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L F Agnati

Publications and source records attributed to L F Agnati.

At least 91 records · Page 5Linked to original sources

Different classes of volume transmission signals exist in the central nervous system and are affected by metabolic signals, temperature gradients and pressure waves.

Volume transmission (VT) is the mode of intercellular communication involving the diffusion of transmitters, via extracellular fluid (ECF) pathways, from nerve cells selectively capable of producing the signal (signal source) to nerve and glial cells selectively capable of recognizing it (signal target). The proposal is now put forward that at least two classes of VT signals can be distinguished: (a) the private-code signals, exemplified by neurotransmitters, which are released by a limited group of nerve cells and recognized, via high affinity G-protein coupled receptors or by cytosolic enzymes such as guanylate cyclase in the case of nitric oxide, by a specific group of cells; and (b) the accessible-code signals, such as the electrical signals that are released by all neuronal cells and decoded by almost every CNS cell. In the present paper, it will be underlined that carbon dioxide, hydrogen ions, temperature gradients and pressure waves may be regulators of wiring transmission and VT.

Animals↗

Antagonistic regulation of alpha 2-adrenoceptors by neuropeptide Y receptor subtypes in the nucleus tractus solitarii.

The modulation of alpha 2-adrenoceptors by neuropeptide Y Y1 and neuropeptide Y Y2 receptor subtypes has been studied in the nucleus tractus solitarii of the male rat. The autoradiographical experiments showed that neuropeptide Y-(1-36), neuropeptide Y-(13-36), a selective neuropeptide Y Y2 receptor agonist, and [Leu31,Pro34]neuropeptide Y, a selective neuropeptide Y Y1 receptor agonist, in the nanomolar range increased the Kd value of the [3H]p-aminoclonidine binding sites in the above rank order of potency without changing the Bmax values. In contrast, in the competition experiments, the neuropeptide Y Y1 and the neuropeptide Y Y2 receptor agonists decreased and increased, respectively, with the same potency the IC50 value of l-adrenaline and especially of clonidine for the alpha 2-adrenoceptor agonist binding sites associated with an increase and a decrease of the B0 value, respectively. Cardiovascular experiments showed that microinjections of clonidine into the nucleus tractus solitarii induced dose-dependent vasodepressor and bradycardiac responses. Threshold doses for vasodepressor effects of neuropeptide Y-(1-36) and of the neuropeptide Y Y1 receptor agonist and for vasopressor effects of the neuropeptide Y Y2 receptor agonist significantly counteracted the vasodepressor action elicited by an ED50 dose of clonidine in the nucleus tractus solitarii, the bradycardiac action of clonidine also being counteracted by the neuropeptide Y Y2 but not the neuropeptide Y Y1 receptor agonist. The present results give indications for the existence of an antagonistic modulation of high affinity alpha 2-adrenoceptors by the neuropeptide Y Y1 and neuropeptide Y Y2 receptor subtype in the nucleus tractus solitarii which may contribute to a reduction of alpha 2-adrenoceptor-mediated cardiovascular depression.

Adrenergic alpha-2 Receptor Antagonists↗

Glial and neuronal glucocorticoid receptor immunoreactive cell populations in developing, adult, and aging brain.

A detailed mapping of glucocorticoid receptor (GR) immunoreactivity (IR) in rat CNS was performed employing a mouse monoclonal antibody against rat liver GR. Subjective comparisons were made between the present results and the available data in the literature. A semiquantitation of GR immunostaining was found necessary and was obtained by microdensitometric and morphometric techniques, which enabled the distinction of neuronal and glial cell populations containing GR IR in various CNS regions. GR IR in the CNS was mainly found in the nuclear compartment. The GR was present in neuronal populations with classical neurotransmitters, especially monoamines and glutamate and with various neuropeptides. The degree of colocalization varied according to the function of the brain area. Functional implications were made in relation to stress sensitivity, mood and nociception/antinociception. The global control of networks by glucocorticoids may allow an optimal integration of different types of circuits. The GR is found already in the fetal rat and the development of GR mRNA and receptor protein was followed during the pre- and postnatal periods. The GR appears to be a major factor in brain maturation and in modulation of stress responses. In aged Brown Norway rat brain GR IR but not mineralocorticoid receptor (MR) IR is reduced in the hippocampal nerve cells. The intensity of GR IR but not the number of nerve cells is altered, indicating a reduced activation of the GR in aging in this rat strain. Overall GR participates in neuronal plasticity from fetal and postnatal life to adult life and aging.

