Brain Distribution and Modulation of Neuronal Excitability by Indicaxanthin From Opuntia Ficus Indica Administered at Nutritionally-Relevant Amounts

Abstract

Several studies have recently investigated the role of nutraceuticals in complex pathophysiological processes such as oxidative damages, inflammatory conditions and excitotoxicity. In this regard, the effects of nutraceuticals on basic functions of neuronal cells, such as excitability, are still poorly investigated. For this reason, the possible modulation of neuronal excitability by phytochemicals (PhC) could represent an interesting field of research given that excitotoxicity phenomena are involved in neurodegenerative alterations leading, for example, to Alzheimer’s disease. The present study was focused on indicaxanthin from Opuntia ficus indica, a bioactive betalain pigment, with a proven antioxidant and anti-inflammatory potential, previously found to cross blood-brain barrier (BBB) and to modulate the bioelectric activity of hippocampal neurons. On this basis, we aimed at detecting the specific brain areas where indicaxanthin localizes after oral administration at dietary-achievable amounts and highlighting eventual local effects on the excitability of single neuronal units. HPLC analysis of brain tissue 1 h after ingestion of 2 μmol/kg indicaxanthin indicated that the phytochemical accumulates in cortex, hippocampus, diencephalon, brainstem and cerebellum, but not in the striato-pallidal complex. Then, electrophysiological recordings, applying the microiontophoretic technique, were carried out with different amounts of indicaxanthin (0.34, 0.17, 0.085 ng/neuron) to assess whether indicaxanthin influenced the neuronal firing rate. The data showed that the bioelectric activity of neurons belonging to different brain areas was modulated after local injection of indicaxanthin, mainly with dose-related responses. A predominating inhibitory effect was observed, suggesting a possible novel beneficial effect of indicaxanthin in reducing cell excitability. These findings can constitute a new rationale for exploring biological mechanisms through which PhC could modulate neuronal function with a relapse on complex cognitive brain process and related neurodegenerative conditions.

Amyloid-Beta Induces Different Expression Pattern of Tissue Transglutaminase and Its Isoforms on Olfactory Ensheathing Cells: Modulatory Effect of Indicaxanthin

“…These conditions contribute to oxidative stress and neural cell death, in which TG2 plays a key role [ 34 ]. It has been reported that hippocampal neurons are more responsive to indicaxanthin [ 36 ]. In particular, it has an important role in several metabolic functions both in vitro and in vivo, reducing inflammation and enhancing immune response [ 22 , 23 , 37 ].…”

Amyloid-Beta induces different expression pattern of tissue transglutaminase and its isoforms on Olfactory Ensheathing Cells: modulatory effect of Indicaxanthin

“…These conditions contribute to oxidative stress and neural cell death, in which TG2 plays a key role [30]. It has been reported that hippocampal neurons are more responsive to Indicaxanthin [39]. In particular, it has an important role in several metabolic functions both in vitro and in vivo, reducing in ammation and enhancing immune response [22,23,40].…”

Haptic Perception in Extreme Obesity: qEEG Study Focused on Predictive Coding and Body Schema

“…Over-eating and obesity are tightly linked to neurobiological, behavioral and cognitive factors such as mood status, addictive behavior, impulsivity and reward processing; cognitive control [19,20,[33][34][35][36][37][38][39][40]. Exploring the effects of external modifications to body homeostasis caused by nutritional, neurophysiological or pharmacological tools is a widely applied approach that provides evidence to fundamental processes of the nervous system [41][42][43]. In this context, although cognitive performance in obese people is far from being elucidated [44], obesity has been recently considered as a risk factor for cognitive impairments [45].…”