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Biomedical subjects

J H Gordon

Publications and source records attributed to J H Gordon.

61 records · Page 4Linked to original sources
PubMed1970

The anaerobic bacterial flora of the mouse cecum.

Refinements of the anaerobic technique such as the utilization of prereduced media and the removal of traces of oxygen from the gases used by passage through a hot copper oven resulted in quantitative and qualitative improvements in the recovery of anaerobic bacteria from the cecum of SPF mice. The commonest morphologic types of bacteria in the mouse cecum were tapered rods. These characteristically gave "speckled" colonies on agar plates. Those identified were species of the genera Fusobacterium, Eubacterium, and Clostridium. Several of the morphologic types seen with phase microscopy still could not be cultivated. The implications of these findings for the study of the intestinal flora are discussed.

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Further characterization of fat diet-induced changes in responsiveness to estrogen and glucose.

Possible reasons for hyperresponsiveness to the anorexic influence of estrogen of rats fed a high-fat (F) diet were explored. It was found that (1) hyperresponsiveness appeared unrelated to body weight, (2) other estrogenic effects (upon vaginal epithelia and upon mating behavior) were normal in F-fed rats, (3) hyperresponsiveness to estrogen was not a result of alterations in brain dopamine or norepinephrine, (4) F-fed rats were also hyperresponsive to postabsorptive satiating effects of intragastric glucose loads. Thus, an altered glucose metabolism of F-fed rats may be related to an increased responsiveness to the anorexic effects of estrogen.

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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.

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PubMedDate not supplied

Modulation of apomorphine-induced stereotypy by estrogen: time course and dose response.

Previous data have indicated that estrogen may either suppress or enhance the potency of dopamine and/or dopamine agonists. The effects of estrogen (estradiol benzoate; EB) in ovariectomized rats were indicative of a dose related suppression of apomorphine-induced stereotypy at 24 hours after the last dose of EB. HOwever, at 48 hours after the last dose of EB, the apomorphine-induced stereotypy was enhanced in those animals that received EB at 100 microgram/kg x 3 days. Ninety-six hours after the last injection of EB, all animals that received either the 100 or 50 microgram/kg dose of EB displayed an enhanced behavioral response to apomorphine. Animals pretreated with a low dose of EB (10 microgram/kg x 3 days) displayed a suppressed apomorphine stereotypy score at 24 hours, after the last dose, but were indistinguishable from Oil injected ovariectomized controls in all subsequent behavioral tests. These data indicate that estrogen can suppress dopamine and/or dopamine agonist potency 24 hours after the last dose of estrogen. However, an enhanced behavioral response to dopamine agonists can been seen at 48 hours (or more) after the last dose of estrogen. The time delay and the dose dependence of the enhanced response to dopamine agonists are indicative of a "withdrawal" phenomenon, suggesting the possibility that the role of endogenous estrogen is to suppress dopaminergic function.

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