Ann Silver

Confirmation from choline acetylase analyses of a massive cholinergic innervation to the rat hippocampus

1. Unilateral lesions were made in the fimbria of adult rats with a stereotaxically‐applied, radio‐frequency current. After 3‐23 days survival, fresh, unfixed, transverse sections were cut of the forebrain. Half the sections were stained histochemically to show the distribution of acetylcholinesterase (AChE) activity. From the other sections, small, anatomically defined areas were dissected out and assayed for choline acetylase (ChAc) activity (acetyl‐CoA: choline‐O‐acetyltransferase EC2.3.1.6).

Fall in blood pressure produced from discrete regions of the ventral surface of the medulla by glycine and lesions

1. In cats anaesthetized with pentobarbitone sodium, atropinized by i.v. atropine methyl nitrate and artificially ventilated, experiments were carried out (a) to localize the site where glycine acts on the ventral surface of the medulla when, on topical application through paired Perspex rings caudal to the trapezoid bodies, it produces a fall in arterial blood pressure, (b) to compare the effects of uni‐ and bilateral application, and (c) to study the blood pressure effects produced by electrolytic lesions of the glycine‐sensitive areas.

The spontaneous release of acetylcholine from the denervated hemidiaphragm of the rat

Brooks (1954) has shown that acetylcholine (ACh) is released from the isolated guinea-pig diaphragm in the absence of nerve stimulation. A comparable resting release has been found in the rat diaphragm by Straughan (1960) and by Krnjevid & Mitchell (1961). Furthermore, in two preliminary experiments Straughan (1960) could detect no great difference between the release from a rat hemidiaphragm denervated by phrenic nerve section 7 days previously, and that from the contralateral control hemidiaphragm acutely denervated at the time of the experiment; he suggested, therefore, that the ACh originated in some non-nervous tissue. Krnjevid & Mitchell (1961), on the other hand, considered it possible that the resting release might represent the ACh responsible for the production of miniature end-plate potentials (m.e.p.p.s). In the work to be described two types of experiment were done. In the first the ACh release from hemidiaphragms which had been denervated for different periods was compared with the release from the corresponding control hemidiaphragms, to determine whether or not the release was altered by chronic phrenic nerve section. In the second series of experiments measurements were made of the spontaneous release of ACh from rat hemidiaphragms subjected to alterations in the potassium concentration or in the temperature of the bathing fluid; these are procedures which are known to alter the m.e.p.p. frequency (Liley, 1956a, c). No attempt was made to measure m.e.p.p.s in either type of experiment; but it should be mentioned that Liley (1956a) could record no m.e.p.p.s from the rat hemidiaphragm from about 18 hr after denervation until the time when the motor nerve terminals were re-established. On the other hand, Katz & Miledi (1959), working on the frog sartorius, found that while the m.e.p.p.s disappeared 3-4 days after denervation, activity was resumed at a much reduced frequency some days later.

Acetylcholine and choline acetyltransferase in the diaphragm of the rat

Although we know that skeletal muscle and many peripheral nerves contain acetylcholine (ACh) and exhibit choline acetyltransferase (ChAc) activity (acetyl-CoA:choline-O-acetyltransferase, EC 2.3.1.6), there is little evidence about how these components are distributed within a muscle. This is of some interest since it has been claimed that the spread of activity along the muscle fibres depends upon a cholinergic mechanism (Nachmansohn, 1959, 1963). If that is the case one might expect to find an even distribution of ACh and ChAc throughout the tissue without any great accumulation in the regions where motor nerve fibres and their endings are situated; particularly if neuromuscular transmission is not mediated by ACh, as is believed by the same author. To investigate this problem, we have examined the gross distribution of ACh and ChAc activity in the rat diaphragm, comparing the zone of innervation with the remainder of the muscle. In addition, we have estimated the ACh content and ChAc activity in the phrenic nerve. A preliminary account of these observations has been given at the 2nd International Pharmacological Meeting (Krnjevic, 1964).

The distribution of cholinesterases in the cat carotid body

1. The distribution of acetyl‐ and butyrylcholinesterase in the carotid body of the cat has been examined histochemically. Studies were made on normal carotid bodies and on carotid bodies from cats in which certain nerves had been cut some time previously. The nerves sectioned were the sinus nerve, the post‐ganglionic sympathetic branch of the superior cervical ganglion or the preganglionic cervical sympathetic trunk.

Electrophoresis in Neuropathology

Agar Gel Electrophoresis in NeurologyBy A. Lowenthal. Pp. 204. (Amsterdam, New York and London: Elsevier Publishing Co., 1964.) 60s.