Nicotinic Acetylcholine Receptors in HIV: Possible Roles During HAND and Inflammation

Capó-Vélez, Coral M.; Delgado-Vélez, Manuel; Baéz-Pagán, Carlos A.; Lasalde‐Dominicci, José A.

doi:10.1007/s10571-018-0603-8

Cited by 7 publications

(4 citation statements)

References 113 publications

(193 reference statements)

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“…The role of this receptor in relation to HIV is currently being investigated in two main lines, namely, chronic inflammation (both neuroinflammation and peripheral inflammation) and HIV-associated neurocognitive disorders. Over the past two decades, a large number of papers have been published studying the molecular mechanisms of the involvement of α7 nAChRs in these two HIV-related processes as well as looking for ways to treat or mitigate the effects of infection, most of which have been considered in recent reviews (see, for example, [ 243 ]).…”

Section: α7- and α9-containing Nachrs As Targets In Viral Infectionmentioning

confidence: 99%

α7- and α9-Containing Nicotinic Acetylcholine Receptors in the Functioning of Immune System and in Pain

Shelukhina

Siniavin

Kasheverov

et al. 2023

IJMS

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Nicotinic acetylcholine receptors (nAChRs) present as many different subtypes in the nervous and immune systems, muscles and on the cells of other organs. In the immune system, inflammation is regulated via the vagus nerve through the activation of the non-neuronal α7 nAChR subtype, affecting the production of cytokines. The analgesic properties of α7 nAChR-selective compounds are mostly based on the activation of the cholinergic anti-inflammatory pathway. The molecular mechanism of neuropathic pain relief mediated by the inhibition of α9-containing nAChRs is not fully understood yet, but the role of immune factors in this process is becoming evident. To obtain appropriate drugs, a search of selective agonists, antagonists and modulators of α7- and α9-containing nAChRs is underway. The naturally occurring three-finger snake α-neurotoxins and mammalian Ly6/uPAR proteins, as well as neurotoxic peptides α-conotoxins, are not only sophisticated tools in research on nAChRs but are also considered as potential medicines. In particular, the inhibition of the α9-containing nAChRs by α-conotoxins may be a pathway to alleviate neuropathic pain. nAChRs are involved in the inflammation processes during AIDS and other viral infections; thus they can also be means used in drug design. In this review, we discuss the role of α7- and α9-containing nAChRs in the immune processes and in pain.

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Section: α7- and α9-containing Nachrs As Targets In Viral Infectionmentioning

confidence: 99%

α7- and α9-Containing Nicotinic Acetylcholine Receptors in the Functioning of Immune System and in Pain

Shelukhina

Siniavin

Kasheverov

et al. 2023

IJMS

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“…Neuronal injury is also observed in the basal ganglia of these mice, including the activation of caspase-3 as well as loss of synaptophysin, GABAnergic, and cholinergic neurons 17 . Gp120, a glycoprotein that forms part of the HIV-1 envelope, interacts with several receptors found in the CNS such as CD4, CCR5, CXCR4, and nAChR [18][19][20] . Gp120 kills neurons by stimulating the neurotoxic pathways mediated by nitric oxide, calcium, glutamate, and superoxide anions 21,22 .…”

Section: Impact Of Hiv-1 Subtypes On the Progression Of Neurological Disordersmentioning

confidence: 99%

Differential Contribution of HIV-1 Subtypes B and C to Neurological Disorders: Mechanisms and Possible Treatments

Santerre¹,

Wang²,

Arjona³

et al. 2019

AIDSRev

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With the introduction of combinatory antiretroviral therapy, patients infected with human immunodeficiency virus type 1 (HIV-1) can live much longer than before. However, the identification of HIV-associated neurocognitive disorder (HAND), especially HIV-associated dementia in 15-20% of patients infected with HIV-1, indicates additional complexity. These disorders turn out to be subtype dependent. Recently, many studies are ongoing trying to understand how the virus induces neuronal injury which could lead to neurological dysfunction. Most of these studies are focusing on the HIV-1 release of proteins such as Tat. However, the exact role of these proteins and their involvement in neuronal degeneration remains unidentified; this is especially true since viral proteins from different HIV-1 subtypes differ in their ability to cause neuronal damage. This review describes the role of different HIV-1 subtypes, identifies probable pathways involved in neuronal damage, the contribution of different HIV-1 subtypes to the progression of HAND, and potential treatments for HAND.

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“…Although the ventral striatum is more closely associated with behavioral reinforcement and associated emotional/motivational processes, dopamine receptor‐expressing neurons in the dorsal striatum are also implicated in reinforcement learning and decision making (Balleine et al., 2007; Kravitz et al., 2012; Loewke et al., 2021). In addition to direct damage to striatal neurons and glia, there is evidence of HIV‐induced disruption to neurochemical systems that modulate neuronal activity in the striatum and guide behavioral outputs (Capó‐Vélez et al., 2018; Gaskill et al., 2017; Kumar et al., 2001; Nolan & Gaskill, 2019).…”

Section: Introductionmentioning

confidence: 99%

HIV‐1 Tat and morphine interactions dynamically shift striatal monoamine levels and exploratory behaviors over time

Lark,

Nass,

Hahn

et al. 2024

Journal of Neurochemistry

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Despite the advent of combination anti‐retroviral therapy (cART), nearly half of people infected with HIV treated with cART still exhibit HIV‐associated neurocognitive disorders (HAND). HAND can be worsened by co‐morbid opioid use disorder. The basal ganglia are particularly vulnerable to HIV‐1 and exhibit higher viral loads and more severe pathology, which can be exacerbated by co‐exposure to opioids. Evidence suggests that dopaminergic neurotransmission is disrupted by HIV exposure, however, little is known about whether co‐exposure to opioids may alter neurotransmitter levels in the striatum and if this in turn influences behavior. Therefore, we assayed motor, anxiety‐like, novelty‐seeking, exploratory, and social behaviors, and levels of monoamines and their metabolites following 2 weeks and 2 months of Tat and/or morphine exposure in transgenic mice. Morphine decreased dopamine levels, but significantly elevated norepinephrine, the dopamine metabolites dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), and the serotonin metabolite 5‐hydroxyindoleacetic acid, which typically correlated with increased locomotor behavior. The combination of Tat and morphine altered dopamine, DOPAC, and HVA concentrations differently depending on the neurotransmitter/metabolite and duration of exposure but did not affect the numbers of tyrosine hydroxylase‐positive neurons in the mesencephalon. Tat exposure increased the latency to interact with novel conspecifics, but not other novel objects, suggesting the viral protein inhibits exploratory behavior initiation in a context‐dependent manner. By contrast, and consistent with prior findings that opioid misuse can increase novelty‐seeking behavior, morphine exposure increased the time spent exploring a novel environment. Finally, Tat and morphine interacted to affect locomotor activity in a time‐dependent manner, while grip strength and rotarod performance were unaffected. Together, our results provide novel insight into the unique effects of HIV‐1 Tat and morphine on monoamine neurochemistry that may underlie their divergent effects on motor and exploratory behavior.

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Nicotinic Acetylcholine Receptors in HIV: Possible Roles During HAND and Inflammation

Cited by 7 publications

References 113 publications

α7- and α9-Containing Nicotinic Acetylcholine Receptors in the Functioning of Immune System and in Pain

α7- and α9-Containing Nicotinic Acetylcholine Receptors in the Functioning of Immune System and in Pain

Differential Contribution of HIV-1 Subtypes B and C to Neurological Disorders: Mechanisms and Possible Treatments

HIV‐1 Tat and morphine interactions dynamically shift striatal monoamine levels and exploratory behaviors over time

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