3 Answers
About what I know, there are 3 ways in animal to trigger / induced REM sleep
a) in albino rats, during the subjective night (and therefore when there is a weak light in the enviroment), by turning the light off. At thermoneutrality the probability of enter REM sleep is very high (see Ruth Benca's work http://www.ncbi.nlm.nih.g
Behav Neurosci. 1999 Aug;113(4):755-65.
The pretectum mediates rapid eye movement sleep regulation by light.Miller AM, Miller RB, Obermeyer WH, Behan M, Benca RM.
Source
Neuroscience Training Program, University of Wisconsin-Madison, 53719, USA.
Abstract
A variety of sensory stimuli (e.g., visual, auditory, and thermal) are known to induce rapid eye movement (REM) sleep in mammals. Studies have examined the induction of REM sleep in albino rats by light-to-dark transitions, a phenomenon referred to as REM sleep triggering. Recent research has demonstrated that aspiration lesions of the superior colliculus (SC) and pretectal area attenuated REM sleep triggering. To define more specifically the area or areas involved in mediating REM sleep responses to changes in illumination, fiber-sparing neurotoxic lesions were made to the pretectum (PT) or the SC. Lesions of the PT attenuated REM sleep triggering, whereas lesions of the SC did not. Thus, the role of the PT may be expanded to include the regulation of REM sleep in response to photic stimulation in albino rats. These findings provide a paradigm in which to study mechanisms of REM sleep generation and the effects of light on behavioral state.
PMID: 10495083 [PubMed - indexed for MEDLINE
J Sleep Res. 2008 Jun;17(2):166-79.
Cold exposure impairs dark-pulse capacity to induce REM sleep in the albino rat.Baracchi F, Zamboni G, Cerri M, Del Sindaco E, Dentico D, Jones CA, Luppi M, Perez E, Amici R.
Source
Department of Human and General Physiology, Alma Mater Studiorum-University of Bologna, Italy.
Abstract
In the albino rat, a REM sleep (REMS) onset can be induced with a high probability and a short latency when the light is suddenly turned off (dark pulse, DP) during non-REM sleep (NREMS). The aim of this study was to investigate to what extent DP delivery could overcome the integrative thermoregulatory mechanisms that depress REMS occurrence during exposure to low ambient temperature (Ta). To this aim, the efficiency of a non-rhythmical repetitive DP (3 min each) delivery during the first 6-h light period of a 12 h:12 h light-dark cycle in inducing REMS was studied in the rat, through the analysis of electroencephalogram, electrocardiogram, hypothalamic temperature and motor activity at different Tas. The results showed that DP delivery triggers a transition from NREMS to REMS comparable to that which occurs spontaneously. However, the efficiency of DP delivery in inducing REMS was reduced during cold exposure to an extent comparable with that observed in spontaneous REMS occurrence. Such impairment was associated with low Delta activity and high sympathetic tone when DPs were delivered. Repetitive DP administration increased REMS amount during the delivery period and a subsequent negative REMS rebound was observed. In conclusion, DP delivery did not overcome the integrative thermoregulatory mechanisms that depress REMS in the cold. These results underline the crucial physiological meaning of the mutual exclusion of thermoregulatory activation and REMS occurrence, and support the hypothesis that the suspension of the central control of body temperature is a prerequisite for REMS occurrence.
PMID: 18482105 [PubMed - indexed for MEDLINE]
b) microinjection of a the cholinergic agonist carbachol (in cats) or the GABA-A antagonist Bicuculline (in rats) whithin the SLD ( pontine sublaterodorsal nucleus)(see Pierre Luppi's work :
http://www.ncbi.nlm.nih.g
Eur J Neurosci. 2002 Nov;16(10):1959-73.
The rat ponto-medullary network responsible for paradoxical sleep onset and maintenance: a combined microinjection and functional neuroanatomical study.Boissard R, Gervasoni D, Schmidt MH, Barbagli B, Fort P, Luppi PH.
