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Biomedical subjects

L Angelucci

Publications and source records attributed to L Angelucci.

140 records · Page 8Linked to original sources
PubMedDate not supplied

Spatial learning and memory in the radial maze: a longitudinal study in rats from 4 to 25 months of age.

This longitudinal study was designed to investigate whether previous experience may influence performances and strategies of rats tested in the radial maze without external cues when aged 4, 13, and 25 months. Their performances and strategies were compared with those of another group of rats tested only when aged 25 months. Expert old animals showed a good retention of previous experiences, whereas age-matched nonexpert animals exhibited some acquisition deficits. On the contrary, in the course of aging, the animals kept modifying their strategies independently of experience. In summary, we can conclude that previous experience is likely to influence performances of the aged rat but not the strategies adopted which are strictly age-dependent and independent of acquired experience.

Aging↗
PubMedDate not supplied

Hippocampal type I and type II corticosteroid receptors are modulated by central noradrenergic systems.

The effects of corticosteroids on various brain functions, including the negative feedback control of hypothalamo-pituitary-adrenal (HPA) axis activity, are mediated by two types of receptors (type I, or mineralocorticoid, and type II, or glucocorticoid) in the central nervous system. Although receptor numbers are thought to be regulated by circulating levels of corticosterone, there may be a direct neural control of corticosteroid receptors. In the present experiments, we demonstrate that 6-OHDA lesioning of noradrenergic (NA) ascending pathways in the pedunculus cerebellaris superior (PCS) reduces corticosterone secretion in response to novelty and increases the number of hippocampal type I corticosteroid receptors in rats 24 hr after adrenalectomy. The same lesion in adrenalectomized animals in which corticosterone levels were maintained within normal limits by corticosterone replacement implants also led to an increase in the number of type I corticosterone receptors and a decrease in the apparent affinity (Kd) of type II receptors in the hippocampus. These results suggest that the NA system may regulate HPA axis activity via a direct control of the number of type I receptors and the apparent affinity of type II receptors in the hippocampus. The possibility that there is a neural control of corticosteroid receptors may throw light on mechanisms controlling HPA axis activity and may suggest other approaches to the treatment of dysregulation of the HPA axis observed during stress and in certain psychopathological conditions.

Adrenalectomy↗
PubMedDate not supplied

A cluster analysis study of acetyl-L-carnitine effect on NMDA receptors in aging.

Aging is associated with a reduction in the maximum density of n-methyl-d-aspartate (NMDA)-sensitive glutamate binding sites in the hippocampus of Fischer 344 rats. This study was designed to investigate the effect of acetyl-l-carnitine (ALCAR) on NMDA receptors in the old rat (24 months) after chronic or single-dose treatments. The number of NMDA receptors was significantly decreased in the old rat hippocampus by 19.5% compared with the young rat. A six-month treatment with ALCAR in the old rat attenuated the loss of NMDA binding sites in the hippocampus. A single-dose treatment with ALCAR in the old rat increased the Bmax value by 35%, while no change was observed in the young group. We conclude that ALCAR can exert two actions: a trophic/neuro-preserving one when chronically administered during aging, and a stimulatory one when given at a single dose in the aged rat.

Acetylcarnitine↗
PubMedDate not supplied

Effect of long-term acetyl-L-carnitine on stress-induced analgesia in the aging rat.

Cold water swim (CWS) analgesia in the rat is mediated by the hypothalamo-pituitary-adrenocortical (HPA) axis. An age-dependent increase of CWS-induced analgesia was observed in male Sprague-Dawley young (4 months), adult (15 months) and old (26 months) rats. Acetyl-L-Carnitine (ALCAR) chronically administered (75 mg/kg/daily in drinking water for 8 months) to old rats was able to maintain the stress-dependent response at the same levels as in adult rats. This effect may be explained by ALCAR capability of retarding the age-dependent loss of glucocorticoid receptors in the hippocampus, thus maintaining the glucocorticoid competence of this structure which exerts a negative feedback control over the HPA axis activity.

Acetylcarnitine↗
PubMedDate not supplied

Acetyl-L-carnitine treatment increases nerve growth factor levels and choline acetyltransferase activity in the central nervous system of aged rats.

The hypothesis that some neurodegenerative events associated with ageing of the central nervous system (CNS) may be due to a lack of neurotrophic support to neurons is suggestive of a possible reparative pharmacological strategy intended to enhance the activity of endogenous neurotrophic agents. Here we report that treatment with acetyl-l-carnitine (ALCAR), a substance which has been shown to prevent some impairments of the aged CNS in experimental animals as well as in patients, is able to increase the levels and utilization of nerve growth factor (NGF) in the CNS of old rats. The stimulation of NGF levels in the CNS can be attained when ALCAR is given either for long or short periods to senescent animals of various ages, thus indicating a direct effect of the substance on the NGF system which is independent of the actual degenerative stage of the neurons. Furthermore, long-term treatment with ALCAR completely prevents the loss of choline acetyltransferase (ChAT) activity in the CNS of aged rats, suggesting that ALCAR may rescue cholinergic pathways from age-associated degeneration due to lack of retrogradely transported NGF.

