Search PubMed⌕ Search

Biomedical subjects

G Taglialatela

Publications and source records attributed to G Taglialatela.

52 records · Page 3Linked to original sources
PubMed1991

Nerve growth factor modulates the activation of the hypothalamo-pituitary-adrenocortical axis during the stress response.

In the present study, we have investigated the functional relationship between the nerve growth factor protein (NGF) and the hypothalamus-pituitary-adrenocortical axis (HPAA). We have found that while iv injected NGF is able to stimulate the HPAA activity in rats, NGF is not able to stimulate the axis after a block of the hypothalamus produced by chlorpromazine-morphine-Nembutal treatment. Also, the stress activation of the HPAA is significantly reduced by pretreatment of the rats with anti-NGF immunoglobulin G. These results suggest that the stimulatory action of NGF on HPAA activity requires the release of ACTH secretagogues from the hypothalamus and that NGF may modulate the HPAA response to stress stimuli.

Animals↗
PubMed1990

125I-beta-nerve growth factor binding is reduced in rat brain after stress exposure.

In the central nervous system (CNS), the presence of nerve growth factor (NGF) and its receptor, NGFR, in cholinergic neurons has been demonstrated. In this study we report that, after exposure to stress, there was a reduction in total binding of NGF in the hippocampus and basal forebrain of 3.5-month-old rats without significant changes in the frontal cortex or cerebellum. Chronic treatment with acetyl-l-carnitine (ALCAR), that prevents some age-related impairments of CNS, for 1.5 months, decreased NGF binding in hippocampus and basal forebrain but abolished the stress-related reduction of NGF binding observed in the hippocampus of untreated rats.

Animals↗
PubMed1990

Nerve growth factor activity and aging in CNS.

This is a discussion of aging in CNS and the influence of the nerve growth factor (NGF) protein. The paper considers neuronal plasticity and neuronotrophic substances, neuronal cell death and the nerve growth factor protein, including its effects, receptors, and model systems for the study of CNS aging.

Aging↗
PubMed1989

Adrenocorticoid receptor binding in the rat hippocampus: strain-dependent covariations with arousal and habituation to novelty.

In order to investigate whether the genotype-dependent behaviour of the Naples high-(NHE) and low-excitability (NLE) rat strains was modulated by differences in the capacity of hippocampal adrenocorticoid receptors, a correlative analysis was made among behavioural scores from exposure to a Làt-maze and in vitro [3H]corticosterone hippocampal binding capacity in these rats and in their random-bred controls (NRB). As previously shown, NHE/NLE-rats differed markedly upon forced exposure to the maze, with the NRB group occupying an intermediate position. No differences were found in maximal binding capacity (Bmax) and dissociation constant (Kd), nor in the individual maximal binding capacity (IMBC) between the two strains, while both showed lower IMBC than NRB-rats. These results tend to exclude that the genetic differences in the behaviour of NHE/NLE-rats are due to distinct patterns in the adrenocorticoid binding capacity in the hippocampus (HPC). Moreover, the intrastrain correlative analysis among IMBC (in the whole HPC and in its dorsal and ventral portion) and the behavioural scores showed that (1) motor and emotional correlates of 'arousal' to novelty were positively correlated in NLE and negatively in NHE-, but not in NRB-rats; (2) a consistent correlation was found with the intertrial activity decrement (long-term habituation), which was negative in both strains, and it was positive in NRB-rats. These complex co-variations are envisioned as possibly due to the differential modulatory components of the activation and inhibition of novelty-induced arousal response. However, our findings support the hypothesized involvement of the HPC, where adrenocorticoid receptors are selectively concentrated, in the modulation of some adaptive behavioural responses.

Animals↗
PubMed1989

Acetyl-L-carnitine reduces the age-dependent loss of glucocorticoid receptors in the rat hippocampus: an autoradiographic study.