Source
CNRS FRE 2469, Institut Fédératif des Neurosciences de Lyon (IFR 19), Université Claude Bernard Lyon I, 8 Avenue Rockefeller, 69373 LYON Cedex 08, France.
Abstract
The neuronal network responsible for paradoxical sleep (PS) onset and maintenance has not previously been identified in the rat, unlike the cat. To fill this gap, this study has developed a new technique involving the recording of sleep-wake states in unanaesthetized head-restrained rats whilst locally administering pharmacological agents by microiontophoresis from glass multibarrel micropipettes, into the dorsal pontine tegmentum and combining this with functional neuroanatomy. Pharmacological agents used for iontophoretic administration included carbachol, kainic acid, bicuculline and gabazine. The injection sites and their efferents were then identified by injections of anterograde (phaseolus vulgaris leucoagglutinin) or retrograde (cholera toxin B subunit) tracers through an adjacent barrel of the micropipette assembly and by C-Fos immunostaining. Bicuculline, gabazine and kainic acid ejections specifically into the pontine sublaterodorsal nucleus (SLD) induced within a few minutes a PS-like state characterized by a continuous muscle atonia, low voltage EEG and a lack of reaction to stimuli. In contrast, carbachol ejections into the SLD induced wakefulness. In PHA-L, glycine and C-Fos multiple double-labelling experiments, anterogradely labelled fibres originating from the SLD were seen apposed on glycine and C-Fos positive neurons (labelled after 90 min of pharmacologically induced PS-like state) from the ventral gigantocellular and parvicellular reticular nuclei. Altogether, these data indicate that the SLD nuclei contain a population of neurons playing a crucial role in PS onset and maintenance. Furthermore, they suggest that GABAergic disinhibition and glutamate excitation of these neurons might also play a crucial role in the onset of PS.
PMID: 12453060 [PubMed - indexed for MEDLINE
c) microinjection of the GABA-A muscimol within the vlPAG (ventrolateral periaqueductal gray). (still Pierre Luppi's work:
http://www.ncbi.nlm.nih.g
PLoS One. 2009;4(1):e4272. Epub 2009 Jan 26.
Localization of the brainstem GABAergic neurons controlling paradoxical (REM) sleep.Sapin E, Lapray D, Bérod A, Goutagny R, Léger L, Ravassard P, Clément O, Hanriot L, Fort P, Luppi PH.
Source
CNRS, UMR5167, Physiopathologie des réseaux neuronaux du cycle veille-sommeil, Lyon, France.
Abstract
Paradoxical sleep (PS) is a state characterized by cortical activation, rapid eye movements and muscle atonia. Fifty years after its discovery, the neuronal network responsible for the genesis of PS has been only partially identified. We recently proposed that GABAergic neurons would have a pivotal role in that network. To localize these GABAergic neurons, we combined immunohistochemical detection of Fos with non-radioactive in situ hybridization of GAD67 mRNA (GABA synthesis enzyme) in control rats, rats deprived of PS for 72 h and rats allowed to recover after such deprivation. Here we show that GABAergic neurons gating PS (PS-off neurons) are principally located in the ventrolateral periaqueductal gray (vlPAG) and the dorsal part of the deep mesencephalic reticular nucleus immediately ventral to it (dDpMe). Furthermore, iontophoretic application of muscimol for 20 min in this area in head-restrained rats induced a strong and significant increase in PS quantities compared to saline. In addition, we found a large number of GABAergic PS-on neurons in the vlPAG/dDPMe region and the medullary reticular nuclei known to generate muscle atonia during PS. Finally, we showed that PS-on neurons triggering PS localized in the SLD are not GABAergic. Altogether, our results indicate that multiple populations of PS-on GABAergic neurons are distributed in the brainstem while only one population of PS-off GABAergic neurons localized in the vlPAG/dDpMe region exist. From these results, we propose a revised model for PS control in which GABAergic PS-on and PS-off neurons localized in the vlPAG/dDPMe region play leading roles.
