Biomedical subjects

S Yatsugi

Publications and source records attributed to S Yatsugi.

24 records · Page 2Linked to original sources

PubMed1991

Anticonvulsive properties of YM-14673, a new TRH analogue, in amygdaloid-kindled rats.

Effects of YM-14673 (N alpha-[( (S)-4-oxo-2-azetidinyl]-carbonyl]-L- prolinamide dihydrate), a new TRH analogue, on the development of kindling and the duration of afterdischarge (AD) were observed in amygdaloid-kindled rats in comparison with those of TRH. The right medial amygdaloid nucleus was electrically stimulated once a day for establishment of kindling. YM-14673 and TRH were administered intraperitoneally 15 and 30 min prior to electrical stimulation from 2 days after the first stimulation, respectively, and the number of stimulations required for the development of generalized seizures was measured. YM-14673 (1 mg/kg) showed tendency to suppress the development of kindling (p less than 0.1), but TRH even at high dose (10 mg/kg) showed little effect on it. In addition, the experiment for the AD duration was conducted in full-kindled rats from one day after at least 3 reproducible generalized seizures were elicited by electrical stimulation of the medial amygdaloid nucleus once a day. Both YM-14673 (1 mg/kg) and TRH (10 mg/kg) administered 15 and 30 min prior to electrical stimulation of the amygdala, respectively, significantly shortened the AD duration in full-kindled rats. At these doses, both drugs desynchronized spontaneous cortical electroencephalogram (EEG) in normal rats. These results indicate that YM-14673 seems to possess anticonvulsive property in rats.

Amygdala↗

PubMed1990

Minaprine improves impairment of working memory induced by scopolamine and cerebral ischemia in rats.

Using a repeated acquisition procedure in a three-panel runway apparatus, the effects of minaprine on the impairment of working memory produced by scopolamine, ethylcholine aziridinium ion (AF64A) or cerebral ischemia were investigated in rats. Minaprine (3.2-32 mg/kg IP) as well as idebenone (10-100 mg/kg IP) and physostigmine (0.1-0.32 mg/kg IP) dose-dependently reduced the increase of errors (pushes made on the two incorrect panels located at each choice point) induced by 0.56 mg/kg IP scopolamine. Cerebral ischemia for 5 min caused a significant increase of errors in the runway task. Minaprine at 3.2 and 10 mg/kg administered IP immediately after blood recirculation and again 30 min before the runway test conducted 24 h after ischemia, significantly reduced increases in errors expected to occur after 5 min of ischemia. Physostigmine 0.1 mg/kg similarly attenuated the increase in errors in ischemic rats. However, minaprine at doses up to 32 mg/kg IP failed to reduce the increase of errors induced by AF64A 2.5 nmol injected into the dorsal hippocampus. These findings suggest that minaprine exerts an ameliorating effect on amnesia produced by scopolamine and cerebral ischemia, probably through mediation of its stimulant action on central cholinergic systems.

Animals↗

PubMed1989

Effect of S-adenosyl-L-methionine on impairment of working memory induced in rats by cerebral ischemia and scopolamine.

A repeated acquisition procedure in a 3-panel runway apparatus was used to investigate the effects to S-adenosyl-L-methionine (SAM) on impairment of working memory produced either by cerebral ischemia or by scopolamine in rats. Cerebral ischemia (2-10 min) produced duration-dependent increases in the number of errors (pushes made on the two incorrect panels located at each choice point) and increased latency (time before the rat reached the goal box). The increase in errors induced by a 5 or 10 min period of ischemia decreased gradually in subsequent training sessions, returning to the control levels in 6 days. The increases in both errors and latency induced by 5 min of ischemia were significantly reduced by 100 and 180 mg/kg SAM administered i.p. immediately after blood recirculation and 1 h before a test conducted 24 h after ischemia. SAM at doses up to 180 mg/kg nevertheless failed to reduce the increases in errors and latency if they were induced by 0.56 mg/kg of scopolamine. These results suggest that SAM has a beneficial effect on memory that has been impaired by cerebral ischemia.

Animals↗

PubMed1989

Inhibition of mouse-killing behavior by S-adenosyl-L-methionine in midbrain raphe-lesioned and olfactory-bulbectomized rats.

The effect of S-adenosyl-L-methionine (SAM), a methyl donor, on mouse-killing behavior in rats with lesions of the midbrain raphe nuclei and in olfactory-bulbectomized rats was investigated. Systemic administration of SAM at doses of 180 and 320 mg/kg IP caused a significant inhibition of both kinds of mouse-killing behavior. The inhibitory effects of SAM on both types of mouse-killing behavior were almost equipotent. Microinjection of SAM at 10-100 micrograms/rat into the lateral ventricle also inhibited mouse-killing behavior induced by raphe lesions in a dose-dependent manner. The ED50 value of SAM for this effect was 38.6 (18.4-81.4) micrograms/rat. It is concluded that SAM has inhibitory effects on mouse-killing behavior in both raphe-lesioned and olfactory-bulbectomized rats through a site of action in the central nervous system.

Animals↗

PubMed1988

Involvement of the medial amygdaloid nucleus in the action of imipramine in rats subjected to the forced swimming test.

A forced swimming test proposed by Porsolt is a useful method for screening antidepressants. To evaluate drug effects more objectively, vibration of the walls of a water tank caused by the escape behavior of the rat was recorded. Imipramine (IMI) increased the number of vibration and this effect was observed in the medial amygdala lesioned rat but not in the central or basolateral amygdala lesioned rat. The present result suggests that the medial amygdala is an important site of action of IMI.

Amygdala↗

PubMed1988

A new method for studying working memory by using the three-panel runway apparatus in rats.

We designed a new method for studying working memory, by using a repeated acquisition procedure in the three-panel runway apparatus. This apparatus is composed of a start box, a goal box and four consecutive choice points; each choice point consists of three panel gates. Male Wistar rats were trained with 6 consecutive trials (one session) per day. Each trial was performed every two minutes. In this apparatus, rats could pass through only one gate (correct gate) among three panel gates in the direction of the goal box and were given 100 mg food pellets as the positive reinforcement. The sequence of correct gate position in each rat was changed everyday, but not in each session. Error responses (pushing the incorrect gate) were gradually reduced as training was repeated, and the learning was established within 16 training sessions to achieve criterion performance. Intraperitoneal scopolamine and intrahippocampal ethylcholine aziridinium ion (AF64A) produced increases in both the number of errors and the latency in a dose-dependent manner. The increase in errors induced by AF64A did not return to the control level, though the prolonged latency returned to normal. As a conclusion, this experimental procedure using the three-panel runway apparatus would be a useful method for studying working memory, and its memory deficit is involved at least in the dysfunction of the cholinergic system in the hippocampus.

Animals↗