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At least 145 records · Page 8Linked to original sources
PubMed1991

[Effect of intraventricular injection of somatostatin on pain threshold, and contents of the monoamines, xanthine, hypoxanthine in rats brain].

Using HPLC with electrochemical detection, we found that icv somatostatin (Som) 5 or 10 micrograms increased rat's pain threshold and contents of 5-HT and 5-HIAA in hippocampus, hypothalamus and brainstem, except the 5-HIAA content of brainstem in Som 5 micrograms group. However, the changes of NE among above three areas of brain were different, the NE contents of hypothalamus and brainstem significantly increased while that of hippocampus markedly decreased. After icv Som 20 micrograms, hypoxanthine and xanthine in hippocampus and hypothalamus decreased significantly, but encephaledema occurred. Som 40 micrograms icv caused necrotic changes of neurons in brain.

Animals↗
PubMed1991

[Influences of intraventricular injection of 6-hydroxydopamine on passive-avoidance response, acetylcholine, and muscarinic receptors in mouse brain].

In step-through and step-down tasks, icv 6-hydroxydopamine (6-OHDA) 20 micrograms on d 14 before training impaired the learning and memory processes in mice. But the amnesic effects in mice received icv 6-OHDA were overcome by ip scopolamine (Scop) 0.5 mg.kg-1 at 15 min before trial. When mice were pretreated with icv 6-OHDA the content of acetylcholine (ACh) in the brain showed no change, whereas the ACh-depleting action of Scop (2 mg.kg-1) was diminished. [3H]Quinuclidinyl benzilate binding assay indicated that the brain muscarinic receptor density (Bmax) and Kd in the mice after icv 6-OHDA were respectively decreased 48% and 57% as compared to the icv sterile water group. These findings suggested a possible participation of brain cholinergic nervous system in memory impairment induced by icv 6-OHDA in mice.

Acetylcholine↗
PubMed1986

[Effects of intraventricular injection of anti-DSIP serum on sleep in rats].

Endogenous delta sleep-inducing peptide (DSIP) has not been demonstrated to be necessary for sleep, although the administration of DSIP has been reported to increase sleep in several mammalian species. The purpose of the present study is to examine whether the immunological neutralization of endogenous DSIP in the brain can modulate sleep in unanesthetized rats. A high titer of the rabbit antiserum specific for the C-terminal of DSIP was used. Sixteen male SD rats were chronically implanted with electrodes for EEG and EMG and with a cannula into the lateral ventricle. The rats were injected with anti-DSIP (ADS) or normal rabbit serum as a control at 10 microliter for 10 min immediately before the onset of the light or dark period, and thereafter the polygraphic recordings were performed for a 24-hr period. The records were scored in 30-sec epochs by visual inspection into 3 stages; wakefulness, slow wave sleep (SWS), and paradoxical sleep (PS). ADS exerted no significant effect on the latencies of SWS and PS after injection in the light or dark period. For SWS and PS, neither the distributions measured each 10 min for the first 4 hr nor the hourly distributions for 24 hr were affected by ADS. The first 12-hr amounts of SWS and PS were also unaffected by ADS. These results may suggest the possibility that endogenous DSIP in the cerebrospinal fluid and/or the periventricular tissues is not responsible for sleep.

Animals↗
PubMed1977

Distribution and degradation of [3H]methotrexate after intravenous and cerebral intraventricular injection in primates.

Four hr after either a single injection or continuous infusion of methotrexate (MTX) plus purified [3',5',9(n)-3H]MTX in cynomolgus or rhesus monkeys, 80 to 98% of the 3H radioactivity present in the plasma was found not to represent intact MTX. The percentage of 3H-containing MTX products in the urine after 4 hr was considerably less, although more variable. This variability seemed to be related to variability in the amount of the total dose excreted. Non-MTX products were also found in selected tissues and the percentage of intact MTX found 4 hr after i.v. injection varied from 2 to 26%. The percentage of intact MTX was routinely measured by comparing the values obtained using the dihydrofolate reductase assay with values based on the specific activity of [3',5',9(n)-3H]MTX. Results obtained by diethylaminoethyl column chromatography on a few samples, however, showed good agreement with results from the reductase assay. [3',5',9(n)-3H]MTX products appeared in peaks eluting from the diethylaminoethyl column both earlier and later than the MTX peak, with the earlier peaks being present in only small amounts in the urine. After continuous i.v. infusion, only 2% or less of the radioactivity found in the cerebrospinal fluid after 4 hr represented intact MTX, with the remaining radioactivity eluting much earlier than MTX. In contrast, after direct injection into the left lateral ventricel, all the 3H radioactivity in both cerebrospinal fluid and brain tissue represented intact MTX for up to 4 hr after injection. The appearance of MTX products in the plasma and selected tissues of these primates a short time after i.v. injection is compared to other work in experimental animals and man and suggests a greater metabolism of MTX than was previously suspected.

Animals↗
PubMed1980

Central action of intraventricularly-injected midodrine in rats.

The aim of the present paper was to investigate the effect of intracerebroventricular (i.v.c.) injections of midodrine on the central nervous system of the rat. It was shown that midodrine increased locomotor activity, decreased body temperature, increased sedation in reserpinized rats and the cataleptic effect of haloperidol. Midodrine enhanced amphetamine-stimulated locomotor activity and reduced the amphetamine and apomorphine sterotypy. Phenoxybenzamine, yohimbine and clonidine inhibited the midodrine-induced hyperactivity. Midodrine depressed the whole brain noradrenaline (NA) and dopamine (DA) concentrations and reduced NA turnover. The results suggest a stimulating action of midodrine on the catecholaminergic neurons.

Animals↗