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Psychiatric Disorders and TRP Channels: Focus on Psychotropic Drugs.

Nazıroğlu M, Demirdaş A - Curr Neuropharmacol (2015)

Bottom Line: Psychiatric and neurological disorders are mostly associated with the changes in neural calcium ion signaling pathways required for activity-triggered cellular events.Evidence substantiates that anandamide and its analog (methanandamide) induce an anxiolytic-like effect via CB1 receptors and TRPV1 channels.Intracellular calcium influx induced by oxidative stress has an significant role in the etiology of bipolar disorders (BDs), and studies recently reported the important role of TRP channels such as TRPC3, TRPM2, and TRPV1 in converting oxidant or nitrogen radical signaling to cytosolic calcium ion homeostasis in BDs.

View Article: PubMed Central - PubMed

Affiliation: Neuroscience Research Center, Süleyman Demirel University, Dekanlık Binası, TR-32260, Isparta, Turkey. mustafanaziroglu@sdu.edu.tr.

ABSTRACT
Psychiatric and neurological disorders are mostly associated with the changes in neural calcium ion signaling pathways required for activity-triggered cellular events. One calcium channel family is the TRP cation channel family, which contains seven subfamilies. Results of recent papers have discovered that calcium ion influx through TRP channels is important. We discuss the latest advances in calcium ion influx through TRP channels in the etiology of psychiatric disorders. Activation of TRPC4, TRPC5, and TRPV1 cation channels in the etiology of psychiatric disorders such as anxiety, fear-associated responses, and depression modulate calcium ion influx. Evidence substantiates that anandamide and its analog (methanandamide) induce an anxiolytic-like effect via CB1 receptors and TRPV1 channels. Intracellular calcium influx induced by oxidative stress has an significant role in the etiology of bipolar disorders (BDs), and studies recently reported the important role of TRP channels such as TRPC3, TRPM2, and TRPV1 in converting oxidant or nitrogen radical signaling to cytosolic calcium ion homeostasis in BDs. The TRPV1 channel also plays a function in morphine tolerance and hyperalgesia. Among psychotropic drugs, amitriptyline and capsazepine seem to have protective effects on psychiatric disorders via the TRP channels. Some drugs such as cocaine and methamphetamine also seem to have an important role in alcohol addiction and substance abuse via activation of the TRPV1 channel. Thus, we explore the relationships between the etiology of psychiatric disorders and TRP channel-regulated mechanisms. Investigation of the TRP channels in psychiatric disorders holds the promise of the development of new drug treatments.

No MeSH data available.


Related in: MedlinePlus

TRPV1 is a polymodal cation channel. TRPV1 is activated by various noxious stimuli such as capsaicin, heat, pH, resiniferatoxin(RTX), and pressure although it was blocked capsazepine (CPZ) and 5'-Iodoresiniferatoxin (IRTX). PKC through phospholipase C and adenylyl cyclase phosphorylates TRPV1 and sensitizes the channel. Increases in intracellular Ca2+ from TRPV1 can activate CaM viacalmodulin to further modulate TRPV1 activity. Supraspinal or spinal inhibition of CaM has been shown to prevent or reverse morphinetolerance and dependence [40]. TRPM2, TRPC3, and TRPV1 respond to mitochondrial-dependent oxidative stress, and indicates the role ofoxidative stress-induced calcium ion signaling in depression and anxiety. AA (arachidonic acid), AEA (anandamide), CB1 (cannabinoidreceptor type I), CB2 (cannabinoid receptor type II), FAAH (fatty acid amide hydrolase), PKC (protein kinase C).
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Figure 1: TRPV1 is a polymodal cation channel. TRPV1 is activated by various noxious stimuli such as capsaicin, heat, pH, resiniferatoxin(RTX), and pressure although it was blocked capsazepine (CPZ) and 5'-Iodoresiniferatoxin (IRTX). PKC through phospholipase C and adenylyl cyclase phosphorylates TRPV1 and sensitizes the channel. Increases in intracellular Ca2+ from TRPV1 can activate CaM viacalmodulin to further modulate TRPV1 activity. Supraspinal or spinal inhibition of CaM has been shown to prevent or reverse morphinetolerance and dependence [40]. TRPM2, TRPC3, and TRPV1 respond to mitochondrial-dependent oxidative stress, and indicates the role ofoxidative stress-induced calcium ion signaling in depression and anxiety. AA (arachidonic acid), AEA (anandamide), CB1 (cannabinoidreceptor type I), CB2 (cannabinoid receptor type II), FAAH (fatty acid amide hydrolase), PKC (protein kinase C).


