Title : Interactions between COX-2 and glutamatergic receptors with CB1 as a novel target in mood and cognitive studies
Abstract:
Glutamate, the brain’s primary excitatory neurotransmitter, maintains neuronal communication and functional stability. Together with gamma-aminobutyric acid (GABA), the primary inhibitory neurotransmitter, it establishes a balance essential for cognitive processes, emotional regulation, and neural plasticity. Dysregulated glutamatergic signaling has been implicated in various psychiatric and neurological disorders, including depression, anxiety, and cognitive impairments.
Glutamate exerts its effects through two receptor types: ionotropic, mediating rapid synaptic transmission, and metabotropic (mGluRs), which modulate neuronal activity over longer timescales. Among these, mGluRs are gaining attention for their role in synaptic plasticity and their therapeutic potential in neuropsychiatric conditions.
Cyclooxygenase-2 (COX-2), an enzyme involved in the inflammatory response, plays a significant role in glutamatergic pathways. Its activity is linked to the production of prostanoids, lipid mediators derived from arachidonic acid (AA), a polyunsaturated omega-6 fatty acid released by phospholipase A2 (PLA2). While inflammation mediated by COX-2 is a natural response to injury, excessive activity can contribute to neuroinflammation, cognitive decline, and mood disorders, making COX-2 an important therapeutic target.
Recent findings reveal a novel interaction between metabotropic glutamate receptor 7 (mGluR7) and cannabinoid receptor 1 (CB1), highlighting their synergistic role in anxiety regulation. This discovery underscores the importance of receptor crosstalk in complex emotional states and suggests potential avenues for developing innovative treatments targeting mGluR7 and CB1.
By bridging the fields of neurotransmission, lipid signaling, and receptor dynamics, these insights deepen our understanding of brain function and its dysregulation in mental health conditions.
