Biomedical subjects

M Bentivoglio

Publications and source records attributed to M Bentivoglio.

At least 55 records · Page 3Linked to original sources

PubMed1998

Contralateral cortical projection to the mediodorsal thalamic nucleus: origin and synaptic organization in the rat.

The origin of the corticothalamic projections to the contralateral mediodorsal nucleus, the collateralization of cortical fibers and their synaptic organization in the ipsi- and contralateral mediodorsal nuclei were investigated in adult rats with double retrograde fluorescent and anterograde tracing. After tracer injections in the mediodorsal nuclei on either side, neurons were retrogradely labeled in all the areas of the contralateral prefrontal cortex in which ipsilateral labeling was also observed. Contralateral corticothalamic cells accounted for 15% of the labeled neurons in the orbital and agranular insular areas, while their proportion was lower (3%) in the anterior cingulate cortex. Up to 70% of the contralateral cortical neurons were double labeled by bilateral injections in the mediodorsal nuclei. At the electron microscopic level, unilateral injections of biotinylated dextran-amine in the orbitofrontal cortex resulted in anterograde labeling of small terminals and a few large boutons in the ipsilateral mediodorsal nucleus, while only small boutons were identified contralaterally. The diameter of postsynaptic dendritic profiles contacted by labeled small cortical endings was significantly larger in the ipsilateral mediodorsal nucleus than contralaterally. These findings demonstrate that dense contralateral cortical projections to the mediodorsal nucleus derive from the orbital and agranular insular areas, and that crossed corticothalamic afferents are mostly formed by collaterals of the ipsilateral connections. Our observations also point out the heterogeneity of corticothalamic boutons in the rat mediodorsal nucleus and morphological differences in the synaptic organization of prefrontal fibers innervating the two sides, indicating that ipsilateral cortical afferents may be more proximally distributed than crossed cortical fibers on dendrites of mediodorsal neurons.

Animals↗

PubMed1998

1898-1998: Camillo Golgi and "the Golgi": one hundred years of terminological clones.

Camillo Golgi discovered, in 1898, the cell organelle that has been called, after him, "the Golgi apparatus" or "the Golgi complex." Because of the necessity of saving words in scientific literature, "the Golgi apparatus" is nowadays frequently referred to only as "the Golgi" or used in an adjectival form in combination with a variety of terms (e.g., Golgi vesicle, Golgi area, Golgi traffic, and so forth). We present here a search of the Medline database for the years 1967 through 1997, which demonstrates that the eponym has lost all connection with Golgi's personal identity. In addition, the search indicates that interest in the Golgi apparatus is steadily increasing, as evidenced in the scientific literature, and that Golgi's name is much more frequently used in association with the cell organelle than with any of the other scientific contributions of this scientist, including the Golgi impregnation of nerve cells.

Eponyms↗

PubMed1998

Altered neuronal activity rhythm and glutamate receptor expression in the suprachiasmatic nuclei of Trypanosoma brucei-infected rats.

The parasites Trypanosoma brucei cause African trypanosomiasis (sleeping sickness), a severe neuropsychiatric disease with marked disturbances of sleep-wake alternation. The sites of brain lesions are not well characterized. The present experimental investigation is focused on the hypothalamic suprachiasmatic nuclei, which play a role of a biological clock entraining endogenous rhythms in the mammalian brain. The electrophysiological properties of these neurons were analyzed in slice preparations from trypanosome-infected rats. The neuronal spontaneous activity, which shows a circadian oscillation, was markedly altered in the infected animals, displaying a reduced firing rate and phase advance of its circadian peak. The direct retinal fibers, which play a pivotal role in entrainment of the circadian pacemaker, displayed a normal density and distribution in the suprachiasmatic nuclei of infected animals after intraocular tracer injections in vivo. At the postsynaptic level, immunohistochemistry and Western blotting revealed in the suprachiasmatic nuclei of infected rats a selective decrease of the expression of glutamate AMPA GluR2/3 and NMDAR1 receptor subunits that gate retinal afferents. These data disclose an impairment of the neuronal functions in the biological clock in African trypanosomiasis, and may serve to unravel functional and molecular mechanisms behind endogenous rhythm disturbances.

Animals↗

PubMed1997

Nitric oxide synthase in the adult and developing thalamus: histochemical and immunohistochemical study in the rat.

