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I Kraulis

Publications and source records attributed to I Kraulis.

14 recordsLinked to original sources
PubMed1991

Modulation by adrenal steroids of limbic function.

The effects of various steroid hormones on the long-term potentiation (LTP) of the rat hippocampus were evaluated. LTP was elicited in the dentate gyrus of adrenalectomized animals with priming tetanic stimulation (200 Hz-0.03 cps) of its main afferent, the perforant pathway. Single pulse EPSP (excitatory post-synaptic potential) slope, and PS (population spike) amplitude values were compared before and after the i.v. injection of the hormones and subsequently after the priming stimulation every 15 min up to 1 h. 18-OH-deoxycorticosterone (18-OH-DOC) produced a significant decrease of the EPSP LTP and arrested the PS enhancement in comparison with vehicle at every time post-tetanic stimulation. Its 21-acetate derivative produced a moderate decrease of the EPSP and had no effect on the PS LTP in comparison with vehicle. Deoxycorticosterone (DOC) exhibited similar effects on the EPSP although less marked than with 18-OH-DOC while the PS only decreased in the first 30 min post-train. Corticosterone decreased both EPSP and PS for the first 15 and 30 min after priming stimulation, respectively, matching values with those of vehicle afterwards. Its 21-acetate produced an initial decrease of the EPSP and had no effect on the PS LTP. Allo-tetrahydro-DOC produced little, if any, initial enhancement of the PS LTP in comparison with vehicle. These results show that the adrenal steroids tested can modulate hippocampal LTP, a plastic phenomenon in the mammalian CNS which is known to be related to memory and learning processes. Moreover, adrenal steroids can independently modify the PS or EPSP components of the LTP, suggesting different loci of action at the neuronal level.

Adrenal Glands↗
PubMed1987

Contrasting effects of 5 alpha- and 5 beta-pregnane-3,20-dione on the motor activity of ovariectomized rats.

While progesterone metabolites have long been known to be potent anesthetics in pharmacological doses, there is no available information as to their effects on behaviour at physiological levels. In this study, 5 alpha- and 5 beta-pregnanediones in silastic capsules were implanted in ovariectomized rats. Approximately 4 mg/kg/day was absorbed over a 24-day period. Rats receiving 5 beta-pregnanedione had decreased motor activity (58% control, P less than or equal to 0.001) while those receiving the 5 alpha-isomer had increased activity (143% control, P = 0.01). These studies suggest that these progesterone metabolites may be responsible for some behavioural changes.

5-alpha-Dihydroprogesterone↗
PubMed1985

Effects of corticosterone and 5 alpha-dihydrocorticosterone on brain excitability in the rat.

The effects of corticosterone (B) and its reduced metabolite 5 alpha-dihydrocorticosterone (DHB) on CNS activity in the rat were examined. Two indices of brain excitability were evaluated: 1) amplitude of population responses (evoked potentials [EP] to sciatic nerve stimulation) and 2) changes in the rate of firing of tonically discharging neurons--both at pontine brainstem regions of the reticular formation. Experiments were carried out in adrenalectomized rats, and recordings were obtained from animals under urethane anesthesia. Steroids were dissolved in a 4:1 saline:Cremophor-El (Sigma) solution and doses of 750 micrograms/0.5 ml were injected (IV). The effects of B on EPs were bidirectional. Increases (8 animals) and decreases (6 animals) of the amplitude responses in different animals were observed. In 4 animals, no changes were detected. In contrast, injection of DHB produced a consistent and significant reduction of brainstem sciatic evoked potentials in 10 of 12 animals tested; 2 animals did not respond to the steroid. At the neuronal level, the effects of the steroids were evaluated by the changes they induced in the mean firing frequency (P less than 0.01) measured during 5-min intervals as determined by a one-way analysis of variance and analysis with a test of multiple comparisons. Only cells that fired in a stationary mode for 15 min before the steroid injection were studied. A more consistent pattern of responses to B was observed at the single-cell level. From 31 neurons that responded to the hormone, of 76 examined, 27 showed an increase in their firing rate and only 4 neurons showed a decrease. The increase in firing rate had an onset latency of 2-5 min (means = 3.5, SE 0.43) with a duration of 16-25 min (means = 17.5, SE 2.7). Of 69 neurons that were tested with DHB, 51 showed a significant decrease in their mean firing frequency. Onset latency of the effect was 2-8 min (means = 4.0, SE 1.21) and the duration of the induced changes was 16-40 min (means = 30.0, SE 3.47). Central interactions of DHB and B when sequentially administered were examined in 28 neurons. Of these, 21 responded to DHB administration with a significant decrease in their firing rates. In 11 of these neurons, injection of B, 5 min after DHB, was followed by a rapid (1-2 min) return of the neurons to baseline firing rates.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1978

