Phenomena In Rats Research Articles

The contextual modulation of conditioned taste aversions by the physical environment and time of day is similar.

In a pair of experiments, we have compared the ability of changes of place (Exp. 1) and changes of time of day (Exp. 2) to separately modulate learned saline-aversion memory phenomena in rats. Neither a spatial nor a temporal change disrupted latent inhibition using the present behavioral procedure. However, pre-exposure to the taste increased the contextual control of the learned aversion expression. The aversion reappeared in the place or at the time of conditioning after extinction in a different context. The results indicate that environmental and temporal contexts can independently, but similarly modulate taste aversion learning.

Attenuation by prolonged nitric oxide synthase inhibition of the enhancement of fibrinolysis caused by environmental stress in the rat.

1. Nitric oxide (NO) suppresses platelet aggregation and plasminogen activator inhibitor (PAI) release from platelets, playing physiological and/or pathological roles in the haemostatic system. We investigated the effect of NG-nitro-L-arginine methyl ester (L-NAME), an NO synthase inhibitor, on the disseminated intravascular coagulation (DIC)-like phenomena in rats under environmental stress, induced by prolonged fluctuation in air temperature, known as SART (specific alternation of rhythm in temperature) stress. 2. Exposure of rats to SART stress for 7 days caused mild DIC-like symptoms such as thrombocytopenia, hypofibrinogenemia, decreased factor VIII: coagulant activity and shortened euglobulin clot lysis time (ECLT). The enhanced fibrinolysis was accompanied by a marked decrease in the activity of plasma PAI. 3. L-NAME, but not its D-enantiomer, when administered orally at 0.3-10 mg kg-1, twice a day for 7-day exposure to stress, inhibited the stress-induced decrease in fibrinogen levels in a dose-dependent manner, whereas it failed to alter platelet count, factor VIII:coagulant activity and plasma protein levels in stressed rats. All these parameters in unstressed rats were resistant to L-NAME at 10 mg kg-1. 4. Repeated treatment with 10 mg kg-1 of L-NAME blocked the shortening of ECLT and the decrease in PAI activity following stress exposure, although it was without effect in unstressed rats. 5. The inhibitory effects of L-NAME at 10 mg kg-1 on the stress-induced alterations in fibrinogen levels and in ECLT were significantly reduced by coadministered L-arginine at 1000 mg kg-1. 6. These findings demonstrate that repeated administration of L-NAME attenuates the enhanced fibrinolysis, without aggravating thrombocytopenia, in SART-stressed rats. Endogenous NO appears to contribute to the stress-induced development of fibrinolysis by suppressing, plasma PAI activity, most probably as a result of inhibition of the PAI release from platelets.

Roles of dopamine D 1 receptors in striatal fos protein induction associated with methamphetamine behavioral sensitization in rats

To elucidate the roles of dopamine D 1 and D 2 receptors in mediating striatal Fos protein induction and behavioral sensitization after methamphetamine administration, we examined the effects of the D 1 receptor antagonist SCH 23390 and D 2 receptor antagonist sulpiride on these phenomena in rats. Intraperitoneal administration of 5.0 mg/kg methamphetamine produced a significant increase in Fos-immunoreactive cells in the medial striatum. Prior exposure to 5.0 mg/kg methamphetamine enhanced ipsilateral rotational behavior in response to subsequent methamphetamine administration in unilateral nigral-lesioned rats (sensitization). Pretreatment with SCH 23390 (0.32 mg/kg IP) suppressed significantly the expression of striatal Fos protein and the development of acute behavioral sensitization following a single injection of 5.0 mg/kg methamphetamine. Sulpiride (50 mg/kg IP) was also effective in suppressing methamphetamine behavioral sensitization, but did not affect the striatal Fos induction. These results suggest that dopamine D 1 receptor-mediated mechanisms are involved in the striatal Fos protein induction associated with behavioral sensitization following exposure to methamphetamine.

NMDA receptor-mediated expression of Fos protein in the rat striatum following methamphetamine administration: relation to behavioral sensitization

In order to clarify the possible involvement of N-methyl- d-aspartate (NMDA) receptors in mediating striatal Fos protein induction and behavioral sensitization after methamphetamine administration, we examined the effects of non-competitive NMDA receptor antagonist MK-801 on these phenomena in rats. A single administration of 1.0 and 5.0 mg/kg methamphetamine resulted in a dose-dependent increase in Fos-immunoreactive cells in the medial striatum. Prior exposure to 5.0 mg/kg methamphetamine enhanced ipsilateral rotational behavior in response to subsequent methamphetamine administration in unilateral nigral-lesioned rats (sensitization). Pretreatment with 1.0 mg/kg MK-801 completely prevented both the expression of striatal Fos protein and the development of acute behavioral sensitization following a single injection of 5.0 mg/kg methamphetamine. These results suggest that NMDA receptor-mediated mechanisms contribute to the expression of striatal Fos protein associated with behavioral sensitization that follows exposure to methamphetamine.

Binding of Ro 5-4864 to brain membranes of rats with and without absence-like phenomena.