The distribution of neuronal elements that express nitric oxide synthase (NOS), the synthetic enzyme of the free radical nitric oxide, was investigated in the adult and developing rat thalamus by means of NADPH-diaphorase (NADPH-d) histochemistry, which is a marker of NOS. Immunocytochemistry was also used to confirm the equivalence between the histochemical pattern of staining and the distribution of the expression of the neuronal NOS isoform. In the adult thalamus, NADPH-d-positive and NOS-immunoreactive perikarya were selectively concentrated along the midline (in the paraventricular, rhomboid, and central medial nuclei) and in the dorsal and ventral lateral geniculate nuclei. Isolated clusters of stained neurons were also observed in the lateral posterior nucleus, in the dorsal part of the medial geniculate nucleus, and in the ventromedial nucleus. Positive perikarya were either absent or very sparse in the other thalamic nuclei. Many thalamic domains were, however, characterized by distinct patterns of NADPH-d-positive fibers, preterminal and terminal-like elements. The highest density of stained neuropil was observed in the anteroventral and anteromedial nuclei, in several of the midline nuclei, in the anterior intralaminar nuclei, and in the lateral and medial geniculate nuclei. Although histochemical reactivity was observed in the thalamus at birth, the intensity and the pattern of distribution of staining observed in adulthood was not achieved until the end of the third postnatal week. The NADPH-d histochemical positivity followed discrete developmental schedules in various thalamic domains, and different areas reached a mature pattern at different ages. In addition, populations of transiently stained neuronal cell bodies were observed in the medial thalamus during the first two postnatal weeks. These results show discrete patterns of expression of NOS in the adult and developing thalamus and suggest that nitric oxide may be involved in selected physiological and developmental roles in different thalamic domains.

Aging↗

PubMed1997

Age-dependent induction of nitric oxide synthase activity in facial motoneurons after axotomy.

The facial nerve was transected in rats at different postnatal ages, from birth to early adulthood. NADPH-diaphorase histochemistry was performed to analyze the induction of nitric oxide synthase, the synthetic enzyme of the free radical nitric oxide, in injured facial motoneurons. In addition, in situ nick-end labeling of DNA fragmentation (TUNEL technique) was performed after axotomy at birth, to verify the occurrence of apoptosis in the damaged facial motoneurons. A striking age-dependency was found in the induction of nitric oxide synthase activity in axotomized facial motoneurons. NADPH-diaphorase positivity was not detectable in these neurons 1 and 2 days after axotomy at birth, when apoptotic changes were evident and marked. In addition, NADPH-diaphorase staining was hardly detectable in the facial nucleus 4 days after axotomies at birth, when extensive motoneuron loss was evident. NADPH-diaphorase positivity was instead induced in the facial motoneurons axotomized from the end of the first postnatal week to adulthood, when the nerve cell loss was less severe than in newborns. However, the time course of the enzyme activity induction varied considerably in relation to the animals' age. These findings are discussed in relation to the role of nitric oxide in motoneuron death or protective response to injury and of oxidative stress in neurodegeneration.

Age Factors↗

PubMed1997

Glutamate, aspartate and co-localization with calbindin in the medial thalamus. An immunohistochemical study in the rat.

Topographical and quantitative features of medial thalamic neurons in which aspartate (ASP) or glutamate (GLU) might act as neurotransmitters were investigated in the rat. The calcium-binding protein calbindin D-28k (CB) was exploited as a marker of neuronal subsets, thus allowing us to study also the relationships between the CB-containing neurons and those immunoreactive to excitatory amino acids. Double immunocytochemistry of ASP and CB or GLU and CB was performed in 40-microm-thick sections. The three markers were distributed in the thalamic midline, mediodorsal, anterior intralaminar and ventromedial nuclei, with regional variations. ASP-immunoreactive neurons appeared more numerous than the GLU-immunoreactive ones throughout these structures; ASP-CB or GLU-CB double-immunostained neurons were evident. ASP-, GLU- and CB-immunoreactive cells were then quantitatively evaluated in 5-microm-thick consecutive sections. Interindividual variations and different anti-ASP and anti-GLU antibodies did not result in significant differences. ASP and GLU were not co-localized. Single ASP- or GLU-immunoreactive neurons accounted for 60% of the total number of immunostained cells, and single ASP-immunopositive cells represented more than half of these neurons. Among the CB-immunoreactive cells (40% of the total), half were double immunostained; the proportion of double CB-ASP-immunopositive neurons was sevenfold higher than that of the CB-GLU-immunoreactive ones. These results indicate that ASP may act as excitatory neurotransmitter in a relatively high proportion of medial thalamic neurons, in which ASP frequently coexists with CB. Approximately 50% of the CB-immunoreactive cells did not contain either ASP or GLU, suggesting that some medial thalamic neurons may utilize a different neurotransmitter.

