GPCR signaling — what immediately changes after ligand binding? Many G-protein–linked receptors trigger short-lived changes in which class of molecules following ligand binding?

Introduction:
G-protein–coupled receptors (GPCRs) translate an outside signal (first messenger) into rapid intracellular changes via second messengers. These changes are typically transient and precisely regulated to encode information without permanently altering cellular components.

Given Data / Assumptions:

• Ligands (first messengers) bind GPCRs at the plasma membrane.
• Activated receptors engage heterotrimeric G proteins and downstream effectors such as adenylyl cyclase or phospholipase C.
• Second messengers include cAMP, cGMP, Ca2+, IP3, and DAG.

Concept / Approach:

Upon ligand binding, GPCRs catalyze GDP–GTP exchange on Gα, which then regulates effectors that synthesize or mobilize second messengers. The resulting brief surge of a second messenger amplifies the signal and activates protein kinases and other targets, producing a coordinated cellular response.

Step-by-Step Solution:

Verification / Alternative check:

Time-resolved imaging shows sharp, short-lived spikes in cAMP or cytosolic Ca2+ after GPCR activation, consistent with second-messenger dynamics.

Why Other Options Are Wrong:

Universal decreases (Option B) are not characteristic; responses can increase or decrease depending on receptor/effector.

Options C and D conflate extracellular ligand concentrations with intracellular second messengers.

Option E describes irreversible changes inconsistent with the transient, reversible nature of GPCR signaling.

Common Pitfalls:

Mixing up first messengers (outside) and second messengers (inside), or assuming second-messenger levels always fall rather than often rise.

Final Answer:

Increase in the concentration of certain intracellular signaling molecules called second messengers