Brain autoradiography in adrenalectomized rats injected with 3H-corticosterone 2 hr before sacrifice was used to study the effect of aging and long-term acetyl-l-carnitine treatment on the hippocampal glucocorticoid receptor. Densitometric analysis of silver grains in individual nerve cells of the hippocampus showed that pyramidal neurones of the CA1 field and granular cells of the dentate gyrus are richest in 3H-corticosterone binding sites, whereas pyramidal neurons of the CA3 field have the lowest number of binding sites. There was a significant decline in the number of glucocorticoid receptors within the various hippocampal areas, both as the total number of 3H-corticosterone binding sites and as the number per single pyramidal or granule neuron associated with aging and perhaps due to loss of adrenocorticoid-competent neurons. The dentate gyrus and the CA1 region were mostly affected by the age-dependent decrease in glucocorticoid receptors of the hippocampus. Twenty-eight-month-old rats, treated with acetyl-l-carnitine for 7 months, showed a significantly higher number of 3H-corticosterone binding sites within the various hippocampal regions examined than did age-matched controls. The CA1 and the dentate gyrus were the regions most susceptible to amelioration by acetyl-l-carnitine treatment. These findings suggest a positive effect of acetyl-l-carnitine treatment on age-related changes which occur in the hippocampus.

Acetylcarnitine↗
PubMed1988

Nerve growth factor binding in aged rat central nervous system: effect of acetyl-L-carnitine.

The nerve growth factor protein (NGF) has been demonstrated to affect neuronal development and maintenance of the differentiated state in certain neurons of the peripheral and central nervous system (CNS) of mammals. In the CNS, NGF has sparing effects on cholinergic neurons of the rodent basal forebrain (BF) following lesions where it selectively induces choline acetyltransferase (ChAT). NGF also induces ChAT in the areas to which BF provides afferents. In aged rats, there is a reduction in the NGF-binding capacity of sympathetic ganglia. Here, we wish to report that there is a decrease in the NGF-binding capacity of the hippocampus and basal forebrain of aged (26-month-old) rats as compared to 4-month-old controls but no change in NGF binding in cerebellum. In all instances, equilibrium binding dissociation constants did not differ significantly. Treatment of rats with acetyl-L-carnitine, reported to improve cognitive performance of aged rats, ameliorates these age-related deficits.

Acetylcarnitine↗
PubMedDate not supplied

Nerve growth factor and neuronal cell death.

The regulation of neuronal cell death by the neuronotrophic factor, nerve growth factor (NGF), has been described during neural development and following injury to the nervous system. Also, reduced NGF activity has been reported for the aged NGF-responsive neurons of the sympathetic nervous system and cholinergic regions of the central nervous system (CNS) in aged rodents and man. Although there is some knowledge of the molecular structure of the NGF and its receptor, less is known as to the mechanism of action of NGF. Here, a possible role for NGF in the regulation of oxidant--antioxidant balance is discussed as part of a molecular explanation for the known effects of NGF on neuronal survival during development, after injury, and in the aged CNS.

Amino Acid Sequence↗
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

Spatial memory and NGF levels in aged rats: natural variability and effects of acetyl-L-carnitine treatment.

The natural variability of behavioral performance of aged rats was used to evaluate the effect of acetyl-L-carnitine (ALCAR) on spatial learning and NGF levels in different brain areas. We used a cluster analysis procedure to subdivide the aged animals into three classes of performance (good, intermediate, and poor). These three classes were equally subdivided into controls and ALCAR-treated animals in order to investigate its effect on spatial retention. The stratification of animals prior to treatment allowed us to highlight the state dependency of the action of ALCAR. The effect of the molecule in improving spatial retention was evident only in the intermediate performance group. Furthermore, the drug reduced the NGF levels in the basal forebrain of treated animals, especially in the intermediate performance group. These results suggest a performance-dependent effect of ALCAR and a nonlinear relationship between NGF levels and learning ability in aged rats.

Acetylcarnitine↗
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↗