Biomedical subjects

E Markel

Publications and source records attributed to E Markel.

13 recordsLinked to original sources

PubMed1994

Life-spanning behavioural and adrenal dysfunction induced by prenatal hypoxia in the rat is prevented by the calcium antagonist nimodipine.

The long-term behavioural effects of prenatal chronic anaemic hypoxia were investigated in young (5 months old), late adult (19 months) and aged Wistar rats (23-26 months). Sodium nitrite (2 g/l) offered in the drinking water during the second half of pregnancy served to evoke prenatal hypoxia. In parallel to nitrite treatment the Ca2+ channel blocker nimodipine (10 mg/kg) or vehicle alone was administered intragastrically once daily. Open-field activity, intermale social behaviour, learning ability in a black-white discrimination paradigm and fear-induced emotionality were assessed at different ages. Plasma corticosterone response to novelty stress was measured by blood sampling through chronic venous canulas at the age of 28 months. The nitrite-exposed 5-month-old offspring started exploration in a novel open-field with considerable delay. This delayed start-latency was augmented in 19- and 23-month-old rats, pointing to exaggerated suppression of behavioural arousal. Nitrite-induced hypoxia decreased the duration of social interactions during ageing. Aged rats exposed to nitrite were unable to learn a black-white discrimination but showed a normal generalized conditioned fear response (immobility) to the test situation as a whole. The conditioned fear-induced vocalization was more frequent among hypoxic aged animals. The aged hypoxic rats displayed a prolonged plasma corticosterone stress response and had higher adrenal weight than their controls. The abnormal open-field, social, learning and emotional behaviours, as well as the altered plasma corticosterone response, were prevented by prenatal nimodipine treatment.

Adrenal Insufficiency↗

PubMed1992

Behavioral and biochemical effects of early postnatal cholinergic lesion in the hippocampus.

The effects of early postnatal (PD 8) intracerebroventricular injection of ethylcholine mustard aziridinium ion (AF64A) on development of open-field and cognitive behaviors and cholinergic markers in several brain areas were examined in the rat. The cholinotoxin was bilaterally administered in a dose range of 0.25 to 2.0 nmol. In the open-field tests, the cholinergic lesion caused a dose-dependent increase in activity at 20 days of age, while it resulted in lengthened latency to initiate exploration and decreased rearing activity at adulthood. Hole-board spatial learning was severely inhibited in adult age. The biochemical activity of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) in the hippocampus was markedly decreased in a dose-dependent manner, but was unchanged in the neocortex and striatum. Histochemical staining of AChE-positive fibers revealed a severe cholinergic denervation of the granular and pyramidal cell layers of the hippocampus. The results showed that a selective cholinergic deafferentation of the hippocampus at a critical stage of development leads to long-lasting abnormal open-field and spatial learning behaviors.

Acetylcholinesterase↗

PubMed1990

Protective effect of the calcium antagonist nimodipine on discrimination learning deficits and impaired retention behavior caused by prenatal nitrite exposure in rats.

Discrimination learning behavior and retention of a passive avoidance response were studied in male adult offspring of gestating rats exposed to drinking water containing 2 g/l sodium nitrite, throughout the second half of pregnancy. Both in an auditory and visual discrimination learning paradigm NaNO2-exposed rats were inferior to controls. The long-term retention of a passive avoidance response was also impaired. The acquisition of simple learning tasks was not significantly disturbed. The concomitant prenatal daily treatment with the calcium antagonist nimodipine in a dose of 10 mg/kg p.o. interfered with the nitrite neurotoxicity and prevented the development of adult behavioral deficits. The results support the hypothesis that Ca2+ homeostasis of neurons is an important factor for normal development of brain and behavior.

Animals↗

PubMed1989

Nitrate induced changes in sensoro-motor development and learning behaviour in rats.

