Interaction between the effects of stress and morphine on body temperature in rats

The relation between stress-induced and morphine-induced body temperature changes was examined in rats. Three groups of eight animals thoroughly habituated to handling and rectal probing, and three groups of eight experimentally naive animals were injected intraperitoneally with either 1, 5, or 30 mg/kg morphine sulphate on each of six consecutive days. Differences in temperature readings from the pre-injection baseline showed that on Day 1 of the experiment stress acted to effectively increase the potency of morphine, causing slightly increased hyperthermia at the lowest dose and greatly increased hypothermia at the highest dose. Thus for habituated animals the dose-response curve for morphine was shifted to the right. By Day 6, after repeated morphine injections, all animals showed a hyperthermic response to morphine and the differences between habituated and unhabituated animals had disappeared. These findings were discussed in terms of the interaction between the temperature changes produced by endogenous opioids in stressed animals and the actions of exogenously administered morphine.     

The effects of narcotic analgesics and narcotic antagonists on ganglionic transmission in the rat.

The effects of narcotic analgesics, narcotic-antagonist analgesics and narcotic antagonists on ganglionic transmission in the superior cervical ganglia of the rat were studied $\text{in}$$\text{vivo}$ and $\text{in}$$\text{vitro}$. $\text{In}$$\text{vivo}$ administration of morphine, meperidine, methadone, pentazocine or naltrexone blocked ganglionic transmission. Levorphanol, cyclazocine, nalorphine and naloxone had no effect on ganglionic transmission in this procedure. $\text{In}$$\text{vitro}$ studies confirmed the $\text{in}$$\text{vivo}$ results with the exception of levorphanol, cyclazocine and nalorphine, which were also found to block ganglionic transmission $\text{in}$$\text{vitro}$. In both preparations, naloxone did not antagonize the effect of morphine, suggesting that the effects of morphine and the other opiates were nonspecific. Similar potency of $\text{d}$- and $\text{l}$-isomers of pentazocine and cyclazocine support this conclusion. The observation that naltrexone blocked ganglionic transmission, but the other pure narcotic antagonist, naloxone, was inactive is somewhat unique to this test procedure and possibly significant.     

Effect of the opiate antagonist naloxone on body temperature in rats.

The specific opiate antagonist naloxone was used to assess the hypothesis that an endogenous opioid plays a significant role in temperature regulation in the rat. A very slight hypothermic effect was observed at a naloxone dose sufficient to block the opiate receptors. Even under conditions of cold stress, the magnitude of the effect was so small as to lend little support to the hypothesis.     

The action of urocortins on body temperature in rats

The actions of individual urocortins on colon temperature were studied in rats. Urocortin 1, urocortin 2 or urocortin 3 was injected into the lateral brain ventricle in conscious rats and the colon temperature was measured at different times following injection, for up to 6 h. In order to study the possible role of prostaglandins, the animals were treated with either a urocortin together with the pyrazolone derivative noraminophenazone to inhibit the action of cyclooxygenase in initiating hyperthermia, or with noraminophenazone 30 min following urocortin administration to act on existing hyperthermia. Noraminophenazone was administered intramuscularly in a dose of 50 mg/kg. Urocortin 1 caused a dose-related increase in colon temperature, maximal action being observed at a dose of 2 microg with the maximal increase in body temperature at 4 h. Noraminophenazone prevented the urocortin-induced increase in colon temperature and attenuated the already existing elevated body temperature. Somewhat similar action was observed with urocortin 2. However, following treatment with 0.5 or 1.0 microg urocortin 2, the action was already over at 2 h, whereas 2 microg increased the colon temperature steadily, with a maximum at 4 h. Noraminophenazone blocked or diminished the action of urocortin 2. Urocortin 3 in a dose of 1 microg was the most effective in increasing the colon temperature; the maximal effect was observed at 2 h. Noraminophenazone blocked the development of urocortin 3-induced hyperthermia, or attenuated it when the hyperthermia was already present. The results demonstrated that urocortin 1, 2 or 3 caused increases in body temperature when injected into the lateral brain ventricle, though the optimal dose and the duration of hyperthermia differed for the individual urocortins. The cyclooxygenase inhibitor blocked or diminished the action of these urocortins, indicating the involvement of prostaglandins in urocortin-induced hyperthermia.     

Action of opiate peptides and narcotic analgesics on the cerebral cortex

The chronic experiments on freely moving cats have shown that the opiate peptides, FK33--824 (Tyr--D--Ala--Gly--MePhe--Met(o)--ol) and tetrapeptide (Tyr--D--Ala--Gly--Phe--NH2), as well as the narcotic analgesics, morphine, phentanyl and pentazocine in doses close to analgesic ones, suppress the recovery cycles of primary responses (PR) in the second somatosensory and associative zones of the brain cortex, recorded at paired stimulation of the fibres of thalamo-cortical radiation (TCR). In larger doses these agents slightly increase PR recorded at single stimulation of TCR, provoke the convulsive discharges on EEG and motor excitation of the animals. Naloxon eliminates all the mentioned effects of the tested opiate peptides and narcotic analgesics.     

Effect of narcotic analgesics on excitatory transmission in the spinal cord]

As demonstrated on nonanesthetized curare-immobilized spinal cats morphine, promedol and fentanyl failed to alter the amplitude of induced potentials in the ventro-lateral columns of the lumbar spinal cord, evoked by a single or repetitive stimulation of the cutaneous or pelvic nerves. In some experiments the same drugs inhibited the nerurons of the posterior horns of the spinal cord activated by the nociceptive stimulation of the peripheral receptors in intraarterial administration of bradykinin. It is suggested that a spinal component was involved in the action of hypnotic analgetics.     

The effects of verapamil and ethanol on body temperature and motor coordination

Male, adult mice of the Binghamton heterogeneous stock received one of two doses of ethanol (1.0 g/kg or 2.0 g/kg in saline) alone or in combination with the calcium (Ca2+) slow channel blocker, verapamil (5.45 mg/kg in 25% v/v ethanol in saline). Hypothermic responses and motor incoordination were assessed in terms of rectal temperatures and rotorod activity both 20 and 60 min after drug administration. Verapamil alone did not affect body temperature, but it potentiated ethanol-induced hypothermia at both post-administration test times. Both verapamil and ethanol impaired muscular coordination and these effects were additive at the two observation periods. Verapamil did not affect ethanol blood levels from 10 to 80 min after administration of the drugs. Since motor impairment was observed when verapamil was administered with only its ethanol vehicle, this suggests a powerful interactive effect between the two drugs.     

The effects of environmental temperature on the body temperature and ear morphology of the mouse

1. 1.|The external temperatures of the trunks and tails of four groups of mice kept at 33, 21, 8 and 4°C for the first 6 months of their life were different depending on the environmental temperature.

2. 2.|The skin temperatures over the tails was lower than those over the trunk at all ambient temperatures but the internal rectal temperature had not changed.

3. 3.|Those ear pinnae are also important in thermoregulation for those of 33°C mice were larger and thinner than those kept at the lower temperatures.

Action of colchicine on analgetic effects of morphine and DADLE in rats

Intracerebroventricular injection of morphine and DADL significantly increased the tail-flick latency in the rat (full analgesia during 1.5-2.5 hours). Previous i. c. v. (lateral ventriculus) injection of colchicine prevented the analgetic effects of these drugs during 5 +/- 1 weeks with subsequent recovery.