Animals↗

PubMed1997

Overlapping ipsilateral and contralateral retinal projections to the lateral geniculate nucleus and superior colliculus in the cat: a retrograde triple labelling study.

To analyze the relative proportion and distribution of retinal ganglion cells projecting ipsilaterally and contralaterally in the cat, large injections of the fluorescent tracers Fluoro Gold, Fast Blue, and Diamidino Yellow were made in the main layers of the lateral geniculate nucleus (LGN) and superior colliculus (SC). One tracer was injected in both the LGN and SC on one side, and the other two tracers were injected contralaterally, in the LGN and SC, respectively; labelled ganglion cells were charted on retinal whole mounts. Ganglion cells labelled from the LGN and SC were highly intermingled in both the ipsilateral and contralateral retinae. The adopted combinations of tracers allowed the detection of cells double labelled from the SC and LGN, supporting the occurrence of branched retino-thalamic axons to the SC. About one-fourth of the ganglion cells labelled from the LGN and SC was located in the eye ipsilateral to the injection. Retrograde labelling from the ipsilateral side was almost entirely confined to the temporal hemiretina. In the contralateral eye, labelled cells were mainly concentrated in the nasal hemiretina, but more than 10% were also detected in the temporal half of the retina. In the latter area, cells displaying the entire range of sizes of the retinal ganglion cells, labelled from the contralateral LGN and SC, were found throughout the entire hemiretina. However, more than 50% of such "wrong" projecting cells were grouped in a strip of 2 mm closest to the nasotemporal division. Control experiments, in which the tracers injections were restricted to the rostral and dorsal portions of the LGN to avoid optic tract contamination, consistently confirmed the occurrence and distribution of the "wrong" projecting cells in the temporal hemiretina. Thus, these latter cells are not grouped in a central strip, where ganglion cells would have the same chance of projecting to the same or to the opposite side, and sparsely distributed in the temporal periphery, as previously believed. Instead, the present findings indicate that the retinal ganglion cells of origin of contralateral projections are distributed more in a continuum, with a naso-temporal gradient of density, across the temporal hemiretina.

Animals↗

PubMed1997

Neurobiology of cerebral malaria and African sleeping sickness.

This review is aimed at emphasizing the need for basic neuroscience research on two tropical diseases, malaria and sleeping sickness (African trypanosomiasis), that still represent major health problems and in which severe involvement of the nervous system is frequently the direct cause of death. The life cycles of the two parasites, the protozoan Plasmodium and Trypanosoma brucei, which are the causative agents of malaria and sleeping sickness, respectively, are briefly reviewed. The historical contribution to the pathogenesis and therapy of malaria by a renowned pioneer in neuroscience, Camillo Golgi, is pointed out. The different strategies for survival in the host by the intracellular Plasmodium and the extracellular African trypanosomes are summarized; such strategies include sites favorable for hiding or replication of the parasites in the host, antigenic variation, and interactions with the cytokine network of the host. In particular, tumor necrosis factor-alpha and interferon-gamma may play a role in these infections. The parasites may paradoxically interact with cytokines to their benefit. However, cytokine receptors are expressed on neuronal subsets sensitive to cytokine action, and stimulation of these subsets may cause neuronal dysfunctions during the infections. Finally, the clinical symptoms of cerebral malaria and African trypanosomiasis and research aiming at deciphering their pathogenetic mechanisms that could affect the nervous system at a molecular level are described. The need for neuroscientists in this endeavor is emphasized.

Animals↗

PubMed1997

The pioneering experimental studies on sleep deprivation.