Spontaneously occurring spike-wave discharges (SWD) in rats are used as a model for absence epilepsy in humans. In vitro, the binding parameters of 3H-Ro 5-4864, a ligand labelling the peripheral benzodiazepine receptor, were determined for brain membranes of WAG/Rij rats, an inbred strain showing SWD, and for ACI rats, an inbred strain showing no SWD. No difference in the Kd but a small difference in the Bmax values between the strains were found. Recently, other investigators reported a correlation between a decrease in affinity for 3H-Ro 5-4864 and the occurrence of SWD. Our results suggest however that it is doubtful that a change in Kd of the peripheral benzodiazepine receptor is causal in the etio-pathology of the spontaneous absence like phenomena in rats.

Synergistic Anticonvulsant Effect of Valproic Acid and Ethosuximide on Pentylenetetrazole-Induced Epileptic Phenomena in Rats

The possible synergistic effect of valproic acid and ethosuximide in combination on pentylenetetrazole-induced epilepsy was investigated in rats. Valproic acid and ethosuximide administered intraperitoneally both showed dose-dependent anti-epileptic activity towards pentylenetetrazole-induced myoclonias and tonic-clonic seizures. The valproic acid-ethosuximide combination had a synergistic pharmacological effect. Against myoclonias combined valproic acid-ethosuximide produced a non-significant decrease in the effective dose of both drugs compared with treatment with either drug alone. In the case of tonic-clonic seizures the protective effect against the seizures was significantly increased by combined treatment compared with treatment with either drug alone. Neither plasma concentrations nor any other pharmacokinetic parameters were significantly changed when the same doses of valproic acid and ethosuximide were given, singly or in combination.

Observations on labeling of neuronal cell bodies, axons, and terminals after injection of horseradish peroxidase into rat brain.

AbstractWe observed with light microscopy the evolution of neuronal labeling phenomena in rats with two hours to eight days survival following injection of horseradish peroxidase (HRP) into the neostriatum. We compared the results of neostriatal injection with those injection of the overlying neocortex. The following conclusions were reached.The zone of diffuse background HRP around the injection site began to shrink after 18 hours. The extent of the early zone of diffusion was marked from 18 hours to two days by a universal granular labeling of neurons. This granular cell labeling appears to be the result of earlier diffuse cell labeling rather than retrograde axonal transport.Retrograde labeling of cells takes place from terminals and from damaged axons. Anterograde labeling of what appear to be terminals and fine preterminal axons takes place only from cells in the injection area, and not from either intact or damaged axons of passage. Usually the axons engaged in such retrograde or anterograde transport are not visibly labeled. Labeling of cells and terminals is generally optimal at 12 to 24 hours, but corticostriatal cells in layer V of the neocortex are seen best at 24 to 36 hours. The area from which retrograde labeling of cells takes place is larger than that from which anterograde labeling of terminals occurs.Massive intra‐axonal movement of HRP away from the injection site occurs within a few hours in axons of passage as well as those originating there. This axonal labeling fades in most axons by 24 hours, but certain axons remain darkly labeled. The latter are probably damaged, since labeled axons which appear to be degenerating are later (3–5 days) seen in the same place, and Fink‐Heimer staining of adjacent sections also shows degenerating axons in these regions. The early massive labeling of axons can lead to short‐lived labeling of complete axonal arborizations within the range of this intra‐axonal movement of HRP. But it seems to have no relation to the longer‐lived labeling of distant cells and terminals, which presumably results from active axonal transport. This suggests that HRP entering axons of passage is not captured by the axonal transport mechanisms.

The effect of clomiphene on parturition and post-partum ovulation in rats.

Laboratory of Animal Reproduction, Faculty of Agriculture, Tohoku University, Sendai, Japan We have previously described studies of parturition and subsequent reproductive phenomena in rats which showed that the time of the LH surge and post-partum ovulation are related to the time of parturition (Hashizume, Sugawara & Takeuchi, 1973a, b, 1975). In an attempt to clarify further the factors governing the timing of the post-partum ovulation in rats, we have examined the effects of an oestrogen antagonist, clomiphene (see Labhsetwar, 1970), on the time of parturition and the post-partum ovulation. Rats of the Wistar strain, bred in our own laboratory and kept in controlled lighting (lights on 06.00-18.00 hours), were used. Rats which had experienced three consecutive 4-day cycles were caged at pro-oestrus with fertile males and mating was verified by finding spermatozoa in the vaginal smear the following morning. This day was designated Day 1 of pregnancy. Clomiphene citrate (Clomid

The inhibition of mast cell damage and histamine release in anaphylaxis by pyridine and diphosphopyridine nucleotidase inhibitors. Comparison with compound 48/80.

In rats and guinea-pigs both mast cell damage and histamine release in anaphylaxis were inhibited by pyridine, nicotinamide, diethylnicotinamide, nicotinic acid, isonicotinic acid and isonicotinic acid hydrazide, which are known to be inhibitors of diphosphopyridine nucleotidases. On the other hand these compounds potentiated histamine release and mast cell damage by compound 48/80 in guinea-pigs although inhibiting the same phenomena in rats. The relationship of these findings with the mechanism of histamine liberation in anaphylaxis is discussed.

Relapse phenomena in rats infected with single spirochetes (Borrelia recurrentis var. turicatae).

Relapse phenomena in rats infected with single spirochetes (Borrelia recurrentis var. turicatae).