1. Intracellular recordings were obtained from seventy-two magnocellular neurosecretory cells (MNCs) confirmed the presence of an apamin-sensitive Ca2+-dependent K+ current.5. Application of apamin produced a threefold increase in the mean firing rate of spontaneously active cells, but was without effect when applied to silent cells (firing rate < 0 5 Hz). 6. Apamin did not affect the ability of MNCs to fire in a phasic manner but caused a dramatic increase in the mean intraburst firing rate. Moreover, inhibition of 'AHP by apamin strongly attenuated spike accommodation normally seen at the onset of phasic bursts. 7. While apamin did not enhance the amplitude of depolarizing after-potentials following single spikes, post-train plateau potentials and associated after-discharges were enhanced. 8. The possible consequences of IAHP modulation are discussed in the context of the regulation of firing rate and pattern in MNCs.

Substance P and choline acetyltransferase have been localised in a small proportion of endothelial cells of rat coronary arteries using electron microscopic immunocytochemistry. During a hypoxic period of 1 min, coronary vasodilatation was produced in the Langendorff heart preparation and increased levels of substance P and acetylcholine were released into the perfusate. The possibility that these substances are released from endothelial cells during hypoxia and contribute to the hyperaemic response is discussed.

1The effect of the A2A adenosine receptor agonist, 2-p-(-2-carboxyethyl)phenethyl-amino-5'-Nethylcarboxamidoadenosine (CGS 21680) on the potassium evoked release of [3H]-y-aminobutyric acid ([3H]-GABA) from nerve terminals derived from the caudate-putamen and the globus pallidus of the rat was compared. In both preparations CGS 21680 (1 nM) inhibited the [3H]-GABA release evoked by 15 mM KCI but had no effect on that evoked by 30 mM KCl. 2 The ability of CGS 21680 (1 nM) to inhibit the release of [3H]-GABA from striatal nerve terminals was unaffected by the presence of the GABA receptor antagonists, bicuculline (10 gM), phaclofen (1001iM) and 2-hydroxysaclofen (100ZtM). Similarly the opioid receptor antagonist, naloxone (10 fiM), the adenosine Al receptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 40 nM), and the cholinoceptor antagonists, mecamylamine (10 lM) and atropine (100 nM) had no effect on this inhibition. 5 It is concluded that the A2A adenosine receptor is present on both GABAergic and cholinergic nerve terminals of the rat striatum and that in both the caudate-putamen and the globus pallidus this receptor inhibits [3H]-GABA release. No evidence was seen for a difference in the ligand binding sites of this receptor in the two groups of nerve terminals.

α‐Adrenoceptor antagonists (prazosin or phentolamine) reduced the contractile response to field stimulation of the isolated vasa deferentia of guinea‐pig, rat and mouse. α, β‐Methylene ATP (α, β‐MeATP) reduced that portion of the contraction which was resistant to α‐adrenoceptor blockade. α, β‐MeATP (1–800 μM) did not affect action potential conduction in the guinea‐pig vas deferens nerves, and (up to 10 μM) did not reduce the stimulation‐evoked overflow of [3H]‐noradrenaline from this tissue. Spontaneous excitatory junction potentials (s.e. j.ps) in the majority of cells of guinea‐pig, rat, and mouse vasa were abolished by α, β‐MeATP (0.1–10 μM). In a small number of cells s.e.j.ps were resistant to the actions of α, β‐MeATP (10 μM). Excitatory junction potentials (e.j.ps) in the majority of cells in vasa of all species studied were abolished by α, β‐MeATP (1–10 μM). E.j.ps elicited in some ‘resistant’ cells demonstrated marked facilitation characteristics. It is concluded that α, β‐MeATP inhibits s.e.j.ps and e.j.ps by a postjunctional action. In all species pretreatment of animals with 6‐hydroxydopamine produced a marked reduction in noradrenaline (NA) content (as determined by fluorescence histochemistry) and abolished e.j.ps, findings which suggest that e.j.ps originated from sympathetic nerves. The results support the hypothesis that NA and ATP are co‐transmitters in the sympathetic nerves of rodent vasa.