Aging↗

Evidence for volume transmission in the dopamine denervated neostriatum of the rat after a unilateral nigral 6-OHDA microinjection. Studies with systemic D-amphetamine treatment.

In the present study the hypothesis has been tested if the dopamine releasing drug D-amphetamine via volume transmission can, at least partly, restore dopamine communication in the dopaminergically denervated neostriatum of rats. The experimental model used, has been a unilateral 6-hydroxydopamine-induced degeneration of the nigrostriatal dopamine neurons, based on nigral microinjections of this neurotoxin. Studies on c-fos like immunoreactivity after systemic D-amphetamine treatment demonstrated a wide-spread appearance of c-fos like immunoreactive neuronal nuclear profiles within the neostriatum on both the unlesioned and denervated side. In the unlesioned neostriatum a peak density of c-fos like immunoreactive profiles was found within the central part of the neostriatum, while on the denervated side the distribution pattern of c-fos like immunoreactive profiles peaked medially and gradually declined in a lateral direction. The microdialysis experiments demonstrated, after systemic d-amphetamine treatment, a marked and sustained increase of extracellular dopamine levels in the neostriatum on the unlesioned side, while no increases in the extracellular dopamine levels were observed on the dopaminergically denervated neostriatum. In the electrophysiological experiments, systemic D-amphetamine treatment produced an inhibition of the neuronal activity on the denervated side which showed a significant increase in basal discharge rate compared with the recordings obtained from the striata on the unlesioned side. The present immunocytochemical microdialysis and electrophysiological analysis provides evidence that in the unilaterally markedly dopamine depleted neostriatum with clearcut signs of dopamine receptor supersensitivity (rotational behaviour results), dopamine transmission may be partly restored via systemic D-amphetamine treatment through the release of dopamine, predominantly from the unlesioned neostriatum, which may diffuse into the cerebrospinal fluid to reach the contralateral dopaminergically denervated neostriatum.

Animals↗

Possible mechanisms for the powerful actions of neuropeptides.

In order to understand the mechanisms underlying the powerful actions of neuropeptides, the present article has emphasized the unique ability of neuropeptides to act as VT signals, which via high-affinity G-protein coupled receptors can exert long-lasting actions and control synaptic transmission via receptor-receptor interactions. Also of substantial importance is the ability of neuropeptides to act as a set of signals via the formation of different types of active fragments, which can act as negative-feedback or positive-feedback signals to modulate the response elicited by the parent peptide and to give origin to syndromic responses. Also in the actions of the fragments on the neuronal network, receptor-receptor interactions may play an important role both by modulating the parent peptide receptors and by modulating other types of VT and/or WT receptors. Future work will have to evaluate the role of neuropeptides as transcellular signals and as regulators of neuronal excitabilities after the formation of carbamates, but certainly new important developments are within the horizon of today's research.

Animals↗

Evidence for an antagonistic angiotensin II/alpha 2-adrenoceptor interaction in the nucleus tractus solitarii.

Interactions between alpha 2-adrenoceptors and angiotensin II receptors were evaluated in the nucleus tractus solitarii of the rat by means of quantitative receptor autoradiography and cardiovascular analysis. In binding experiments using l-noradrenaline to compete for [3H]p-aminoclonidine binding sites, angiotensin II (1 nM) increased the IC50 value of l-noradrenaline by 50%. The angiotensin AT1 receptor antagonist, DUP753 (losartan), not only blocked this action but also decreased the IC50 value of l-noradrenaline. The modulatory effect of angiotensin II was also evaluated after addition of both DUP753 and PD123319, an angiotensin AT2 receptor antagonist, and counteraction of the reduction in the IC50 value of l-noradrenaline was observed. In saturation experiments angiotensin II increased the KD and Bmax values of [3H]p-aminoclonidine binding sites, compatible with possible uncoupling of the alpha 2-adrenoceptors. Cardiovascular analysis demonstrated that a threshold dose of angiotensin II (0.05 pmol) counteracted the vasodepressor effect produced by an ED50 dose of l-adrenaline, l-noradrenaline or clonidine coinjected in the nucleus tractus solitarii. DUP753 fully blocked this in vivo modulation of alpha 2-adrenoceptors by angiotensin II. These findings suggest the existence of an antagonistic angiotensin AT1/alpha 2-adrenoceptor interaction in the nucleus tractus solitarii. Therefore, it can be surmised that the activation of angiotensin II AT1 receptors may reduce the transduction of the alpha 2-adrenoceptors and thus the alpha 2-mediated vasodepressor responses.