The experimental studies on sleep deprivation were initiated by the Russian physician and scientist, Marie de Manacéine, who studied sleep-deprived puppies kept in constant activity. She reported in 1894 that the complete absence of sleep was fatal in a few days, pointing out that the most severe lesions occurred in the brain. In 1898, the Italian physiologists Lamberto Daddi and Giulio Tarozzi also kept dogs awake by walking them; the animals died after 9-17 days, and their survival was unrelated to food consumption. In the histological study performed by Daddi, degenerative alterations, mainly represented by chromatolytic changes, were observed in neurons of the spinal ganglia, Purkinje cells of the cerebellum, and neurons of the frontal cortex. Daddi ascribed these changes to a state of autointoxication of the brain during insomnia. In 1898, the psychiatrist Cesare Agostini, interested in the psychic phenomena caused by prolonged insomnia in humans, sleep deprived dogs by keeping them in a metallic cage in order to avoid fatigue. The dogs survived about 2 weeks, and degenerative changes were observed in their brains. In these experimental paradigms, the effect of sleep loss was confounded by motor exhaustion and/or intense sensory stimulation. In spite of the absence of adequate controls, the pioneering studies performed at the end of the 19th century represented the first experimental attempts to relate sleep with neural centers and suggested that sleep is a vital function and that the brain may be affected by insomnia.

Animals↗

PubMed1997

Combined therapy with benazepril and amlodipine in the treatment of hypertension inadequately controlled by an ACE inhibitor alone.

In a multicenter, randomized, double-blind, placebo-controlled study, we evaluated the efficacy and tolerability of the combination of benazepril, 10 mg, and amlodipine, 2.5 or 5 mg once daily, compared with benazepril, 10 mg, monotherapy in patients with hypertension inadequately controlled with angiotensin-converting enzyme (ACE)-inhibitor monotherapy. After a 2-week placebo and 4-week single-blind benazepril, 10 mg once daily, run-in period, 448 patients, 213 men and 235 women, aged 24-73 years (mean, 55 years), with mean diastolic blood pressure (DBP) > or =95 and < or =120 mm Hg at the end of the benazepril run-in period, were randomized to receive one of the following treatments once daily for 8 weeks: (a) benazepril, 10 mg, plus placebo (BZ10); (b) benazepril, 10 mg, plus amlodipine, 2.5 mg (BZ10/AML2.5); or (c) benazepril, 10 mg, plus amlodipine, 5 mg (BZ10/AML5). Before the patients were admitted to the trial, at the end of the placebo run-in and the benazepril run-in period and at the end of weeks 4 and 8 of the treatment period, sitting and standing blood pressure (BP), heart rate (HR), and body weight were measured 22-26 h after the intake of the trial medication. Both BZ10/AML2.5 and BZ10/AML5 combinations showed better antihypertensive activity than did BZ10 monotherapy at the terminal visit as demonstrated by (a) the 24-h postdosing sitting and standing systolic BP (SBP) and DBP values, which were statistically lower with combination therapy than with BZ10; (b) the success rate, which was statistically higher with both the combinations (69.2% in the BZ10/AML2.5 and 65.8% in the BZ10/AML5 group) compared with the BZ10 group (40.5%). The tolerability was good in the three treatment groups. No significant abnormal laboratory data were detected. There was no difference in efficacy and safety/tolerability between the BZ10/AML2.5 and BZ10/AML5 groups.

Adolescent↗

PubMed1996

Botulinum toxin induces nitric oxide synthase activity in motoneurons.

Intramuscular injections of botulinum toxin A were made into the snout of 3-month- and 3-week-old rats, resulting in transient paralysis of the facial muscles. Nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase histochemistry, which is a marker of nitric oxide synthase activity in fixed tissue and, in particular, in injured motoneurons, was studied in the facial nucleus. At variance with control injections of saline, the histochemical staining was found to be induced in facial motoneurons after botulinum toxin injection. The occurrence and persistence of the histochemical positivity in facial motoneurons paralleled that of muscle paralysis. These findings indicate that the enzyme of synthesis of the free radical nitric oxide can be induced in motoneurons after a functional disconnection from the target, which spares the axon and is associated with cell survival.

Animals↗

PubMed1996

Induction of NADPH-diaphorase activity in the rat forebrain after middle cerebral artery occlusion.