Development of sensoro-motor functions and adult learning behaviour was studied in rats subjected to nitrate exposure. Pregnant and lactating dams and their offspring were supplied with drinking water containing nitrate, 1.12 or 2.24 mM KNO3, and compared with nitrate-free controls. Postnatal maturation of reflexes, that of sensory and somatic parameters and motor activity, furthermore, the acquisition of one-way avoidance and rewarded discriminative learning behaviour in adulthood were examined. Reflexes (righting, cliff-avoidance) and hearing startle reaction maturated earlier in nitrate treated groups. No difference was found in olfactory homing behaviour, in the time of eye opening and in body weight growth. Open-field motor activity was higher at days 5, 7, 10 after birth, but hypoactivity ensued after day 20. A marked learning deficit was observed both in punished and in rewarded learning paradigms. The results indicate a nitrate induced deviation in behavioural development, and an impairment in learning behaviour, particularly of discriminative type.

Animals↗

PubMed1987

Effect of 1-desamino-D-arginine vasopressin, ACTH 4-10 and adrenaline on acquisition of active avoidance response in prenatally ethanol-treated rats.

The acquisition of active avoidance response was studied in 45 to 50-day old rats exposed to ethanol during pregnancy. The offsprings showed no retardation in somatic development although there was a marked deficit in learning of avoidance response. Daily administration of 1-desamino-D-arginine vasopressin (0.1 to 5 micrograms/100 g b.w.), ACTH 4-10 (0.1 to 2 micrograms/100 g b.w.) and adrenaline (0.2 to 2.0 micrograms/100 g b.w.) facilitated the learning performance in a dose-dependent manner. The retention of responding was tested after the interruption of training for 7 days. The prenatally ethanol-exposed rats with DDAVP pretreatment during the 5-day training procedure showed a better performance than that of the vehicle-treated ethanol-exposed rats but they were inferior to the controls. The present data indicate a complexity of biochemical changes due to the prenatal exposure to ethanol and the learning deficit can be modified by either neuropeptides or catecholamines, by such humoral mediators which are known to influence learning behavior and memory consolidation under different experimental conditions and due to different noxious stimuli from noxious stimuli from either external or internal environment.

Adrenocorticotropic Hormone↗

PubMed1986

Effects of arginine-vasopressin and ACTH 4-10 on acquisition of active avoidance response in rats with alcohol pretreatment in prenatal and adult age.

Alcohol administration in drinking water to mother rats during gestation resulted in a permanent learning deficit of the offspring when behavioural reactions were tested in active avoidance conditioned reflex situation in adult age. A similar deficit of learning capacity was observed in adult rats following alcohol administration for two weeks; the acquisition of active avoidance response was tested later. Administration of arginine-vasopressin and ACTH 4-10 during behavioural test led to a significant improvement of learning ability of the animals pretreated with alcohol. The observations indicate that the ethanol-induced deficit of learning capacity involves peptidergic mechanisms and the behavioural manifestations following chronic alcohol treatment are not irreversible processes.

Adrenocorticotropic Hormone↗

PubMed1986

Changes in avoidance behaviour following ethanol treatment in rats of different ages.

Avoidance learning and pain sensitivity were studied in rats after chronic ethanol administration (1.1 to 1.7 g per kg b.w. in drinking water) at prenatal, adolescent and adult ages. The behavioural reactions were tested in adulthood by studying passive and active avoidance learning and the threshold of pain sensitivity to electric tail shock. Chronic ethanol consumption led to an impairment of avoidance learning and to hyperalgesia in each experimental series, although the alterations were greater in the prenatally treated groups. The experimental observations are discussed in the light of fetal alcohol syndrome.

Alcoholism↗

PubMed1984

Footshock sensitivity of rats after adrenalectomy and glucocorticoid treatments.

The threshold of flinch-jump response to electric footshock was measured after adrenalectomy (ADX) in male albino rats. The ADX-rats showed higher threshold from the 2nd to 6th postoperative days than the sham-operated animals. Daily subcutaneous administration of 100 micrograms/100 g b.w. corticosterone (CS) led to restoration of the footshock sensitivity of ADX-rats. The same effect was observed following dexamethasone (DEX) treatment. DEX but not CS administration resulted in a decrease of the footshock sensitivity in the sham-operated rats. On the 9th and 18th days after adrenalectomy, in contrast to the early postoperative period, the threshold for footshock sensitivity was significantly lower than in sham-operated controls. It is suggested that an excess release of endogenous opiates from the pituitary are involved in the changes of pain threshold under the conditions studied.

Adrenalectomy↗

PubMed1971