Huperzine A, but not tacrine, stimulates S100B secretion in astrocyte cultures

Abstract

Our data reinforce the idea that AChE inhibitors, particularly HupA, do not act exclusively on the acetylcholine balance. This effect of HupA could contribute to improve the cognitive deficit observed in patients, which are attributed to cholinergic dysfunction. In addition, for the first time, to our knowledge, these data indicate that S100B secretion can be modulated by nicotinic receptors, in addition to glutamate, dopamine and serotonin receptors.

Cholinergic Hypofunction in Presbycusis-Related Tinnitus With Cognitive Function Impairment: Emerging Hypotheses

“…The activation of α7nAChRs in neural cells suppresses central inflammatory responses in mice with Parkinson disease (Stuckenholz et al, 2013 ), stroke (Han et al, 2014 ), or traumatic brain injury (Kelso and Oestreich, 2012 ), and also suppresses glutamate-induced neurotoxicity in vitro (Shimohama et al, 1998 ; Iwamoto et al, 2013 ). Futhermore, the activation of α7nAChRs in astrocytes down-regulates Aβ1–42-induced increases in NF-κB in in vitro (Xie et al, 2016 ), and improves neurotrophic cytokine S100B secretion, which is decreased in the cerebrospinal fluid in rat models of dementia (Lunardi et al, 2013 ). Moreover, the upregulation of α7nAChR expression induced by neuregulin in microglial cells suppresses neuroinflammation in vitro (Mencel et al, 2013 ).…”

Nicotine induces intracellular Ca<sup>2+</sup> increases in cultured hippocampal astrocytes by nAChR-dependent and -independent pathways

“…These glial receptors are activated by nAChRs agonists, resulting in increases of the [Ca 2+ ] i [16,17], and it is very likely that these receptors are involved in glial cell functions, including bidirectional glia-neuron communication. For instance, neuronal and glial nAChRs participate in modulating both hippocampal synaptic transmission and long-term memory [14,37,38], neuroprotection, and inflammation [18,19,39].…”

“…In the brain, nicotine acts on neurons and astrocytes [10][11][12], enhancing hippocampal synaptic transmission and long-term memory [13,14]. Furthermore, activation of astrocytic nAChRs increases their intracellular Ca 2+ concentration ([Ca 2+ ] i ) [12,[15][16][17]; upregulating the expression of the glial derived neurotrophic factor implicated in neuroprotection [18], and increasing S100B secretion, a possible indicator of brain injury [19]. It is known that glial Ca 2+ signaling is triggered by activation of multiple metabotropic and ionotropic transmitter receptors, and this signal is an important way for neurons and astrocytes to communicate [16,[20][21][22][23][24].…”

Faradarmani Consciousness Field Suppresses Alzheimer’s Disease Development in Both in Vitro and in Vivo Models of The Disease

“…The loss of cholinergic function in the central nervous system contributes to cognitive decline and dementia [26], which has been the target of anti-AD drugs [27]. Pharmacologic treatments temporarily improve symptoms but can't slow or stop the degeneration of neurons [28].…”