Induction of NADPH-diaphorase (NDP) following ischemic infarction was studied by means of histochemistry in the rat cerebral cortex 1,2,7, and 14 days after distal occlusion of the right middle cerebral artery (MCA). The fine structure of cells in the penumbra region of the necrotic center was also investigated. MCA distal occlusion resulted in ischemic lesion of the frontoparietal cortex of variable extent; NDP induction was detected in neurons, astrocytes, macrophages, and endothelial cells, with regional specificity and a temporal gradient. One, two, and seven days after MCA occlusion, weak NDP positivity was consistently induced in some pyramidal neurons in cortical areas neighboring the necrotic area; NDP induction was also seen in pyramidal neurons of the ipsilateral anterior cingulate and infralimbic cortices and in the tenia tecta. In addition, numerous NDP-positive pyramidal neurons were detected in the contralateral frontoparietal cortex after relatively large ischemic lesions. Two weeks after MCA occlusion, NDP induction in neurons was only evident in the deep cortical layers near the lesion. NDP histochemistry combined with glial fibrillary acidic protein immunofluorescence, performed 7 days after MCA occlusion, indicated that the astrocytes at the periphery of the necrotic area were hypertrophic and some of them were also NDP-positive. One and two days after MCA occlusion, numerous macrophages displaying NDP positivity of variable intensity were seen at the periphery of the necrotic area and in the external capsule of the ischemic cerebral hemisphere. Many endothelial cells in the cortex and subcortical white matter were consistently NDP-positive in all rats. Electron microscopic studies indicated that the area adjacent to the necrotic center was composed of fibrous astrocytes, with the morphological characteristics of proliferation, and numerous lysosome-filled macrophages. Altogether the present results suggest that focal cerebral ischemia may induce in different cell types nitric oxide synthase, which is equivalent to NDP in fixed tissue. The induction of nitric oxide synthase may be related to (1) blood-flow regulation at relatively early postischemic stages, which may decline when collateral circulation is established, and/or (2) cytotoxic or neuroprotective mechanisms.

Animals↗

PubMed1996

Trends in the anatomical organization and functional significance of the mammalian thalamus.

The last decade has witnessed major changes in the experimental approach to the study of the thalamus and to the analysis of the anatomical and functional interrelations between thalamic nuclei and cortical areas. The present review focuses on the novel anatomical approaches to thalamo-cortical connections and thalamic functions in the historical framework of the classical studies on the thalamus. In the light of the most recent data it is here discussed that: a) the thalamus can subserve different functions according to functional changes in the cortical and subcortical afferent systems; b) the multifarious thalamic cellular entities play a crucial role in the different functional states.

Animals↗

PubMed1996

Neuronal and synaptic organization of the centromedian nucleus of the monkey thalamus: a quantitative ultrastructural study, with tract tracing and immunohistochemical observations.

The ultrastructure of the centromedian nucleus of the monkey thalamus was analysed qualitatively and quantitatively and projection neurons, local circuit neurons, and synaptic bouton populations identified. Projection neurons were mostly medium-sized, with oval-fusiform or polygonal perikarya, few primary dendrites, and frequent somatic spines; local circuit neurons were smaller. Four basic types of synaptic boutons were distinguished: (1) Small- to medium-sized boutons containing round vesicles (SR) and forming asymmetric contacts, identified as corticothalamic terminals. (2) Heterogeneous medium-sized boutons with asymmetric contacts and round vesicles, similar to the so-called large round (LR) boutons, which were in part of cortical origin. (3) Heterogeneous GAD-positive small- to medium-sized boutons, containing pleomorphic vesicles and forming symmetric contacts (F1 type), which included pallidothalamic terminals. (4) Presynaptic profiles represented by GAD-positive vesicle-containing dendrites of local circuit neurons. Complex synaptic arrangements, serial synapses and triads with LR and SR boutons engaging all parts of projection neuron dendrites and somata, were seen consistently, whereas classical glomeruli were infrequent. LR and SR boutons also established synapses on dendrites of local circuit neurons. F1 boutons established synapses on projection neuron somata, dendrites and initial axon segments. Compared to other previously studied motor-related thalamic nuclei, differences in synaptic coverage between proximal and distal projection neuron dendrites were less pronounced, and the density of synapses formed by local circuit dendrites on projection neuron dendrites was lower. Thus, compared to other thalamic nuclei, the overlap of different inputs was higher on monkey centromedian cells, and centromedian inhibitory circuits displayed a different organization.

Animals↗

PubMed1996

Diencephalic asymmetries.