Acetylcarnitine↗
PubMedDate not supplied

Nerve growth factor brain concentration and stress: changes depend on type of stressor and age.

In the relationship between the hippocampus and the hypothalamo-pituitary-adrenocortical axis, trophic and tropic actions of nerve growth factor are involved in parallel with those on the cholinergic nuclei of the basal forebrain. Here, we report the changes produced by stress activation of the hypothalamo-pituitary-adrenocortical axis on hippocampal and basal forebrain nerve growth factor concentrations in 3-month-old male Wistar rats. The stressors used were: restraint; cold exposure; foot-shock; and rotatory platform. Restraint stress tended to reduce nerve growth factor in the hippocampus and reduced it significantly in the basal forebrain. Nerve growth factor levels in the hippocampus were not modified by cold exposure. However, a single unrepeated exposure significantly increased nerve growth factor in the basal forebrain. Both acute and chronic foot-shock reduced nerve growth factor in the hippocampus, leaving the levels in the basal forebrain unmodified. Acute but not chronic rotatory platform reduced nerve growth factor in the hippocampus, while showing a tendency, more pronounced after chronic application, toward an increase in the basal forebrain. Since with aging both activity of the hypothalamus-pituitary-adrenal axis and nerve growth factor trophic and tropic functions change, we studied the effect of restraint and cold stress in the 24-month-old male rat. The variations in nerve growth factor concentrations in the basal forebrain following stress activation are no longer present in the aged rat. The picture that emerges is indicative of a complex relationship between stress and nerve growth factor which is influenced by the kind of stressor and by age. Lack of uniformity in the effects produced by different stressors might reside in different qualitative and/or quantitative degree of involvement of neurotransmitters and/or neurohormones for each of them.

Aging↗
PubMedDate not supplied

[Pharmacologic profile of protirelin tartrate].

Pharmacological interest in the tripeptide thyrotropin-releasing hormone (TRH) is due to the multiple effects it produces. In fact, apart from taking part in regulating the activity of the hypothalamo-pituitary-thyroid axis, TRH produces various neuropharmacological effects which indicate a biological role that is probably more important than that of a releasing hormone. Trials performed in animals have shown, for example, the dose-dependent capacity of TRH to induce analgesia, probably by interacting with the opioid peptide system. Motor activity is affected by TRH. In fact this tripeptide elicits an increase in spontaneous motor and explorative activities by interacting with the dopaminergic neurotransmitter system at the nucleus accumbens level. The neuropharmacological activities of TRH include an interesting arousal effect and an analeptic action on generalized depression of the CNS whether this depression is of natural origin, such as hibernation, or induced pharmacologically (barbiturates, ethanol) or of a traumatic origin (coma). This analeptic action is attributable to stimulation of cholinergic neurons in the septo-hippocampal area and to the presence of terminals containing TRH in the lateral septum and TRH receptors concentrated especially in the medial septum and diagonal band of Broca. It has also been suggested that TRH localized in the pineal gland has a part in activating the neuronal mechanisms of arousal. Associated with the arousal effect and especially evident in variously originated shock conditions are the activating effects of TRH on vegetative functions (body temperature, circulation, the gastrointestinal tract). These stimulatory activities on the CNS were the rationale for therapeutic use of TRH in the initial treatment of coma due to brain trauma and for the treatment of endogenous depression. A most interesting property of TRH is that of counteracting the neurological deficit due to experimental lesion of the spinal cord particularly with regard to spasticity and ataxia. Electrophysiological trials have shown that TRH depolarizes the motoneurons in frog spinal cord thereby increasing the monosynaptic reflex. Furthermore, TRH has recently been shown to have a trophic effect on cultures of rat fetus spinal cord. On this basis TRH has been used successfully for the treatment of amyotropic lateral sclerosis (Charcot's syndrome) and spinocerebellar degeneration. Further support for this therapeutic strategy is given by the demonstration that deafferentiation of rat spinal cord produces an increased density of TRH spinal receptors. Recent studies have also given encouraging results on the possible therapeutic use of TRH for the treatment of Alzheimer's disease.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMedDate not supplied

A model for later-life effects of perinatal drug exposure: maternal hormone mediation.

In the female rat chronic ethanol intake increased plasma levels of corticosterone; acute stress in the pregnant or lactating rat increased plasma levels of corticosterone in the fetuses or sucklings. In the lactating rat, corticosterone rapidly equilibrated between plasma and milk, so that variations in the mother's adrenocortical secretion could be promptly reflected in the suckling's body. The role of maternal adrenocortical hormone with regard to the development of pituitary-adrenocortical and behavioral activities was indicated by endocrine (plasma corticosterone), neurochemical (hippocampal corticosterone binding) and behavioral (avoidance performance) anomalies in the adult offspring of lactating rats with adrenocortical "hyperfunction" or "insufficiency." Further, the offspring of rats with adrenocortical "insufficiency" showed abnormalities in "in vitro" hypothalamus, pituitary and adrenocortex release of hormones. When searching for later effects in the offspring of drugs given to the mother in perinatal life one must be cognizant that, aside from their expected pharmacological action, drugs can produce variations in the mother pituitary-adrenocortical activity, sensed by the conceptus through the placenta or milk.

Adrenocortical Hyperfunction↗