Adrenergic alpha-Antagonists↗

Generalized presence of a PEC-60-like peptide in catecholamine neurones.

PEC-60, a 60-residue intestinal peptide structurally related to the pancreatic secretory type of trypsin inhibitor, has been isolated, characterized and molecularly cloned. It shows biological activity as a hormone in both the gastrointestinal tract and in the immune system. We now report immunohistochemical evidence suggesting its neural localization exclusively within central and peripheral catecholamine (CA) neurones. PEC-60-like immunoreactivity was present in cell bodies, dendrites and nerve terminals of virtually all catecholamine neurones examined and including the noradrenergic gland cells of the adrenal medulla. PEC-60-like immunoreactivity was not seen, however, within the tyrosine hydroxylase-positive but CA-negative arcuate neurones producing growth hormone releasing hormone. The findings open up the possibility that a PEC-60-like peptide may represent a generalized co-transmitter in the peripheral and central CA neurones.

Animals↗

Selective modulation of the NPY receptors of the Y2 subtype by alpha 2 receptors in the nucleus tractus solitarii of the rat. A cardiovascular and quantitative receptor autoradiographical analysis.

The modulation of neuropeptide Y (NPY) receptors by alpha 2 receptors in the nucleus tractus solitarii (Sol) of the rat was evaluated using quantitative receptor autoradiography and measurements of mean arterial blood pressure and heart rate. The receptor autoradiographical experiments showed that clonidine (10 nM), a selective alpha 2 receptor agonist, induced a 59% increase in the B0 value and a 47% decrease in the IC50 value of NPY(1-36) when competing for [125I]peptide YY ([125I]PYY)-binding sites in the presence of [Leu31, Pro34]NPY (100 nM), a selective NPY Y1 receptor agonist, to block the binding to NPY Y1 receptors. In contrast, when NPY(13-36) (300 nM), a selective NPY Y2 receptor agonist, was used to block the binding to NPY Y2 receptors, clonidine (1-30 nM) did not affect the B0 value and the IC50 value of NPY(1-36) when competing for [125I]PYY-binding sites, suggesting that the stimulation of alpha 2 receptors can selectively increase the affinity of NYP(1-36) for the NPY Y2 receptor. Microinjections of threshold doses of adrenaline or clonidine into the Sol not only counteracted the vasopressor action of a close to ED50 dose of coinjected NPY(13-36), but also changed the vasopressor and tachycardic response produced by NPY(13-36) into a vasodepressor and bradycardic response. However, threshold doses of adrenaline or of clonidine microinjected into the Sol did not modify the vasodepressor responses to a close to ED50 dose of NPY(1-36) or of [Leu31, Pro34]NPY.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Dopamine D1 receptors are involved in the modulation of D2 receptors induced by cholecystokinin receptor subtypes in rat neostriatal membranes.

The action of cholecystokinin octapeptide (CCK-8) on rat neostriatal dopamine (DA) D2 receptors was evaluated in membrane binding experiments. 0.1 nM of CCK-8 increased the Kd value of the D2 agonist [3H]N-propylnorapomorphine (NPA) binding sites by 42%. The CCKB antagonist PD134308 blocked this action. Kinetic analysis demonstrated that this effect of CCK-8 was related to a reduction by 45% of the association rate constant of [3H]NPA. In contrast, 1 nM of CCK-8 decreased the KH and the KL values of DA for the D2 antagonist [3H]raclopride binding sites by 56% and 50%, respectively. Both the CCKA antagonist L364718 and the CCKB antagonist PD134308 blocked this effect. The D1 antagonist SCH23390 counteracted the CCK-8 induced decrease in the KH and the KL values of DA, and allowed 1 nM of CCK-8 to produce a significant increase in the IC50 value of NPA for the [3H]raclopride binding sites. These results indicate that CCK-8 can reduce the affinity of the neostriatal D2 agonist binding sites, but increase the affinity of D2 receptors for DA. D1 receptors may exert a switching role in the modulation of the neostriatal D2 receptors by the CCK receptors.