Structural asymmetry in diencephalic regions has been reported in a number of studies since the pioneering observations by Kemali and Braitenberg, Atlas of the frog's brain. Springer Verlag: 1969. Anatomical differences between the left and right habenulae have been identified in many lower vertebrate species. While there are few reports of structural asymmetry in the dorsal thalamus, there is evidence that asymmetrical thalamofugal projections can be induced in the visual system of chicks by lateralized sensory stimulation prior to hatching. Finally, there have been consistent reports of differences between and right sides of the hypothalamus in their sensitivity to the effects of circulating gonadal hormones in rats. In most cases, these asymmetries are sex-linked and correspond to a lateralization of function. Although the significance of these diencephalic asymmetries is still enigmatic, their existence indicates that asymmetry is not a phylogenetically recent feature of the brain, and the left-right differences in the brain may be mediated by a common ontogenetic mechanism and may underlie the development of highly specialized functions.

Animals↗

PubMed1996

NADPH-diaphorase activity in brain macrophages during postnatal development in the rat.

NADPH-diaphorase histochemistry, that allows the visualization of cells producing the gaseous intercellular messenger nitric oxide, was used in the study of the forebrain during the first three postnatal weeks in the rat. Subpopulations of NADPH-diaphorase positive neurons were observed at all ages studied. In addition, non-neuronal NADPH-diaphorase-stained cells were detected in the subcortical white matter, and were very numerous in the supraventricular portion of the corpus callosum, and in the internal and external capsules. These cells were present during the first two postnatal weeks, and were especially prominent at the end of the first postnatal week. They were round-shaped and morphologically similar to the brain macrophages, whose phagocytic activity has been shown in previous studies to play a role in naturally occurring cell death and elimination of exhuberant axons. Series of sections adjacent to those stained with NADPH-diaphorase were processed with immunohistochemistry, using two different antibodies (OX-42 and ED-1) that detect macrophagic and microglial markers, and antibodies that recognize the neuronal form of nitric oxide synthase. Furthermore, brain sections from rats at postnatal day 7 were sequentially processed for either OX-42 or nitric oxide synthase immunohistochemistry followed by NADPH-diaphorase histochemistry. The morphological features and distribution of the non-neuronal NADPH-diaphorase-positive cells were superimposable to those obtained with OX-42 and ED-1 immunohistochemistry. In addition, these cells did not display nitric oxide synthase immunoreactivity. Double-labelled NADPH-diaphorase-positive and OX-42-immunoreactive cells were detected at postnatal day 7. The present results show that brain macrophages express NADPH-diaphorase activity during the early stages of the normal postnatal maturation and suggest that nitric oxide produced by brain macrophages could be involved in the development reshaping of the central nervous system.

Animals↗

PubMed1996

Upregulation of spinal glutamate receptors in chronic pain.

Recent studies indicate that glutamate binding to N-methyl-D-aspartate receptors in the spinal cord is involved in triggering the development of chronic pain However, the processes which directly underlie the increased pain remain unclear. Here we report that, following peripheral nerve injury (ligation of the sciatic nerve) in the rat, there is an increase in immunoreactive labelling of non-N-methyl-D-asparatate, AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionate), glutamate receptors in the superficial laminae of the lumbar spinal cord ipsilateral to the ligation. The increase in AMPA receptor expression peaks 14 days after nerve ligation and decreases 35 days post-ligation, corresponding to the time-course of heightened sensitivity to mechanical and thermal noxious stimuli (hyperalgesia) induced by the ligation. Given evidence that AMPA receptors in the superficial laminae mediate fast nociceptive transmission in the spinal cord, our findings suggest that an upregulation of spinal AMPA receptors contributes to hyperalgesia following peripheral nerve injury.

Animals↗

PubMed1996

Melatonin and its new agonist S-20098 restore synchronized sleep fragmented by experimental trypanosome infection in the rat.

The experimental infection with the parasite Trypanosoma brucei in the rat provides a unique model of dysfunction of the sleep regulatory mechanisms, because the length of synchronized sleep episodes is selectively and dramatically reduced in the advanced stages of the disease. In the present study, melatonin was acutely administered (3 mg/kg SC) to trypanosome-infected rats, before the sleep onset. This treatment resulted in a significant increase of the length of synchronized sleep episodes in respect to the infected animals and to those that had received only the vehicle. Thus, melatonin restored a normal sleep pattern during the infection. Similar findings were obtained with the new melatonin agonist S-20098. The sleep parameters were not significantly modified by either melatonin or S-20098 acute administration to noninfected animals. These findings indicate that exogenous melatonin and S-20098 exert a selective regulatory action on sleep fragmentation during experimental trypanosomiasis.

Acetamides↗