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Start Over Author "Livio, Luongo" Journal molecular brain
3 results on '"Livio, Luongo"'

1. 2-Pentadecyl-2-oxazoline ameliorates memory impairment and depression-like behaviour in neuropathic mice: possible role of adrenergic alpha2- and H3 histamine autoreceptors

Author

Serena Boccella, Francesca Guida, Monica Iannotta, Fabio Arturo Iannotti, Rosmara Infantino, Flavia Ricciardi, Claudia Cristiano, Rosa Maria Vitale, Pietro Amodeo, Ida Marabese, Carmela Belardo, Vito de Novellis, Salvatore Paino, Enza Palazzo, Antonio Calignano, Vincenzo Di Marzo, Sabatino Maione, and Livio Luongo

Subjects
Neuropathic pain, Depression, Cognitive impairments, H3 receptors, Locus coeruleus, Mice, Neurology. Diseases of the nervous system, RC346-429
Abstract

Abstract Neuropathic pain (NP) remains an untreatable disease due to the complex pathophysiology that involves the whole pain neuraxis including the forebrain. Sensory dysfunctions such as allodynia and hyperalgesia are only part of the symptoms associated with neuropathic pain that extend to memory and affectivity deficits. The development of multi-target molecules might be a promising therapeutic strategy against the symptoms associated with NP. 2-pentadecyl-2-oxazoline (PEA-OXA) is a plant-derived agent, which has shown effectiveness against chronic pain and associated neuropsychiatric disorders. The molecular mechanisms by which PEA-OXA exerts its effects are, however, only partially known. In the current study, we show that PEA-OXA, besides being an alpha2 adrenergic receptor antagonist, also acts as a modulator at histamine H3 receptors, and report data on its effects on sensory, affective and cognitive symptoms associated with the spared nerve injury (SNI) model of neuropathic pain in mice. Treatment for 14 days with PEA-OXA after the onset of the symptoms associated with neuropathic pain resulted in the following effects: (i) allodynia was decreased; (ii) affective/cognitive impairment associated with SNI (depression, spatial, and working memories) was counteracted; (iii) long-term potentiation in vivo in the lateral entorhinal cortex-dentate gyrus (perforant pathway, LPP) was ameliorated, (iv) hippocampal glutamate, GABA, histamine, norepinephrine and dopamine level alterations after peripheral nerve injury were reversed, (v) expression level of the TH positive neurons in the Locus Coeruleus were normalized. Thus, a 16-day treatment with PEA-OXA alleviates the sensory, emotional, cognitive, electrophysiological and neurochemical alterations associated with SNI-induced neuropathic pain.

Published
2021
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2. Correction to: 2-Pentadecyl-2-oxazoline ameliorates memory impairment and depression-like behaviour in neuropathic mice: possible role of adrenergic alpha2- and H3 histamine autoreceptors

Author

Serena Boccella, Francesca Guida, Monica Iannotta, Fabio Arturo Iannotti, Rosmara Infantino, Flavia Ricciardi, Claudia Cristiano, Rosa Maria Vitale, Pietro Amodeo, Ida Marabese, Carmela Belardo, Vito de Novellis, Salvatore Paino, Enza Palazzo, Antonio Calignano, Vincenzo Di Marzo, Sabatino Maione, and Livio Luongo

Subjects
Neurology. Diseases of the nervous system, RC346-429
Abstract

An amendment to this paper has been published and can be accessed via the original article.