Animals↗

Coinjections of NPY(1-36) or [Leu31,Pro34]NPY with adrenaline in the nucleus tractus solitarius of the rat counteract the vasodepressor responses to adrenaline.

The cardiovascular effects of adrenaline microinjected alone or together with neuropeptide Y (NPY) receptor agonists into the nucleus tractus solitarius (Sol) of the anaesthetized rat have been investigated in order to evaluate NPY/adrenergic receptor interactions. In the dose range 0.05-20 nmol, adrenaline microinjected unilaterally into the Sol produced significant dose-related reductions in mean arterial blood pressure and heart rate. The vasodepressor action of a close to ED50 dose of adrenaline (0.5 nmol) was significantly counteracted by a threshold dose of NPY (1-36) (1 pmol) and of the NPY Y1 receptor agonist [Leu31,Pro34]NPY (2.5 pmol) microinjected into the Sol, but not by a threshold dose of NPY(13-36)(50 fmol), a selective Y2 receptor agonist. The present study provides evidence for an antagonistic NPY Y1/adrenergic receptor interaction in the Sol of the rat, involved in cardiovascular regulation.

Animals↗

Evidence for a regional distribution of hyaluronic acid in the rat brain using a highly specific hyaluronic acid recognizing protein.

By means of a highly specific hyaluronic acid-recognizing protein the localization and regional distribution of hyaluronic acid was demonstrated in the tel- and diencephalon and in the midbrain of the adult rat nervous system. Histochemistry revealed labeling associated with the plasma membrane in highly discrete nerve cell bodies of the frontoparietal cortex, the red nucleus, the zona reticulata of the substantia nigra, the oculomotor nucleus and the reticular thalamic nucleus. A strong labeling without association with perikarya was demonstrated in the subgranular zone of the dentate gyrus of the hippocampal formation. The present results open up the possibility that the hyaluronic acid found in high concentrations associated with some perikarya may have a special role in plasticity responses in these discrete nerve cell populations.

Animals↗

On the regional distribution of heparan sulfate proteoglycan immunoreactivity in the rat brain.

By means of two monoclonal antibodies specific for heparan sulfate (HS)-related epitopes, one (10E4) against native HS chains and one (3G10) against desaturated uronates, a highly regional and differential distribution of these two epitopes have been observed in the adult rat brain. The 10E4 epitope immunoreactivity (IR) is mainly found in the substantia nigra, the red nucleus and the subgranular zone of the dentate gyrus, while the 3G10 epitope IR is mainly found in the CA2 area of the hippocampal formation and the pyramdial cells in the layer V of the frontoparietal cortex. The codistribution of both types of IRs with basic fibroblast growth factor (bFGF, FGF-2) in neurons and astroglia supports the notion that heparan sulfate proteoglycans (HSPG) in the extracellular matrix may serve as a site for storage of bFGF and assist in the bFGF-induced activation of the high-affinity FGF receptors linked to astroglia and neurons in these discrete areas.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

Chronic continuous infusion of nicotine increases the disappearance of choline acetyltransferase immunoreactivity in the cholinergic cell bodies of the medial septal nucleus following a partial unilateral transection of the fimbria fornix.

