Effects of whole body microwave exposure on the rat brain contents of biogenic amines.

The effects of whole body microwave exposure on the central nervous system (CNS) of the rat were investigated. Rats weighing from 250 to 320 g were exposed for 1 h to whole body microwave with a frequency of 2450 MHz at power densities of 5 and 10 mW.cm-2 at an ambient temperature of 21-23 degrees C. The rectal temperatures of the rats were measured just before and after microwave exposure and mono-amines and their metabolites in various discrete brain regions were determined after microwave exposure. Microwave exposure at power densities of 5 and 10 mW.cm-2 increased the mean rectal temperature by 2.3 degrees C and 3.4 degrees C, respectively. The noradrenaline content in the hypothalamus was significantly reduced after microwave exposure at a power density of 10 mW.cm-2. There were no differences in the dopamine (DA) content of any region of the brain between microwave exposed rats and control rats. The dihydroxyphenyl acetic acid (DOPAC) content, the main metabolite of DA, was significantly increased in the pons plus medulla oblongata only at a power density of 10 mW.cm-2. The DA turnover rates, the DOPAC:DA ratio, in the striatum and cerebral cortex were significantly increased only at a power density of 10 mW.cm-2. The serotonin (5-hydroxytryptamine, 5-HT) content in all regions of the brain of microwave exposed rats was not different from that of the control rats. The 5-hydroxyindoleacetic acid (5-HIAA) content in the cerebral cortex of microwave exposed rats was significantly increased at power densities of 5 and 10 mW.cm-2.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of ceruletide and haloperidol on the hypothalamo-pituitary beta-endorphin system and brain beta-endorphin contents in the rat: with special reference to effects of ceruletide in chronically haloperidol-treated rats.

Subcutaneous (sc) administration of 200 micrograms/kg ceruletide (CER), a decapeptide chemically related CCK-8, and 5 mg/kg haloperidol (HLP) to rats increased the plasma immunoreactive beta-endorphin (ir-beta-END) level. The combined injection of CER and haloperidol caused higher plasma ir-beta-END levels than either drug alone. High plasma ir-beta-END levels returned to control levels on the 2nd day. Prior intraperitoneal (ip) administration of a CCK receptor antagonist, L-364,718 (3 mg/kg), but not proglumide (400 mg/kg, ip), inhibited CER-induced, but not HLP-induced, elevation in plasma ir-beta-END levels. The dopamine agonist, bromocriptine (1 mg/kg, ip) decreased plasma ir-beta-END levels, but had not effect on CER-induced elevation in plasma ir-beta-END levels, whereas bromocriptine-induced reduction in plasma ir-beta-END levels was antagonised by HLP. CER injection to chronically HLP-treated rats caused a greater elevation of plasma ir-beta-END levels compared to saline-injected rats. In contrast to the acute experiment, plasma ir-beta-END levels remained elevated over a period of 24 h. In the acute experiment, CER, HLP or the combined treatment with these two drugs had no effect on ir-beta-END contents in the pituitary gland and brain. In the chronic experiment, HLP increased the adenohypophyseal and septal ir-beta-END contents and decreased the hippocampal ir-beta-END contents 24 h after the final HLP injection. CER caused a small reduction only in the hippocampal ir-beta-END contents of CER-injected rats 15 min after injection. When determined on the 2nd day, however, the increases in the adenohypophyseal and septal ir-beta-END contents and the decrease in the hippocampal ir-beta-END contents observed in CER-injected rats were of the same magnitude as those of rats not given the CER injection. These findings indicate that CER stimulates the release of ir-beta-END from the adenohypophysis through CCK-A receptors and that elevated plasma ir-beta-END levels is partly involved in some behavioural effects induced by CER. Furthermore, sustained elevation of plasma ir-beta-END levels after a single injection of CER to chronically HLP-treated rats may explain its long-lasting therapeutic and behavioural effects.

Effects of whole-body vibration stress on substance P- and neurotensin-like immunoreactivity in the rat brain.

In order to clarify the involvement of substance P (SP) and neurotensin (NT) neurons in the response of organisms to stress, SP-like immunoreactivity (SP-LI) and NT-like immunoreactivity (NT-LI) were determined in various regions of the rat brain following exposure to the whole-body vibration (20 Hz, 4 G, 90 min). SP-LI and NT-LI in the rat brain were measured by means of a sensitive and specific double-antibody solid-phase enzyme immunoassay. SP-LI in the frontal cortex was significantly reduced following whole-body vibration, while that in the nucleus accumbens and amygdala was significantly increased. NT-LI in both the frontal cortex and the hypothalamus of rats exposed to the whole-body vibration was significantly increased. However, striatal SP-LI and NT-LI remained unchanged. The present findings indicate that the SP and NT neuronal systems in various brain areas are involved in the response to stress. The frontal and amygdalofugal SP and hypothalamic NT neuronal systems, in particular, may have an important role in mediating the response of organisms to the whole-body vibration-induced stress.

A study of non-isotopic in situ hybridization histochemistry on postmortem changes in vasopressin mRNA in rat brain.

Rat models which stimulated various postmortem conditions were used to determine postmortem changes in the vasopressin mRNA content of the brain. In situ hybridization histochemistry experiments using biotinylated oligonucleotide probes revealed that vasopressin mRNA could be detected in the rat hypothalamic nuclei, even though the rats had been killed and left for 8 h postmortem at room temperature and the brains were then fixed by immersion in 4% paraformaldehyde instead of by transcardial perfusion. However, these signals were greatly reduced in the nuclei if the brains were removed after a 24-h delay. These results suggest that gene expression study of neuropeptides at the cellular level can be performed on postmortem human brains after a short postmortem delay.

A therapeutic trial of caerulein to a long-term heavy marihuana user with amotivational syndrome.

A male marihuana user with amotivational syndrome who responded poorly to neuroleptic therapy was treated four times with weekly intramuscular injection of caerulein in a dose of 0.6 micrograms/kg. He was maintained on his previous neuroleptic medication during the study period. The BPRS was used to rate the patient's symptoms. There were remarkable improvements in the total scores and the psychosis subscale score, which consists of the following symptoms that do not respond well to neuroleptic therapy in chronic schizophrenia: emotional withdrawal, mannerisms and posturing, uncooperativeness, and blunted affect. These improvements persisted for two weeks after cessation of caerulein administration, after which the patient's condition gradually worsened. Nevertheless, the improvement recurred upon reinjection of caerulein. These findings indicate that the improvement observed seems to be due to caerulein, and suggest that caerulein may be a useful and effective therapeutic drug for marihuana user with amotivational syndrome.