Published
2021
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3. Palmitoylethanolamide reduces pain-related behaviors and restores glutamatergic synapses homeostasis in the medial prefrontal cortex of neuropathic mice

Author

Livio Luongo, Francesco Napolitano, Danilo De Gregorio, V. de Novellis, V. Di Marzo, A. de Bartolomeis, Francesca Guida, Fabiana Piscitelli, Ida Marabese, Federica Marmo, Antimo D'Aniello, Alessandro Usiello, Roberta Lattanzi, Sabatino Maione, F. Rossi, Carmela Belardo, Rosaria Romano, Monica Iannotta, Guida, F., Luongo, L., Marmo, F., Romano, R., Iannotta, M., Napolitano, F., Belardo, C., Marabese, I., D'Aniello, A., De Gregorio, D., Rossi, F., Piscitelli, F., Lattanzi, R., De Bartolomeis, A., Usiello, A., Di Marzo, V., De Novellis, V., Maione, S., Guida, F, Luongo, L, Marmo, Federica, Romano, R, Iannotta, M, Napolitano, Francesco, Belardo, C, Marabese, I, D'Aniello, A, De Gregorio, D, Rossi, F, Piscitelli, F, Lattanzi, R, DE BARTOLOMEIS, Andrea, Usiello, A, Di Marzo, V, DE NOVELLIS, Vincenzo, Guida, Francesca, Luongo, Livio, Marmo, F, Napolitano, F, Marabese, Ida, Rossi, Francesca, de Bartolomeis, A, Usiello, Alessandro, DE NOVELLIS, Vito, and Maione, Sabatino

Subjects
receptor, Palmitic Acid, microglia, neurons, neuralgia, electrophysiological phenomena, tail, chemistry.chemical_compound, 0302 clinical medicine, homeostasis, Ethanolamine, animal, Prefrontal cortex, Cells, Cultured, prefrontal cortex, 0303 health sciences, Behavior, Animal, brain-derived neurotrophic factor, Chronic pain, Synapse, Microinjection, 3. Good health, animals, trkB, Neuropathic pain, ethanolamines, Glutamatergic synapse, glutamic acid, medicine.symptom, Psychology, signal transduction, SNi, mice, proto-oncogene proteins c-akt, palmitic acids, 03 medical and health sciences, Cellular and Molecular Neuroscience, Glutamatergic, male, Homeostasi, medicine, Receptor, trkB, cultured, Molecular Biology, 030304 developmental biology, Palmitoylethanolamide, behavior, Research, Neuron, Nerve injury, medicine.disease, Amides, chemistry, cells, immobilization, microinjections, receptor, trkB, synapses, cellular and molecular neuroscience, molecular biology, Neuroscience, 030217 neurology & neurosurgery
Abstract

Background Enhanced supraspinal glutamate levels following nerve injury are associated with pathophysiological mechanisms responsible for neuropathic pain. Chronic pain can interfere with specific brain areas involved in glutamate-dependent neuropsychological processes, such as cognition, memory, and decision-making. The medial prefrontal cortex (mPFC) is thought to play a critical role in pain-related depression and anxiety, which are frequent co-morbidities of chronic pain. Using an animal model of spared nerve injury (SNI) of the sciatic nerve, we assess bio-molecular modifications in glutamatergic synapses in the mPFC that underlie neuropathic pain-induced plastic changes at 30 days post-surgery. Moreover, we examine the effects of palmitoylethanolamide (PEA) administration on pain-related behaviours, as well as the cortical biochemical and morphological changes that occur in SNI animals. Results At 1 month, SNI was associated with mechanical and thermal hypersensitivity, as well as depression-like behaviour, cognitive impairments, and obsessive-compulsive activities. Moreover, we observed an overall glutamate synapse modification in the mPFC, characterized by changes in synaptic density proteins and amino acid levels. Finally, with regard to the resolution of pain and depressive-like syndrome in SNI mice, PEA restored the glutamatergic synapse proteins and changes in amino acid release. Conclusions Given the potential role of the mPFC in pain mechanisms, our findings may provide novel insights into neuropathic pain forebrain processes and indicate PEA as a new pharmacological tool to treat neuropathic pain and the related negative affective states. Graphical Abstract Palmitoylethanolamide: a new pharmacological tool to treat neuropathic pain and the related negative affective states. Electronic supplementary material The online version of this article (doi:10.1186/s13041-015-0139-5) contains supplementary material, which is available to authorized users.

Published
2015
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