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Biomedical subjects

C J Wallis

Publications and source records attributed to C J Wallis.

30 records · Page 2Linked to original sources
PubMed1982

Effect of phencyclidine on [3H]QNB binding.

Intraperitoneal injection of phencyclidine before intravenous injection of [3H] Quinuclidinyl benzilate (QNB, 1.6 micrograms/kg) significantly increased the amount of radioactivity found in the brains of female C57BL/6J mice one hour after the 3H-QNB administration. This effect was found in hypothalamus, cortex, hippocampus and striatum and was decreased by pretreatment of the animal with atropine. The magnitude of the enhancement varied as a function of dose but did not change across the time span studied. These data are in contrast to our findings and those of others of inhibition of the specific binding of 3H-QNB to muscarinic cholinergic receptors by PCP in vitro. When atropine or PCP was administered in vivo and the tissue later analyzed in vitro, no effects of the drugs were observed on 3H-QNB binding. The reasons for the differences remain a matter of speculation.

Animals↗
PubMed1982

Relationship between regional brain angiotensinogen and local blood flow and volume in the adrenalectomized rat: application of approach to quantification of brain corticosterone receptors.

Prior studies from this laboratory have established that angiotensinogen, the prohormone of angiotensin, is unevenly distributed in the rat brain and that adrenalectomy selectively perturbs levels of the prohormone in regions associated with cardiovascular neural pathways. However, plasma angiotensinogen levels are 10(2)--10(3) times higher in plasma than in brain, so that the observation of a unique distribution of brain angiotensinogen may reflect variable plasma contamination. Studies were therefore undertaken to establish whether adrenalectomy selectively alters regional blood flow, blood volume, or plasma contamination of brain tissue, thereby artifactitiously altering apparent angiotensinogen levels. Radioactive 2-deoxyglucose, iodoantipyrine, and inulin were employed in these analyses. We conclude that variations in blood flow do not explain the selective effects of adrenalectomy, but that a variable extent of residual plasma contamination (remaining after transcardiac perfusion) is partially reflected in our earlier data. However, after correcting for plasma contamination, we still find significant changes in selected areas of the rat brain following adrenalectomy. Finally, our results demonstrate the necessity for direct quantitation of plasma contamination od brain tissue segments. This is shown to have relevance in other situations, such as corticosterone binding globulin contamination of brain corticosterone receptor binding.

Adrenalectomy↗
PubMed1975

Stimulation of male and female sexual behavior in gonadectomized rats with estrogen and androgen therapy and its inhibition with concurrent anti-hormone therapy.

In the first experiment gonadectomized male rats were injected daily with various combinations of vehicle (V), estradiol benzoate (E), dihydrotestosterone (D) and/or the anti-androgen cyproterone acetate (CA). The eight treatment combinations consisted of V, E, D, CA, E + D, E + CA, D + CA and E + D + CA. Only those males treated with both E and D were found to display ejaculations. Concurrent treatment with CA completely blocked ejaculatory behavior and it significantly reduced both mount and intromission frequencies. Examination of peripheral androgen target tissues indicated that following stimulation with D, CA effectively reduced seminal vesicle and penile weights, and penile lengths, but it did not reduce penile spines. In the second experiment gonadectomized female rats were treated with two daily injections of E, E + CA or E + the anti-estrogen CI-628. A second set of gonadectomized females received three daily injections of testosterone (T), T + CA or T + CI-628. On the day after completion of these injections all females received progesterone and were tested for sexual receptivity three hours later. Both E and T treated females were found to display the lordotic posture in response to mounting stimulation while both CI-628 and CA were found to block this behavior. In E treated females, CI-628 and CA were also found to reduce uterine weight. Thus, CA was shown to have anti-estrogenic as well as anti-androgenic properties. These results were discussed in terms of the aromatization and 5alpha reduction theories of testosterone action in sexual behavior.

Androgens↗
PubMed1975

Maintenance of male sexual behavior by combined treatment with oestrogen and dihydrotestosterone in CD-1 mice.

After castration, adult male sexually experienced CD-1 strain mice were treated with dihydrotestosterone (200 mug/day, DHT), oestradiol benzoate (1 mug/day, OB) or DHT (200 mug/day) plus OB (1 mug/day). Oestradiol benzoate and the combined treatment DHT + OB maintained male sexual behaviour at levels comparable to a group of intact control mice, while DHT m maintained behaviour at a lower level. Having all hormone dosages resulted in a decrease in the number of OB-treated animals mating and a complete loss of mating in the DHT-treated animals. The decrease in dosage did not result in any change in the behavior of the mice receiving both hormones. Adrenalectomy was found to have no effect on the mating behaviour of the OB-treated and untreated animals, but it did reduce the number of DHT+ OB-treated animals mating. Thus, both OB alone and combined DHT+OB treatment can maintain male mating behaviour in castrated CD-1 strain mice and these effects do not appear to be due to the effects of oestradiol on the adrenal.

