergic and adrenergic antagonists, but also to H1 and H2 histaminergic antagonists and to the serotoninergic antagonist, methysergide. It is concluded that the non-adrenergic non-cholinergic contraction is mediated by an efferent action of the sensory system because it is resistant to ganglionic nicotinic antagonists and because it is elicited specifically by stimulation of the peripheral cut end of the dorsal root. 5-Hydroxytryptamine is a potent and specific inhibitor of the sensory non-adrenergic non-cholinergic contraction. Although the bladder smooth muscle is innervated by terminals containing a somatostatin-like substance, somatostatin does not cause a bladder contraction. Luteinizing hormone-releasing hormone, enkephalin, histamine, 5-hydroxytryptamine, adenosine and adenosine 5 monophosphate are also unlikely candidates for the non-adrenergic non-cholinergic transmitter because they do not produce bladder contractions and/or their antagonists are ineffective on the nerve-evoked contraction. A putatively sensory network of fibers containing a substance P-like material is located within the wall of the bladder. Substance P produces bladder contractions at concentrations as low as 10(-9) M and so it, or a related substance, is a viable transmitter candidate in this system. Adenosine 5'-triphosphate (ATP)(10(-5) M) also causes a bladder contraction and remains a possible candidate as well. The data demonstrate that the bladder contraction resulting from electrical stimulation of the bladder nerves is due in large part to the "antidromic" stimulation of sensory axons. The likely presence therefore of potent and releasable substances in the peripheral sensory terminals of the bladder suggests that this sensory system may exert significant local, efferent control of bladder smooth muscle (i.e. independent from the central nervous system).

Neurotoxins from Plectreurys spider venom are potent presynaptic blockers in Drosophila.

Studies of presynaptic events in synaptic transmission may be facilitated through the use of specific ligands for functional components of the transmitter release mechanism and through the use of genetics. For this purpose, neurotoxins that affect neuromuscular transmission in Drosophila have been identified and purified from Plectreurys spider venom (PLTX). One class of toxins causes irreversible presynaptic block, probably by blocking calcium entry or by acting on other closely associated processes. These toxins have been highly purified and are peptides of about 7 kDa in molecular weight. They specifically block transmitter release at nanomolar concentrations and may be useful in further biochemical studies.

Sites of action of lead on spontaneous transmitter release from motor nerve terminals.

Lead ions have potent neurotoxic activities. At the neuromuscular junction, they depress the neurally evoked release, but strongly facilitate the spontaneous release of transmitter quanta from motor nerve terminals. The mechanisms underlying the latter action of lead were studied in the isolated frog neuromuscular preparation. The evidence presented in this article is consistent with the hypothesis that lead ions inhibit some membranal and intracellular calcium regulatory mechanisms, consequently producing an increase in the intraterminal concentration of ionized calcium, and hence, in spontaneous transmitter release.