Steroid induction of gonadotropin surges in the immature rat. I. Priming effects of androgens.

Sexually immature female rats were either primed with estradiol benzoate on day 23 or given daily injections of various androgens on days 23--25. Plasma for LH and FSH determinations was collected on day 26, 5 h after an injection of progesterone. Massive gonadotropin surges were found after priming with estradiol benzoate or treatment with dehydroepiandrosterone (DHEA), delta 4-androstenedione, and testosterone, but not with ring A-reduced androgens (5 alpha-dihydrotestosterone, 5 alpha-androstane-3 alpha,17 beta-diol, its 3 beta-epimer, and androsterone) or the nonaromatizable 11 beta-hydroxy- and 11-ketoderivatives of delta 4-androstenedione. Rats bearing DHEA-containing Silastic implants also produced LH surges in response to progesterone. A single injection of an antiestrogen antiserum abolished gonadotropin surges in rats primed with estradiol benzoate or DHEA and greatly reduced the accompanying uterine hypertrophy. DHEA and delta 4-androstenedione were barely uterotrophic in ovariectomized rats but sustained progesterone-induced gonadotropin surges. The results indicate that certain (adrenal?) androgens are able to induce maturation of the steroid-sensitive surge system via extragonadal aromatization, whereas their uterotrophic effect is largely mediated by the ovaries. Coordinated increased conversion of androgens at central and peripheral sites may be of physiological importance for the triggering of puberty.

Androgens↗
PubMed1978

Steroid induction of gonadotropin surges in the immature rat. II. Triggering ability of progesterone metabolites, adrenocortical hormones, and adrenocorticotropin.

Several adrenocortical steroids were tested for their ability to trigger LH release in estrogen-primed sexually immature female rats. Massive LH surges, approaching these known to be triggered by progesterone (P), followed the injection of depot ACTH1-24 and also of the adrenal steroids deoxycorticosterone (DOC) and 4-pregnen-21-ol-3,20-dione 21-acetate, but not of 5 alpha- and 5 beta-pregnan-21-of-3,20-dione, corticosterone, or aldosterone. Estrogen-primed adrenalectomized/ovariectomized rats also responded to DOC, albeit to a lesser extent. The P metabolites 5 alpha-pregnana-3,20-dione, 4-pregnen-20 alpha-ol-3-one, and 3 alpha-hydroxy-5 alpha-pregnan-20-one proved ineffective, although their triggering ability in adults was confirmed. It is concluded that adrenal P and DOC are potent activators of the gonadotropin surge system underlying pubertal ovulation and that P metabolites may acquire biological properties during sexual maturation.

Adrenal Cortex Hormones↗
PubMed1975

Distribution, metabolism and biological activity of deoxycorticosterone in the central nervous system.

Intravenously injected [1,2-3H]deoxycorticosterone (DOC) readily enters all parts of the central nervous system. In intact and eviscerated rats the highest concentration of radioactive label was recovered from areas corresponding to the reticular formation from the brain stem. In addrenalectomized animals, in addition to high brain stem concentration, there was also a marked increase in the uptake of radioactivity in the septum, hippocampus and pituitary. Data from the eviscerated rat point to a uniform distribution of [1,2-3H]DOC in neural tissues and suggest that the higher levels of radioactivity found in the brain stem may be due to a DOC metabolite with the chromatographic characteristics of allo-tetrahydro-DOC, an anaesthetic-type steroid. A decrease in the amplitude of evoked sciatic potentials in brain stem sites but not in the thalamic relay nucleus was observed in 52% of the cases studied, following the i.v. injection of 100-150 mug DOC.

Adrenalectomy↗