Adrenal Glands↗
PubMedDate not supplied

Effects of septal lesions and chronic estrogen treatment on dopamine, GABA and lordosis behavior in male rats.

Septal lesions (SL) in female rats result in an increased sensitivity to the behavioral effects of acute estradiol benzoate (ACUTE-EB; 2 microgram/day X 3) treatment as measured by the lordosis quotient (LQ: number of lordotic responses X 100/number of mounts). Male rats, intact or castrated, do not show this enhanced behavioral response to ACUTE-EB unless they are treated with EB (2 microgram/day) for 2--4 weeks immediately following the production of SL. The present study was undertaken to examine possible neurochemical alterations which could account for the enhanced behavioral sensitivity to ACUTE-EB seen in the SL male rat treated chronically with EB during the postlesion period (SL-EB). Three groups, normal males, SL-EB and SL males chronically treated with oil (SL-oil), were subdivided and treated with ACUTE-EB or oil and decapitated. The brains were removed, frozen and stored at -50 degrees C prior to dissection and assay. Tyrosine hydroxylase (TH) activity was assayed in the dopamine (DA) rich areas of the forebrain (striatum, STR, nucleus accumbens septi, ACB; and olfactory tubercle). The TH activity was significantly suppressed in both the STR and ACB of the SL-EB males treated with ACUTE-EB. The glutamic acid decarboxylase (GAD) activity in both the substantia nigra and ventral tegmentum was significantly increased in the SL-EB males given ACUTE-EB relative to that of all other groups. In summary, SL-EB males given ACUTE-EB show (1) an enhanced LQ, (2) decreased TH activity in the region of DA terminals, and (3) increased GAD activity in the region of DA cell bodies. The increase in GAD activity is suggested to be a result of an altered neuronal feedback because of plastic changes that occur during chronic EB treatment following production of SL. This probable increase in inhibitory tone in the region of the DA cell bodies may explain the observation that the SL-EB male exhibits decreased DA turnover following ACUTE-EB treatment. Moreover, since DA may be inhibitory to the display of lordosis behavior, the SL-EB males may show an enhanced LQ, at least partially, because of this reduction in DA activity.

Animals↗
PubMedDate not supplied

GM1 ganglioside reduces ethanol intoxication and the development of ethanol dependence.

The monosialoganglioside, GM1, protects the nervous system against a variety of insults. In this study, we evaluated the protective properties of GM1 on ethanol intoxication and development of dependence. GM1 (20-40 mg/kg, IP) reduced the extent and duration of ataxia produced by ethanol (2 g/kg, IP, 15-95 min), and delayed the onset of loss and reduced the duration of the righting reflex (LORR) produced by ethanol (4.2 g/kg, IP). GM1 did not alter ethanol-induced hypothermia or the rate of ethanol clearance. Rather, GM1 increased the waking blood ethanol concentration. In animals fed a complete liquid diet containing 4.5% ethanol, concurrent administration of GM1 (40 mg/kg/day) blocked the tremors, hypolocomotion, and anxiety-like behavior associated with ethanol withdrawal. These findings demonstrate that GM1 reduces both ethanol's acute intoxication and the signs and symptoms of ethanol withdrawal by a mechanism not related to ethanol pharmacokinetics.

Alcoholic Intoxication↗
PubMedDate not supplied

Regional changes in rat brain angiotensinogen following bilateral nephrectomy.

One approach to establish the existence and functionality of a brain angiotensin system is to demonstrate selective alterations in that system following perturbation of peripheral cardiovascular functions. The present study utilized this approach to quantify regional angiotensinogen levels in the rat brain following bilateral nephrectomy, a perturbation that severely disrupts salt and water homeostasis. Angiotensinogen, the precursor of any centrally-derived angiotensin, was analyzed since it should provide a marker for a putative angiotensin peptidergic system. Net brain angiotensinogen was determined by correcting total tissue concentrations of angiotensinogen with accurate values of contaminating plasma angiotensinogen. The latter was determined by quantifying regional plasma space utilizing tritiated inulin as a marker of cerebral vascular space. It was found that there were no detectable alterations in regional net brain angiotensinogen in the first 24 hours following nephrectomy despite over a twofold increase in plasma angiotensinogen and the absence of significant plasma renin. By 32 hours postnephrectomy, certain areas of the rat hypothalamus and midbrain exhibited significant elevations in net angiotensinogen content. These areas coincided with regions traversed by neural pathways shown to mediate angiotensin-induced drinking or blood pressure elevations. The results lend further support to the concept of an independent brain angiotensin system.

Angiotensinogen↗