Previous studies have demonstrated that chronic continuous nicotine treatment via minipumps partially protects against mechanically induced degeneration of the nigrostriatal dopamine neurons in the male Sprague-Dawley rat. In the present study we investigated how a 4-week continuous infusion with (-)-nicotine via minipumps implanted subcutaneously in the male Sprague-Dawley rat (0.125 mg/kg-1 h-1) influences the anterograde and retrograde changes occurring in the septohippocampal cholinergic neurons following a unilateral transection of the fimbria fornix. Choline acetyltransferase and acetylcholinesterase immunocytochemistry was performed in combination with computer-assisted morphometry and microdensitometry. Measurements of choline acetyltransferase enzyme activity was performed in the dorsal hippocampus. The chronic nicotine infusion significantly increased the disappearance of the choline acetyltransferase immunoreactive nerve cell area within the medial septal nucleus of the lesioned side. However, the disappearance of the acetylcholinesterase immunoreactive nerve terminals within the dentate gyrus (molecular layer) and of choline acetyltransferase enzyme activity within the dorsal hippocampus was not found to be influenced by the chronic nicotine infusion. Thus, chronic infusion of (-)-nicotine does not appear to exert any protective activity on mechanically injured septohippocampal cholinergic neurons but may instead increase their dysfunction. In comparison with the dopaminergic neurons it may therefore be that the continuous chronic nicotine exposure does not lead to sufficient desensitization of the nicotinic cholinoceptors of the cholinergic neurons to reduce the chronic influx of sodium and calcium ions via the nicotinic ion channels and thus intraneuronal calcium levels and energy demands.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholinesterase↗

The concept of astrocyte-kinetic drug in the treatment of neurodegenerative diseases: evidence for L-deprenyl-induced activation of reactive astrocytes.

Basic fibroblast growth factor (bFGF) increases neuronal survival and growth in cell cultures and stimulates functional recovery from brain lesion. In addition, bFGF is able to induce glial cell proliferation and differentiation. Recently, L-deprenyl has been shown to potentiate astrocyte reaction to a mechanical lesion and to possess a trophic-like activity in several experimental models. In the present paper, we have therefore investigated if the enhancing effect of L-deprenyl on astrocyte reactivity is accompanied by increased levels of bFGF. The effect of L-deprenyl (0.25 mg/kg/day) on bFGF immunoreactivity (IR) after the insertion of an injection cannula in rat neostriatum have been investigated. It has been found that subchronic L-deprenyl treatment potentiates both the lesion-induced increase of glial fibrillary acidic protein (GFAP) and bFGF IRs (P < 0.01). These data suggest that a possible mechanism for L-deprenyl-induced neuroprotection may be the activation of astrocytes associated with increased secretion of trophic factors that promote neuronal survival and growth. This "astrocyte-kinetic" action of L-deprenyl could represent a new therapeutical approach to increase trophic support of lesioned neurons.

Animals↗

Basic fibroblast growth factor and steroid receptors in the aging hippocampus of the brown Norway rat: immunocytochemical analysis in combination with stereology.

The effect of aging on the hippocampal formation of the male Brown Norway rat was studied by immunohistochemistry and measurements of the immunoreactive hippocampal cells using stereological techniques. The total estimated number of glucocorticoid receptor (GR) immunoreactive neurons of the CA1-CA2 area did not differ in the 3- and the 36-month-old rat. However, the intensity of the GR immunoreactivity was decreased in the aged animals. A gradual decrease of the immunoreactivity for the mineralocorticoid receptor was also observed in the CA1-CA2 area. In the stratum oriens and the stratum radiatum of the CA1-CA2 area the immunoreactivity for basic fibroblast growth factor (bFGF) present in the glia was found to be reduced [20,000 +/- 2100 (n = 6)] in the 36-month-old rat vs the 3-month-old rat [28,500 +/- 4500 (n = 4) (*P = 0.05)]. However, there was no difference in the number of glial fibrillary acidic protein immunoreactive cells of this area in these two age groups. The present findings give evidence that in the Brown Norway rat there is no loss of the neuronal population containing glucocorticoid receptors of the CA1-CA2 area during aging but suggest that aging is characterized by deficits of glially derived growth factors, such as bFGF.

Aging↗

Mapping and computer assisted morphometry and microdensitometry of glucocorticoid receptor immunoreactive neurons and glial cells in the rat central nervous system.

