Protein metabolism in the rat cerebral cortex in vivo and in vitro as affected by the acquisition enhancing drug piracetam

The effect of Piracetam on rat cerebral protein metabolism in vivo and in vitro was studied. It was found that the drug stimulates the uptake of labelled leucine by cerebral cortex slices, has no effect on the incorporation of leucine into cerebral protein, neither in slices nor in vivo, but inhibits the breakdown of newly formed protein in slices. Chemicals/CAS: piracetam, 7491-74-9; protein, 67254-75-5; Leucine, 61-90-5; Nerve Tissue Proteins; Piracetam, 7491-74-9; Pyrrolidinone

On the oscillatory decay of the myotonic action of 9 anthroic acid. Influence of cholinesterase inhibition

The effects of the myotonic agent, 9-anthroic acid (ANCA), and the acetylcholinesterase (AChE) inhibitor, soman, on the isolated phrenic nerve-diaphragm preparation of the rat were studied. ANCA induced after-contractions which followed the twitches evoked by either direct or indirect stimulation. In the intermittently stimulated muscle the height of the after-contractions decreased rather rapidly and in an oscillatory fashion. The maximum height of each after-contraction was attained after the twitch had reached its peak. AChE inhibition changed the shape of these after-contractions in the indirectly, but not in the directly stimulated diaphragm. After AChE inhibition, the after-contractions decreased more slowly and in a non-oscillatory manner. Similar phenomena were observed in vivo in the gastrocnemius-soleus muscles. The effects of ANCA in the AChE-inhibited and in the non-inhibited diaphragm could be mimicked by incubation in low chloride media. Addition of ouabain to the non-inhibited diaphragm treated with ANCA, caused an immediate and striking enhancement followed by a rapid loss of the after-contractions, whereas the twitches remained fairly constant. In the AChE-inhibited diaphragm treated with ANCA, ouabain caused no increase but only a rapid and complete decay of the after-contractions with a decrease of the twitches. It is suggested that after inhibition of the AChE in the ANCA-treated muscle fibre, the site of initiation of the repetitive action potentials which cause the after-contractions shifts from the transverse tubular system to the motor end-plate. Moreover, it is suggested that the sodium pump is involved in the gradual decay of the myotonic action of ANCA. Chemicals/CAS: 9 anthroic acid, 723-62-6; acetylcholinesterase, 9000-81-1; curare, 8063-06-7; ouabain, 11018-89-6, 630-60-4; soman, 96-64-0; Anthracenes; Calcium, 7440-70-2; Carboxylic Acids; Chlorides; Cholinesterase Inhibitors; Magnesium, 7439-95-4; Ouabain, 630-60-4; Potassium, 7440-09-7; Sodium, 7440-23-5; Soman, 96-64-

Age-related acquisition deficits and activity in rats

Spontaneous motor activity and physically undemanding conditioned suppression of drinking behavior were assessed in rats of 3, 12, 18 or 30 months (M) age. Initial spontaneous motor activity of 12 M rats was as low as that of 30 M rats and both were significantly lower than that of 3 M rats. The performance of 3, 12 and 18 M rats were similar to each other, whereas 30 M rats started to perform poorer after one week of training. It is concluded that the acquisition deficits observed here in aged rats occur only after 18 months age and appear to be independent of the subjects' reactivity to punishment and their activity prior to training. © 1976

Changes in rat brain norepinephrine levels and turnover after olfactory bulbectomy

After bilateral olfactory bulbectomy in rats a significant increase of norepinephrine (NE) level in the hypothalamus was found. However, no difference was observed between hypothalamic NE turnover of bulbectomized and sham operated animals. In the amygdaloid cortex the NE level was not affected by bulbectomy. In this area, however, the NE turnover appeared to be decreased after bulbectomy. The latter finding may be related to the deficits in passive avoidance behaviour as found in bulbectomized rats