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T. M. Jessell

Bio: T. M. Jessell is an academic researcher. The author has contributed to research in topics: Stimulation & Substance P. The author has an hindex of 1, co-authored 2 publications receiving 940 citations.

Papers
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Journal ArticleDOI
11 Aug 1977-Nature
TL;DR: It is reported here that opiate analgesics are able to suppress the stimulus-evoked release of SP, which may represent a mechanism for the direct spinal analgesic actions of opiates.
Abstract: THE undecapeptide substance P (SP) may act as a transmitter released from the terminals of primary sensory nerves in the spinal cord1–2. SP has been shown to be highly concentrated in the terminals of small diameter fibres in the substantia gelatinosa of the dorsal horn in mammalian spinal cord, and these terminals disappear after dorsal root section3–6. Sensory nuclei of some of the cranial nerves, such as the spinal trigeminal nucleus, also contain a high density of SP nerve terminals6–7. SP is released by a calcium-dependent mechanism from the isolated rat spinal cord during electrical stimulation of the dorsal roots8. The peptide is also a powerful excitant of neurones in the spinal cord2, and seems to excite selectively those cells in dorsal horn that respond to noxious stimuli9–10. SP may, therefore, represent the excitatory transmitter, or one of the transmitters, released from primary fibres involved in the transmission of pain. We have examined the stimulus-evoked release of SP from rat spinal trigeminal nucleus slices in vitro to explore the factors which may control its release from primary sensory terminals. We report here that opiate analgesics are able to suppress the stimulus-evoked release of SP. These findings may represent a mechanism for the direct spinal analgesic actions of opiates.

941 citations

Journal ArticleDOI
01 Feb 1979-Pain
TL;DR: A strong case is made for a descending inhibitory raphe-spinal pathway in the DLF that mediates opiate and brain stimulation induced analgesia.
Abstract: THE undecapeptide substance P (SP) may act as a transmitter released from the terminals of primary sensory nerves in the spinal cord1–2. SP has been shown to be highly concentrated in the terminals of small diameter fibres in the substantia gelatinosa of the dorsal horn in mammalian spinal cord, and these terminals disappear after dorsal root section3–6. Sensory nuclei of some of the cranial nerves, such as the spinal trigeminal nucleus, also contain a high density of SP nerve terminals6–7. SP is released by a calcium-dependent mechanism from the isolated rat spinal cord during electrical stimulation of the dorsal roots8. The peptide is also a powerful excitant of neurones in the spinal cord2, and seems to excite selectively those cells in dorsal horn that respond to noxious stimuli9–10. SP may, therefore, represent the excitatory transmitter, or one of the transmitters, released from primary fibres involved in the transmission of pain. We have examined the stimulus-evoked release of SP from rat spinal trigeminal nucleus slices in vitro to explore the factors which may control its release from primary sensory terminals. We report here that opiate analgesics are able to suppress the stimulus-evoked release of SP. These findings may represent a mechanism for the direct spinal analgesic actions of opiates.

3 citations


Cited by
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Journal ArticleDOI
TL;DR: The body of scientific evidence regarding the mechanisms and effects of nociceptive activity in newborn infants has not been addressed directly and the pervasive view of neonatal pain is that newborns are frequently not given analgesic or anesthetic agents during invasive procedures, including surgery.
Abstract: THE evaluation of pain in the human fetus and neonate is difficult because pain is generally defined as a subjective phenomenon.1 Early studies of neurologic development concluded that neonatal responses to painful stimuli were decorticate in nature and that perception or localization of pain was not present.2 Furthermore, because neonates may not have memories of painful experiences, they were not thought capable of interpreting pain in a manner similar to that of adults.3 4 5 On a theoretical basis, it was also argued that a high threshold of painful stimuli may be adaptive in protecting infants from pain during birth.6 These traditional . . .

1,507 citations

Journal ArticleDOI
TL;DR: It was difficult to identify substance-P immunoreactive axons in the rats studied, and further experimental studies are necessary to elucidate the projections of the substance P-immunoreactive neurons in the rat central nervous system.

1,403 citations

Journal ArticleDOI
TL;DR: The relationship of trigeminovascular fibers to the pathogenesis of vascular head pain sheds light on possible mechanisms of migraine and other central nervous system conditions associated with headache and inflammation.
Abstract: Nervous connections between the trigeminal ganglia and cerebral blood vessels have recently been identified in experimental animals and have been termed the trigeminovascular system. Existence of this system in humans is inferential. Trigeminovascular neurons and their peripheral unmyelinated nerve fibers contain the neurotransmitter peptide substance P. Most newly synthesized substance P is transported from ganglion cell bodies to afferent nerve fibers, where depolarization-induced release of neurotransmitter into the wall of the cerebral blood vessel occurs. Substance P dilates pial arteries, increases vascular permeability, and activates cells that participate in the inflammatory response. The relationship of trigeminovascular fibers to the pathogenesis of vascular head pain sheds light on possible mechanisms of migraine and other central nervous system conditions associated with headache and inflammation.

899 citations

Journal ArticleDOI
TL;DR: Findings indicate that substance P and 5-HT may coexist not only in some cell bodies but also in axons and nerve endings in neurons of the lower medulla oblongata.

804 citations