Scholarlink

<p>Cyclic adenosine monophosphate (cAMP) and Ca²⁺ are ubiquitous second messengers that regulate gene expression, metabolism, and synaptic plasticity. Here, we identified a complex interplay between Ca²⁺ and cAMP signaling pathways in mouse olfactory bulb astrocytes. Norepinephrine (NE) elevated both Ca²⁺ and cAMP levels via α<sub>₁</sub> and α<sub>₂</sub> adrenergic receptors, whereas β receptors triggered only cAMP responses. The α<sub>₁</sub> receptor agonist phenylephrine increased cAMP, but this effect was suppressed when Ca²⁺ elevations were blocked by Ca²⁺ depletion and removal of external Ca²⁺. We found that α<sub>₁A</sub> and α<sub>1D</sub> receptors are key targets for phenylephrine, acting through Ca²⁺/calmodulin-dependent adenylyl cyclases AC1 and AC3 downstream of α<sub>₁</sub> receptor activation. Moreover, α<sub>₂</sub> receptor stimulation raised Ca²⁺ levels, thereby stimulating cAMP production, yet also reduced forskolin-induced cAMP elevations, indicating that α<sub>₂</sub> receptors can both inhibit adenylyl cyclase via G<sub>i</sub> and stimulate AC1/AC3 via Ca²⁺ signaling. Together, these findings reveal intricate crosstalk between noradrenergic Ca²⁺ and cAMP signaling in olfactory bulb astrocytes mediated by all three adrenergic receptor subtypes.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Crosstalk of noradrenergic Ca2+ and cAMP signaling in astrocytes of the murine olfactory bulb

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月11日

查看全文
  • Jessica Sauer,
  • Antonia Beiersdorfer,
  • Franz Lennart Schmidt,
  • Mathias Nordbeck,
  • Oana Constantin,
  • Daniela Hirnet,
  • Christine E. Gee,
  • Christian Lohr

摘要

Cyclic adenosine monophosphate (cAMP) and Ca²⁺ are ubiquitous second messengers that regulate gene expression, metabolism, and synaptic plasticity. Here, we identified a complex interplay between Ca²⁺ and cAMP signaling pathways in mouse olfactory bulb astrocytes. Norepinephrine (NE) elevated both Ca²⁺ and cAMP levels via α₁ and α₂ adrenergic receptors, whereas β receptors triggered only cAMP responses. The α₁ receptor agonist phenylephrine increased cAMP, but this effect was suppressed when Ca²⁺ elevations were blocked by Ca²⁺ depletion and removal of external Ca²⁺. We found that α₁A and α1D receptors are key targets for phenylephrine, acting through Ca²⁺/calmodulin-dependent adenylyl cyclases AC1 and AC3 downstream of α₁ receptor activation. Moreover, α₂ receptor stimulation raised Ca²⁺ levels, thereby stimulating cAMP production, yet also reduced forskolin-induced cAMP elevations, indicating that α₂ receptors can both inhibit adenylyl cyclase via Gi and stimulate AC1/AC3 via Ca²⁺ signaling. Together, these findings reveal intricate crosstalk between noradrenergic Ca²⁺ and cAMP signaling in olfactory bulb astrocytes mediated by all three adrenergic receptor subtypes.