The results confirm that "hot" tonsillectomy techniques carry a substantially elevated risk of postoperative hemorrhage when diathermy is used as a dissection tool in tonsillectomy.

Neuronal nicotinic ␣7 acetylcholine receptors (␣7nAChRs) are expressed primarily in the brain and are implicated in modulating many cognitive functions (e.g., attention, working and episodic memory). Not surprisingly, much effort has been committed to the development of molecules acting at ␣7nAChRs as potential therapies for a variety of central nervous system diseases (e.g., Alzheimer's). N-[(3S)-1-azabicyclo[2.2.2]oct-3-yl]-1H-indazole-3-carboxamide hydrochloride (RG3487) binds potently to the human ␣7nAChR (K i ϭ 6 nM), in which it acts as a partial agonist (63-69% of acetylcholine) as assessed by whole-cell patch-clamp recordings in both oocytes and QM7 cell lines. RG3487 activates human ␣7nAChRs with an EC 50 of 0.8 M (oocytes) and 7.7 M (QM7 cells). RG3487 also exhibits antagonist properties at the serotonin 3 receptor [IC 50 ϭ 2.8 nM (oocytes), 32.7 nM (N1E-115 cells)]. In vivo, RG3487 improved object recognition memory in rats after acute [minimally effective dose (MED) 1.0 mg/kg p.o.] or repeated (10 day) administration at brain and plasma concentrations in the low-nanomolar range. Spatial learning deficits in age-impaired rats were reversed after RG3487 administration (MED: 0.03 mg/kg i.p.) as evaluated in the Morris water maze task. In the prepulse inhibition (PPI) of startle model of sensorimotor gating, RG3487 improved apomorphine-induced deficits in PPI performance (MED: 0.03 mg/kg i.p.) and reversed phencyclidine-induced impairments in an attentional set-shifting model of executive function (MED: Յ0.03 mg/kg i.p.). Cumulative evidence from these studies indicates RG3487 is a novel and potent ␣7nAChR partial agonist that improves cognitive performance and sensorimotor gating.

SUMMARY1. The existence and functional significance of Na channels in pancreatic fl-cell membranes were investigated by studying the effects of the plant alkaloid veratridine on the temporal release of insulin from perfused isolated rat islets of Langerhans.2. 100 /SM veratridine evoked a sustained threefold increase in insulin release which was almost completely inhibited by 3 /LM tetrodotoxin (TTX). This action of TTX was rapidly reversible.3. The simultaneous presence of 100 /tM propranolol, 100 /LM phenoxybenzamine and 10/M atropine did not alter the magnitude of the response to 100 #UM veratridine, indicating that the action of veratridine on the fl-cells was direct and was not mediated via the release of neurotransmitters from nerve endings within the islets.4. 45Ca uptake by isolated islets in static incubation was increased almost threefold by 100 ItM veratridine. This increase was completely inhibited by the simultaneous presence of 3 /LM TTX.5. Replacement of Nao by choline caused a transient fourfold increase in insulin release which was associated with an increase in the uptake of 45Ca from the extracellular space of similar magnitude. Subsequent exposure of islets to 100 /tM veratridine still evoked some insulin release but this only achieved 32 % of that secreted by islets exposed to veratridine in medium of normal [Na]0. 6. The addition of 2-5 mm CoCl2 to the medium caused a 62 5 % inhibition of veratridine-mediated insulin release.7. In Ca-free medium supplemented with 1 mm EGTA, 100 fUM veratridine evoked insulin release of equal magnitude and of similar temporal relationship to that obtained in the presence of normal [Ca]0. [Ca]i by altering the equilibria of intracellular Casequestering mechanisms. The small but significant reduction of glucosemediated insulin release by TTX indicates that glucose has a rather weak action on the Na channel and a more pronounced effect on the voltagedependent (o2+-blockable Ca channel.

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