Psychiatric Disorders and TRP Channels: Focus on Psychotropic Drugs.

Nazıroğlu M, Demirdaş A - Curr Neuropharmacol (2015)

TRPV1 is a polymodal cation channel. TRPV1 is activated by various noxious stimuli such as capsaicin, heat, pH, resiniferatoxin(RTX), and pressure although it was blocked capsazepine (CPZ) and 5'-Iodoresiniferatoxin (IRTX). PKC through phospholipase C and adenylyl cyclase phosphorylates TRPV1 and sensitizes the channel. Increases in intracellular Ca2+ from TRPV1 can activate CaM viacalmodulin to further modulate TRPV1 activity. Supraspinal or spinal inhibition of CaM has been shown to prevent or reverse morphinetolerance and dependence [40]. TRPM2, TRPC3, and TRPV1 respond to mitochondrial-dependent oxidative stress, and indicates the role ofoxidative stress-induced calcium ion signaling in depression and anxiety. AA (arachidonic acid), AEA (anandamide), CB1 (cannabinoidreceptor type I), CB2 (cannabinoid receptor type II), FAAH (fatty acid amide hydrolase), PKC (protein kinase C).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4598437&req=5

Figure 1: TRPV1 is a polymodal cation channel. TRPV1 is activated by various noxious stimuli such as capsaicin, heat, pH, resiniferatoxin(RTX), and pressure although it was blocked capsazepine (CPZ) and 5'-Iodoresiniferatoxin (IRTX). PKC through phospholipase C and adenylyl cyclase phosphorylates TRPV1 and sensitizes the channel. Increases in intracellular Ca2+ from TRPV1 can activate CaM viacalmodulin to further modulate TRPV1 activity. Supraspinal or spinal inhibition of CaM has been shown to prevent or reverse morphinetolerance and dependence [40]. TRPM2, TRPC3, and TRPV1 respond to mitochondrial-dependent oxidative stress, and indicates the role ofoxidative stress-induced calcium ion signaling in depression and anxiety. AA (arachidonic acid), AEA (anandamide), CB1 (cannabinoidreceptor type I), CB2 (cannabinoid receptor type II), FAAH (fatty acid amide hydrolase), PKC (protein kinase C).
Bottom Line: Psychiatric and neurological disorders are mostly associated with the changes in neural calcium ion signaling pathways required for activity-triggered cellular events.Evidence substantiates that anandamide and its analog (methanandamide) induce an anxiolytic-like effect via CB1 receptors and TRPV1 channels.Intracellular calcium influx induced by oxidative stress has an significant role in the etiology of bipolar disorders (BDs), and studies recently reported the important role of TRP channels such as TRPC3, TRPM2, and TRPV1 in converting oxidant or nitrogen radical signaling to cytosolic calcium ion homeostasis in BDs.

View Article: PubMed Central - PubMed

Affiliation: Neuroscience Research Center, Süleyman Demirel University, Dekanlık Binası, TR-32260, Isparta, Turkey. mustafanaziroglu@sdu.edu.tr.

ABSTRACT
Psychiatric and neurological disorders are mostly associated with the changes in neural calcium ion signaling pathways required for activity-triggered cellular events. One calcium channel family is the TRP cation channel family, which contains seven subfamilies. Results of recent papers have discovered that calcium ion influx through TRP channels is important. We discuss the latest advances in calcium ion influx through TRP channels in the etiology of psychiatric disorders. Activation of TRPC4, TRPC5, and TRPV1 cation channels in the etiology of psychiatric disorders such as anxiety, fear-associated responses, and depression modulate calcium ion influx. Evidence substantiates that anandamide and its analog (methanandamide) induce an anxiolytic-like effect via CB1 receptors and TRPV1 channels. Intracellular calcium influx induced by oxidative stress has an significant role in the etiology of bipolar disorders (BDs), and studies recently reported the important role of TRP channels such as TRPC3, TRPM2, and TRPV1 in converting oxidant or nitrogen radical signaling to cytosolic calcium ion homeostasis in BDs. The TRPV1 channel also plays a function in morphine tolerance and hyperalgesia. Among psychotropic drugs, amitriptyline and capsazepine seem to have protective effects on psychiatric disorders via the TRP channels. Some drugs such as cocaine and methamphetamine also seem to have an important role in alcohol addiction and substance abuse via activation of the TRPV1 channel. Thus, we explore the relationships between the etiology of psychiatric disorders and TRP channel-regulated mechanisms. Investigation of the TRP channels in psychiatric disorders holds the promise of the development of new drug treatments.

No MeSH data available.


Related in: MedlinePlus