By means of a monoclonal mouse immunoglobulin G2a antibody against the rat liver glucocorticoid receptor and the indirect immunoperoxidase technique, the distribution of glucocorticoid receptors in neuronal and glial cell populations was mapped in the central nervous system of the male rat. The mapping was complemented by computer-assisted morphometric and microdensitometric evaluation of glucocorticoid receptor immunoreactivity in many brain regions. The quantitative analysis allowed us to achieve for the first time an objective characterization of glucocorticoid receptor distribution in the CNS, thus avoiding the ambiguities of previous mapping studies based on subjective evaluations. In addition, a taxonomic analysis of central nervous system regions containing glucocorticoid receptor immunoreactivity was carried out utilizing the quantitative parameters obtained in the morphometric evaluation. Nuclei of neuronal and glial cells containing glucocorticoid receptor immunoreactivity were detected in a widespread, but still highly heterogeneous, fashion in the central nervous system, underlining the view that glucocorticoids can control a large number of central nervous system target cells via effects on gene expression. Many nerve cell populations have been shown to contain substantial amounts of nuclear glucocorticoid receptor immunoreactivity, whereas only a low density of glial cells, in both gray and white matter, show nuclear glucocorticoid receptor immunoreactivity. Thus, in most brain areas, the major target for glucocorticoids appears to be the nerve cells. Interestingly, an inverse correlation was found in the regional density of glucocorticoid receptor-immunoreactive nerve and glial cells, suggesting that glucocorticoids may influence a brain area either via glial cells or, more frequently, via nerve cells. The results on mapping highlight the impact of glucocorticoids in areas both traditionally and not traditionally involved in stress responses. The distribution of glucocorticoid receptor immunoreactivity also emphasizes a role of glucocorticoids in the regulation of the afferent regions of the basal ganglia and the cerebellar cortex, and of both afferent and efferent layers of the cerebral cortex. Glucocorticoid receptor immunoreactivity is widely distributed over the thalamus, probably leading to modulation of activity in the various thalamocortical pathways transmitting inter alia specific sensory information to the cerebral cortex. Many unspecific afferents to the cerebral cortex are potentially regulated by glucocorticoid receptors such as the noradrenaline and 5-hydroxytryptamine afferents, since their nerve cells of origin contain strong glucocorticoid receptor immunoreactivity. Eight brain regions involving sensory, motor and limbic areas were shown to have a similarity with regard to glucocorticoid receptor-immunoreactive parameters at the level of 95%. The density of glucocorticoid receptor-immunoreactive nerve cells appeared to be the main factor in determining such a very high level of similarity. Overall, our results emphasize that glucocorticoids may appropriately tune networks of different areas to obtain optimal integration and in this way improve survival of the animal under challenging conditions.

Adrenalectomy↗

Basic fibroblast growth factor (bFGF, FGF-2) immunoreactivity exists in the noradrenaline, adrenaline and 5-HT nerve cells of the rat brain.

By means of two colour immunofluorescence procedures it has been possible to demonstrate in the rat brain the coexistence of TH and bFGF immunoreactivities (IRs) in the perikarya of large numbers of noradrenaline (NA) nerve cells of the locus coeruleus and of the NA cell groups A1, A5 and A7 and in many perikarya of the adrenaline (A) cell groups C1, C2 and C3. The coexistence of 5-hydroxytryptamine (5-HT) and bFGF IRs was demonstrated in the perikarya of large numbers of 5-HT nerve cells of practically all raphe nuclei. These results open up the possibility that bFGF may have a trophic role in the NA, A and 5-HT cell groups of the rat brain.

Animals↗

Microinjections of subpicomolar amounts of NPY(13-36) into the nucleus tractus solitarius of the rat counteract the vasodepressor responses of NPY(1-36) and of a NPY Y1 receptor agonist.

Microinjections of neuropeptide Y (NPY) (1-36) and of the NPY Y1 agonist [Leu31,Pro34]NPY into the caudal dorsomedial part of the nucleus tractus solitarius (Sol) in the anaesthetized rat led to the development of dose-related vasodepressor and bradycardic responses. The threshold dose of the NPY Y2 agonist NPY(13-36) (50 fmol) significantly counteracted the vasodepressor actions of a close to ED50 dose of NPY(1-36) (2.5 pmol) and of the NPY Y1 agonist (5 pmol). These results indicate that NPY Y1 receptor activation in the Sol leads to the development of a vasodepressor response, which can be counteracted by NPY Y2 receptor activation in the Sol. The results support the existence of a Y2/Y1 receptor-receptor interaction in the Sol, via which NPY Y2 receptors may reduce transduction over NPY Y1 receptors.

Animals↗