Effects of pain and of several central analgesics on cortex, hippocampus and reticular formation of brain stem

Soulairac, A; Gottesmann, Claude; Charpentier, J.

doi:10.1016/0028-3908(67)90055-x

Cited by 20 publications

(6 citation statements)

References 5 publications

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“…This processing might have included the hippocampus as this structure is involved in phase 2, but not phase 1, of the formalin test (McKenna & Melzack, 1992). The involvement of the hippocampus in pain processing is also supported by results from physiological (Dutar et al ., 1985), pharmacological (Soulairac et al ., 1967; Dutar et al ., 1985; McKenna & Melzack, 1992), and behavioural (Corkin, 1984; Wei et al ., 2000) studies. Furthermore, hippocampal activity is changed by persistent pain and these effects are different in males and females (Aloisi et al ., 1996).…”

Section: Discussionmentioning

confidence: 99%

Environmental conditions influence hippocampus‐dependent behaviours and brain levels of amyloid precursor protein in rats

Teather

Magnusson

Chow

et al. 2002

Eur J of Neuroscience

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Sprague-Dawley rats were reared in enriched (EC; group housing, exposure to stimulating objects, frequent handling) or restricted (RC; individual housing, no exposure to stimulating objects, minimal handling) environments starting on day 23 of life. At six months of age, they underwent behavioural tests to assess 'cognitive' and 'stimulus-response' memory, selective attention, and inflammatory pain processing. Alterations in synapses and cell survival may occur as a result of environment differences; therefore we assessed the brain levels of several proteins implicated in neurite outgrowth, synaptogenesis, and cell survival. Brains were dissected and analysed for amyloid precursor protein (APP) and other synaptic and cytoskeletal proteins using Western blotting. The performance of EC animals in a hidden platform water maze task, and in a test of selective attention (both of which are thought to involve the hippocampus) was superior to that of RC animals. In contrast, performance of RC animals on two stimulus-response tasks, the visible platform water maze test and simple visual discrimination (both of which are thought to be hippocampal independent) was indistinguishable from that of EC animals. Male EC rats displayed a different behavioural response to formalin during the inflammatory phase of nociception--the phase affected by hippocampal processing; a similar trend was observed in females. Female but not male RC rats exhibited elevated plasma corticosterone levels; adrenal weights were unaffected by environmental conditions. Region-specific increases in brain levels of APP, neurofilament-70 (NF-70), and platelet-activating factor receptor (PAF-R) were found in EC rats. These data suggest that enriched animals manifest enhanced functioning of certain hippocampus-mediated behaviours when compared with that of their restricted counterparts; and that brain levels of various synaptic and structural proteins involved in neurite outgrowth, cell survival, and synaptogenesis, are affected by environmental factors.

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Section: Discussionmentioning

confidence: 99%

Environmental conditions influence hippocampus‐dependent behaviours and brain levels of amyloid precursor protein in rats

Teather

Magnusson

Chow

et al. 2002

Eur J of Neuroscience

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Section: Vasoactive Intestinal Peptidementioning

confidence: 99%

“…As early as 1960s, Soulairac et al [142] reported that strong electrical stimulation of the tail in conscious animals synchronized the hippocampal EEG and produced a 'hippocampal awakening' which lasted several seconds and was correlated with the rat vocalizing and biting the electrodes. Morphine and related agents blocked all of these responses [142] . Subsequently, Sinnamon and Schwartzbaum [143] examined the response of Another EEG study regarding hippocampus and nociception derives from Archer and Roth [144] , who explored the pharmacodynamic relationship between thiopentone concentrations and both hippocampal EEG and nocifensive reflexes, measured as mechanical withdrawal threshold to noxious pressure stimulation on the tail.…”

Section: Vasoactive Intestinal Peptidementioning

confidence: 99%

Roles of the hippocampal formation in pain information processing

2009

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Abstract:Pain is a complex experience consisting of sensory-discriminative, affective-motivational, and cognitive-evaluative dimensions. Now it has been gradually known that noxious information is processed by a widely-distributed, hierarchicallyinterconnected neural network, referred to as neuromatrix, in the brain. Thus, identifying the multiple neural networks subserving these functional aspects and harnessing this knowledge to manipulate the pain response in new and beneficial ways are challenging tasks. Albeit with elaborate research efforts on the cortical responses to painful stimuli or clinical pain, involvement of the hippocampal formation (HF) in pain is still a matter of controversy. Here, we integrate previous animal and human studies from the viewpoint of HF and pain, sequentially representing anatomical, behavioral, electrophysiological, molecular/ biochemical and functional imaging evidence supporting the role of HF in pain processing. At last, we further expound on the relationship between pain and memory and present some unresolved issues.

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“…This raises the possibility that opiate/opioid rigid immobility might be based on an epileptiform limbic state, accompanied by inhibition of the neocortex. The mechanism of neocortical EEG synchronization during morphine-induced "stupor" (Khazan, Weeks, & Schroeder, 1967;Tortella, Moreton, & Khazan, 1978) is conceivably unlike that of normal slow wave sleep, because opiate-induced neocortical "somnolence" coexists with desynchronized EEG activity in the mesencephalic reticular formation (Soulairac, Gottesmann, & Charpentier, 1967; for another example of subcorticalneocortical disconnection in a "somnolent" state, see Shoham & Teitelbaum, 1982). On the other hand, the contribution of hippocampal mechanisms to opiate/opioid rigid immobility and explosive motor behavior should not be ruled out.…”

Section: Neural Mechanisms Of Morphine Catalepsymentioning

confidence: 99%

Morphine catalepsy as an adaptive reflex state in rats.

Ryck¹,

Teitelbaùm²

1984

Behavioral Neuroscience

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These experiments demonstrate that morphine-induced catalepsy consists of two complementary, but opposite, behavioral extremes (rigid immobility and sudden locomotor bursts), each of which can be controlled by distinct classes of external stimuli. When stimuli that involve pain and/or nonnociceptive skin pressure are tonic (continuous), morphine-induced electroencephalographic (EEG) deactivation and behavioral immobility are potentiated, even to the extent that a stimulation-bound reversible coma results. In contrast, phasic (discrete) stimulation produces behavioral and/or EEG activation. EEG and behavioral rebound effects are observed following stressful (intense, prolonged) stimuli. On the basis of the observed stimulus controls, sensorimotor characteristics, and EEG reactions, it is suggested that similarities may exist between morphine-induced catalepsy and defensive reactions of immobility and escape in drug-free animals (i.e., the adaptive death- feigning reflex).

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Effects of pain and of several central analgesics on cortex, hippocampus and reticular formation of brain stem

Cited by 20 publications

References 5 publications

Environmental conditions influence hippocampus‐dependent behaviours and brain levels of amyloid precursor protein in rats

Environmental conditions influence hippocampus‐dependent behaviours and brain levels of amyloid precursor protein in rats

Roles of the hippocampal formation in pain information processing

Morphine catalepsy as an adaptive reflex state in rats.

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