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Analgesia evoked from the posterior diencephalon (anterior pretectal nucleus)
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ANALGESIA EVOKED FROM THE POSTERIOR DIENCEPHALON (ANTERIOR 60 Poster PRETECTAL NUCLEUS). H. Rees*, D.G. Wilson* and M.H.T. Mon Room 3 Roberts. Department ofphysiology, University College, Board 27 / Cardiff, U.K. Aims Electrical stimulation of the anterior pretectal nucleus (APtN) cauza prolonged increase in the latency of the tail flick reflex to noxious heat (Roberts & Rees, 1986). The present study examines the effects of stimulating the APtN in greater detail. Methods In the unanaesthetisedanimal the effects of stimulation have been examined on paw pressure and formalin test. In the halothane anesthetised rat microelectroderecordings have been made in the APtN and spinal cord. Results Brief (15 set) and mild (35 PA r.m.s.) stimulation of the APtN was effective in both the paw pressure and formalin tests. In both cases APtN stimulation was as effective as morphine (3 mg/kg s.c.). Following APtn stimulation there was no deficit in either motor performance or startle response. In electrophysiologicalexperiments APtN stimulation specifically inhibits the noxious responses of Lamina V-type neurones for periods up to 35 min. Many of these cells were identified as projection neurones by antidromic invasion from the antero-lateral funiculus. Sections of the DLF abolishes the effects of stimulation but lesions of raphe magnus do not. The noxious responses of Lamina I and the low threshold responses of Lamina V-type neurones were unaffected. Cells in the APtN were excited by low threshold stimulation of the dorsal column pathways. Conclusions Electrical stimulation of the APtN, a nucleus where cells are excited by low threshold sensory stimulation, causes behavioural analgesia and inhibition of Lamina V-type but not Lamina I neurones. Roberts M.H.T. & Rees H. Pain 25: 83-93, 1986.
MESOLIMBIC NEURCNAL CIRCUITRI INVOLVED IN ANTINCCICEPTICN J.S. Han and L.S. Yu*, Department of physiology, Beijing Medical University, Beijing 100083, China. Aim of Investigation: Compared to the extensive research on the medulla-spinal descending control of nociception, less attension has been payed on the cerebral neuronal circuitry involved in antinociceptive activities. This study examines the possible neuronal connection between the periaqueductal grey (PAG) and the nucleus accumbens (NA) or other related nuclei subserving analgesic effect. Methods: Nociception was measured by the latency of the escape response elicited by radiant heat focused on the nostrils. Rabbits were equipped Should an enkephal iwith intracerebral cannulae directing to PAG and NA. nergic pathway is sent from nucleus A to B, subserving analgesia, the analgesia elicited by stimulating A should be blocked by microinjection of naloxone or enkephalin antiserum into nucleus B, and vice versa. Results: Analgesia produced by morphine administered into PAGwas markedly attenuated by the 5-HT antagonist cinanserin injected into NA, and the analgesia elicited by 5-HT in NA could be blocked by metUsing the enkephalin antiserum (ME AS) adm inistered into the same site. same approach, an enkephalinergic connection was found extending from NA was also and from habenula to PAG. A GABAergic connection to habenula, a mechanism of disinhibition in suggested within the area of PAG, implying its efferent pathways. Conclusions: A msso-limbic neuronal loop of analgesia seem to exist between PAG-NA-Habenula-PAG, using 5-HT and ME sequentially as This neuronal loop may constitute an important part neurotransmitters. in the endogenous analgesia system.
ANALGESIA EVOKED FROM THE POSTERIOR DIENCEPHALON (ANTERIOR 60 Poster PRETECTAL NUCLEUS). H. Rees*, D.G. Wilson* and M.H.T. Mon Room 3 Roberts. Department ofphysiology, University College, Board 27 / Cardiff, U.K. Aims Electrical stimulation of the anterior pretectal nucleus (APtN) cauza prolonged increase in the latency of the tail flick reflex to noxious heat (Roberts & Rees, 1986). The present study examines the effects of stimulating the APtN in greater detail. Methods In the unanaesthetisedanimal the effects of stimulation have been examined on paw pressure and formalin test. In the halothane anesthetised rat microelectroderecordings have been made in the APtN and spinal cord. Results Brief (15 set) and mild (35 PA r.m.s.) stimulation of the APtN was effective in both the paw pressure and formalin tests. In both cases APtN stimulation was as effective as morphine (3 mg/kg s.c.). Following APtn stimulation there was no deficit in either motor performance or startle response. In electrophysiologicalexperiments APtN stimulation specifically inhibits the noxious responses of Lamina V-type neurones for periods up to 35 min. Many of these cells were identified as projection neurones by antidromic invasion from the antero-lateral funiculus. Sections of the DLF abolishes the effects of stimulation but lesions of raphe magnus do not. The noxious responses of Lamina I and the low threshold responses of Lamina V-type neurones were unaffected. Cells in the APtN were excited by low threshold stimulation of the dorsal column pathways. Conclusions Electrical stimulation of the APtN, a nucleus where cells are excited by low threshold sensory stimulation, causes behavioural analgesia and inhibition of Lamina V-type but not Lamina I neurones. Roberts M.H.T. & Rees H. Pain 25: 83-93, 1986.
MESOLIMBIC NEURCNAL CIRCUITRI INVOLVED IN ANTINCCICEPTICN J.S. Han and L.S. Yu*, Department of physiology, Beijing Medical University, Beijing 100083, China. Aim of Investigation: Compared to the extensive research on the medulla-spinal descending control of nociception, less attension has been payed on the cerebral neuronal circuitry involved in antinociceptive activities. This study examines the possible neuronal connection between the periaqueductal grey (PAG) and the nucleus accumbens (NA) or other related nuclei subserving analgesic effect. Methods: Nociception was measured by the latency of the escape response elicited by radiant heat focused on the nostrils. Rabbits were equipped Should an enkephal iwith intracerebral cannulae directing to PAG and NA. nergic pathway is sent from nucleus A to B, subserving analgesia, the analgesia elicited by stimulating A should be blocked by microinjection of naloxone or enkephalin antiserum into nucleus B, and vice versa. Results: Analgesia produced by morphine administered into PAGwas markedly attenuated by the 5-HT antagonist cinanserin injected into NA, and the analgesia elicited by 5-HT in NA could be blocked by metUsing the enkephalin antiserum (ME AS) adm inistered into the same site. same approach, an enkephalinergic connection was found extending from NA was also and from habenula to PAG. A GABAergic connection to habenula, a mechanism of disinhibition in suggested within the area of PAG, implying its efferent pathways. Conclusions: A msso-limbic neuronal loop of analgesia seem to exist between PAG-NA-Habenula-PAG, using 5-HT and ME sequentially as This neuronal loop may constitute an important part neurotransmitters. in the endogenous analgesia system.