Journal of Nippon Medical School: Vol.69 No.4 page.322

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ArticleTitle Tachykininergic Neurotransmission in the Central Nervous System

AuthorList Hidenori Suzuki

Affiliation Department of Pharmacology, Nippon Medical School

Language JA

Volume 69

Issue 4

Year 2002

Page 322-327

Received March 2, 2002

Accepted April 18, 2002

Keywords amygdala, anxiety, pain, tachykinins, tachykinin receptor antagonist

Abstract Tachykinins are widely distributed in mammalian central nervous system and exert a variety of actions through individual specific receptors. Neurotransmitter functions of substance P (SP), a member of mammalian tachykinins, have been firmly established in the spinal cord; SP is highly concentrated in the superficial layers of the dorsal horn, is released upon electrical stimulation, produces a slow excitatory postsynaptic potential in second-order neurons and is inactivated by peptidases. Since SP is contained in unmyelinated primary afferent fibers, which mediate nociception, SP is thought to transmit nociceptive information and contribute to occurrence of pathological pain states such as inflammation and nerve injury. Based on these findings, great effort has been devoted to developing NK-1 tachykinin receptor antagonists as a potent antinociceptive drug, but up to the present such effective drugs are unavailable. Tachykinin receptor antagonists have been also attracting much attention as a novel therapeutic drug for anxiety and depression other than pain. The amygdala, a key brain structure associated with emotional responses, is thought to be a target of tachykinin receptor antagonists for exerting psychopharmacological actions. Indeed, tachykinins enhance inhibitory synaptic transmission in the basolateral complex of the amygdala. Further study of tachykininergic transmission in the central nervous systems will open novel fields for pharmacology and therapeutics in neuropsychiatric disorders.

Correspondence to Hidenori Suzuki, MD, Department of Pharmacology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan
hsuzuki@nms.ac.jp

ArticleTitle	Tachykininergic Neurotransmission in the Central Nervous System
AuthorList	Hidenori Suzuki
Affiliation	Department of Pharmacology, Nippon Medical School
Language	JA
Volume	69
Issue	4
Year	2002
Page	322-327
Received	March 2, 2002
Accepted	April 18, 2002
Keywords	amygdala, anxiety, pain, tachykinins, tachykinin receptor antagonist
Abstract	Tachykinins are widely distributed in mammalian central nervous system and exert a variety of actions through individual specific receptors. Neurotransmitter functions of substance P (SP), a member of mammalian tachykinins, have been firmly established in the spinal cord; SP is highly concentrated in the superficial layers of the dorsal horn, is released upon electrical stimulation, produces a slow excitatory postsynaptic potential in second-order neurons and is inactivated by peptidases. Since SP is contained in unmyelinated primary afferent fibers, which mediate nociception, SP is thought to transmit nociceptive information and contribute to occurrence of pathological pain states such as inflammation and nerve injury. Based on these findings, great effort has been devoted to developing NK-1 tachykinin receptor antagonists as a potent antinociceptive drug, but up to the present such effective drugs are unavailable. Tachykinin receptor antagonists have been also attracting much attention as a novel therapeutic drug for anxiety and depression other than pain. The amygdala, a key brain structure associated with emotional responses, is thought to be a target of tachykinin receptor antagonists for exerting psychopharmacological actions. Indeed, tachykinins enhance inhibitory synaptic transmission in the basolateral complex of the amygdala. Further study of tachykininergic transmission in the central nervous systems will open novel fields for pharmacology and therapeutics in neuropsychiatric disorders.
Correspondence to	Hidenori Suzuki, MD, Department of Pharmacology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan hsuzuki@nms.ac.jp