Modulating cyclic nucleotides pathways by bioactive compounds in combatting anxiety and depression disorders.

Anxiety and depression disorders are highly prevalent neurological disorders (NDs) that impact up to one in three individuals during their lifetime. Addressing these disorders requires reducing their frequency and impact, understanding molecular causes, implementing prevention strategies, and improving treatments. Cyclic nucleotide monophosphates (cNMPs) like cyclic adenosine monophosphate (cAMP), cyclic guanosine monophosphate (cGMP), cyclic uridine monophosphate (cUMP), and cyclic cytidine monophosphate (cCMP) regulate the transcription of genes involved in neurotransmitters and neurological functions.

Effect of subchronic exposure to ambient fine and ultrafine particles on rat motor activity and striatal dopaminergic transmission.

Alterations in dopaminergic transmission are associated with neurological disorders, such as depression, autism, and Parkinson's disease. Exposure of rats to ambient fine (FP) or ultrafine (UFP) particles induces oxidative and inflammatory responses in the striatum, a neuronal nucleus with dense dopaminergic innervation and critically involved in the control of motor activity. We used an system to evaluate the effect of inhalation exposure to FP and UFP on motor activity and dopaminergic transmission.

Adenosine A and histamine H receptors interact at the cAMP/PKA pathway to modulate depolarization-evoked [H]-GABA release from rat striato-pallidal terminals.

We previously reported that the activation of histamine H receptors (HRs) selectively counteracts the facilitatory action of adenosine A receptors (ARs) on GABA release from rat globus pallidus (GP) isolated nerve terminals (synaptosomes). In this work, we examined the mechanisms likely to underlie this functional interaction. Three possibilities were explored: (a) changes in receptor affinity for agonists induced by physical AR/HR interaction, (b) opposite actions of ARs and HRs on depolarization-induced Ca entry, and (c) an AR/HR interaction at the level of adenosine 3',5'-cyclic monophosphate (cAMP) formation.

The Histamine H3 Receptor: Structure, Pharmacology, and Function.

Among the four G protein-coupled receptors (H-H) identified as mediators of the biologic effects of histamine, the H receptor (HR) is distinguished for its almost exclusive expression in the nervous system and the large variety of isoforms generated by alternative splicing of the corresponding mRNA. Additionally, it exhibits dual functionality as autoreceptor and heteroreceptor, and this enables HRs to modulate the histaminergic and other neurotransmitter systems. The cloning of the HR cDNA in 1999 by Lovenberg et al.

Histamine H3 receptor activation counteracts adenosine A2A receptor-mediated enhancement of depolarization-evoked [3H]-GABA release from rat globus pallidus synaptosomes.

High levels of histamine H3 receptors (H3Rs) are found in the globus pallidus (GP), a neuronal nucleus in the basal ganglia involved in the control of motor behavior. By using rat GP isolated nerve terminals (synaptosomes), we studied whether H3R activation modified the previously reported enhancing action of adenosine A2A receptor (A2AR) stimulation on depolarization-evoked [(3)H]-GABA release. At 3 and 10 nM, the A2AR agonist CGS-21680 enhanced [(3)H]-GABA release induced by high K(+) (20 mM) and the effect of 3 nM CGS-21680 was prevented by the A2AR antagonist ZM-241385 (100 nM).