Activation of Astrocytes in the Dorsomedial Striatum Facilitates Transition From Habitual to Goal-Directed Reward-Seeking Behavior

Kang, Seungwoo; Hong, Sa-Ik; Lee, Jeyeon; Peyton, Lee; Baker, Matthew; Choi, Sun Hee; Kim, Hyun-Jung; Su, Chang; Choi, Doo Sup

doi:10.1016/j.biopsych.2020.04.023

“…By activating Gq signaling within GFAP-expressing cells directly, the present work extends these findings to the in vivo situation in which the entire hypothalamo-pituitary gonadal axis can interact, and indicates a role for these cells within the preoptic area in ultimately increasing LH release in males. In other brain regions, when astrocytes were activated with either DREADDs or by agonists of native GPCRs, the timecourse of increases in intracellular calcium are similar to changes in firing rate in the present study 56,57 . This suggests that the GnRH neuron response may be dependent upon the elevation of calcium in astrocytes, and also that the signal conveyed to the GnRH neuron produces a prolonged response consistent with activation of a G-protein-coupled receptor within the neurons.…”

Section: Discussionsupporting

confidence: 67%

A role for glial fibrillary acidic protein (GFAP)-expressing cells in the regulation of gonadotropin-releasing hormone (GnRH) but not arcuate kisspeptin neuron output in male mice

Vanacker

¹

,

DeFazio

²

,

Sykes

³

et al. 2021

eLife

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GnRH neurons are the final central neural output regulating fertility. Kisspeptin neurons in the hypothalamic arcuate nucleus (KNDy neurons) are considered the main regulator of GnRH output. GnRH and KNDy neurons are surrounded by astrocytes, which can modulate neuronal activity and communicate over distances. Prostaglandin E2 (PGE2), synthesized primarily by astrocytes, increases GnRH neuron activity and downstream pituitary release of luteinizing hormone (LH). We hypothesized GFAP-expressing astrocytes play a role regulating GnRH and/or KNDy neuron activity and LH release. We used adenoassociated viruses to target designer receptor exclusively activated by designer drugs (DREADDs) to GFAP-expressing cells to activate Gq or Gi-mediated signaling. Activating Gq signaling in the preoptic area, near GnRH neurons, but not in the arcuate, increases LH release in vivo and GnRH firing in vitro via a mechanism in part dependent upon PGE2. These data suggest astrocytes can activate GnRH/LH release in a manner independent of KNDy neurons.

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“…By activating Gq signaling within GFAP-expressing cells directly, the present work extends these findings to the in vivo situation in which the entire hypothalamo-pituitary gonadal axis can interact, and indicates a role for these cells within the preoptic area in ultimately increasing LH release in males. In brain slices from these mice, CNO increased intracellular calcium with a similar timecourse to that observed in other brain regions when astrocytes were activated with either DREADDs or by agonists native GPCRs 55,56 . In the present work, the increase in astrocyte intracellular calcium occurred with a shorter lag and had a shorter duration than the changes in neuronal firing rate.…”

Section: Discussionsupporting

confidence: 63%

A role for glial fibrillary acidic protein (GFAP)-expressing cells in the regulation of gonadotropin-releasing hormone (GnRH) but not arcuate kisspeptin neuron output

Vanacker

¹

,

DeFazio

²

,

Sykes

³

et al. 2021

Preprint

0

View full text Add to dashboard Cite

GnRH neurons are the final central neural output regulating fertility. Kisspeptin neurons in the hypothalamic arcuate nucleus (KNDy neurons) are considered the main regulator of GnRH output. GnRH and KNDy neurons are surrounded by astrocytes, which can modulate neuronal activity and communicate over distances. Prostaglandin E2 (PGE2), synthesized primarily by astrocytes, increases GnRH neuron activity and downstream pituitary release of luteinizing hormone (LH). We hypothesized GFAP-expressing astrocytes play a role regulating GnRH and/or KNDy neuron activity and LH release. We used adenoassociated viruses to target designer receptor exclusively activated by designer drugs (DREADDs) to GFAP-expressing cells to activate Gq or Gi-mediated signaling. Activating Gq signaling in the preoptic area, near GnRH neurons, but not in the arcuate, increases LH release in vivo and GnRH firing in vitro via a mechanism in part dependent upon PGE2. These data suggest astrocytes can activate GnRH/LH release in a manner independent of KNDy neurons.

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“…Astrocyte activities are essential for addictive behaviors (Scofield and Kalivas, 2014 ; Corkrum et al, 2020 ; Kang et al, 2020 ; Kang and Choi, 2021 ), especially for AUD (Ayers-Ringler et al, 2016 ; Erickson et al, 2018 , 2021 ; Lindberg et al, 2018 ). Astrocytes regulate neuronal activities of glutamatergic neurons in the cortico-striatal and dopaminergic neurons in the ventral tegmental area (VTA)-nucleus accumbens (NAc) circuits (Scofield and Kalivas, 2014 ; Corkrum et al, 2020 ).…”

Section: Alcohol and Cell-specific Neuroinflammatory Responsementioning

confidence: 99%

Alcohol-Induced Neuroinflammatory Response and Mitochondrial Dysfunction on Aging and Alzheimer’s Disease

León

¹

,

Kang

²

,

Franca-Solomon

³

et al. 2022

Front. Behav. Neurosci.

Self Cite

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Mitochondria are essential organelles central to various cellular functions such as energy production, metabolic pathways, signaling transduction, lipid biogenesis, and apoptosis. In the central nervous system, neurons depend on mitochondria for energy homeostasis to maintain optimal synaptic transmission and integrity. Deficiencies in mitochondrial function, including perturbations in energy homeostasis and mitochondrial dynamics, contribute to aging, and Alzheimer’s disease. Chronic and heavy alcohol use is associated with accelerated brain aging, and increased risk for dementia, especially Alzheimer’s disease. Furthermore, through neuroimmune responses, including pro-inflammatory cytokines, excessive alcohol use induces mitochondrial dysfunction. The direct and indirect alcohol-induced neuroimmune responses, including pro-inflammatory cytokines, are critical for the relationship between alcohol-induced mitochondrial dysfunction. In the brain, alcohol activates microglia and increases inflammatory mediators that can impair mitochondrial energy production, dynamics, and initiate cell death pathways. Also, alcohol-induced cytokines in the peripheral organs indirectly, but synergistically exacerbate alcohol’s effects on brain function. This review will provide recent and advanced findings focusing on how alcohol alters the aging process and aggravates Alzheimer’s disease with a focus on mitochondrial function. Finally, we will contextualize these findings to inform clinical and therapeutic approaches towards Alzheimer’s disease.

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Activation of Astrocytes in the Dorsomedial Striatum Facilitates Transition From Habitual to Goal-Directed Reward-Seeking Behavior

Cited by 48 publications

References 67 publications

A role for glial fibrillary acidic protein (GFAP)-expressing cells in the regulation of gonadotropin-releasing hormone (GnRH) but not arcuate kisspeptin neuron output in male mice

A role for glial fibrillary acidic protein (GFAP)-expressing cells in the regulation of gonadotropin-releasing hormone (GnRH) but not arcuate kisspeptin neuron output in male mice

A role for glial fibrillary acidic protein (GFAP)-expressing cells in the regulation of gonadotropin-releasing hormone (GnRH) but not arcuate kisspeptin neuron output

Alcohol-Induced Neuroinflammatory Response and Mitochondrial Dysfunction on Aging and Alzheimer’s Disease

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