PMID: 19169414 [PubMed - indexed for MEDLINE] PMCID: PMC2629845
a) in albino rats, during the subjective night (and therefore when there is a weak light in the enviroment), by turning the light off. At thermoneutrality the probability of enter REM sleep is very high (see Ruth Benca's work http://www.ncbi.nlm.nih.g
Behav Neurosci. 1999 Aug;113(4):755-65.
The pretectum mediates rapid eye movement sleep regulation by light.Miller AM, Miller RB, Obermeyer WH, Behan M, Benca RM.
Source
Neuroscience Training Program, University of Wisconsin-Madison, 53719, USA.
Abstract
A variety of sensory stimuli (e.g., visual, auditory, and thermal) are known to induce rapid eye movement (REM) sleep in mammals. Studies have examined the induction of REM sleep in albino rats by light-to-dark transitions, a phenomenon referred to as REM sleep triggering. Recent research has demonstrated that aspiration lesions of the superior colliculus (SC) and pretectal area attenuated REM sleep triggering. To define more specifically the area or areas involved in mediating REM sleep responses to changes in illumination, fiber-sparing neurotoxic lesions were made to the pretectum (PT) or the SC. Lesions of the PT attenuated REM sleep triggering, whereas lesions of the SC did not. Thus, the role of the PT may be expanded to include the regulation of REM sleep in response to photic stimulation in albino rats. These findings provide a paradigm in which to study mechanisms of REM sleep generation and the effects of light on behavioral state.
PMID: 10495083 [PubMed - indexed for MEDLINE
J Sleep Res. 2008 Jun;17(2):166-79.
Cold exposure impairs dark-pulse capacity to induce REM sleep in the albino rat.Baracchi F, Zamboni G, Cerri M, Del Sindaco E, Dentico D, Jones CA, Luppi M, Perez E, Amici R.
Source
Department of Human and General Physiology, Alma Mater Studiorum-University of Bologna, Italy.
Abstract
In the albino rat, a REM sleep (REMS) onset can be induced with a high probability and a short latency when the light is suddenly turned off (dark pulse, DP) during non-REM sleep (NREMS). The aim of this study was to investigate to what extent DP delivery could overcome the integrative thermoregulatory mechanisms that depress REMS occurrence during exposure to low ambient temperature (Ta). To this aim, the efficiency of a non-rhythmical repetitive DP (3 min each) delivery during the first 6-h light period of a 12 h:12 h light-dark cycle in inducing REMS was studied in the rat, through the analysis of electroencephalogram, electrocardiogram, hypothalamic temperature and motor activity at different Tas. The results showed that DP delivery triggers a transition from NREMS to REMS comparable to that which occurs spontaneously. However, the efficiency of DP delivery in inducing REMS was reduced during cold exposure to an extent comparable with that observed in spontaneous REMS occurrence. Such impairment was associated with low Delta activity and high sympathetic tone when DPs were delivered. Repetitive DP administration increased REMS amount during the delivery period and a subsequent negative REMS rebound was observed. In conclusion, DP delivery did not overcome the integrative thermoregulatory mechanisms that depress REMS in the cold. These results underline the crucial physiological meaning of the mutual exclusion of thermoregulatory activation and REMS occurrence, and support the hypothesis that the suspension of the central control of body temperature is a prerequisite for REMS occurrence.
PMID: 18482105 [PubMed - indexed for MEDLINE]
b) microinjection of a the cholinergic agonist carbachol (in cats) or the GABA-A antagonist Bicuculline (in rats) whithin the SLD ( pontine sublaterodorsal nucleus)(see Pierre Luppi's work :
http://www.ncbi.nlm.nih.g
Eur J Neurosci. 2002 Nov;16(10):1959-73.
The rat ponto-medullary network responsible for paradoxical sleep onset and maintenance: a combined microinjection and functional neuroanatomical study.Boissard R, Gervasoni D, Schmidt MH, Barbagli B, Fort P, Luppi PH.
Source
CNRS FRE 2469, Institut Fédératif des Neurosciences de Lyon (IFR 19), Université Claude Bernard Lyon I, 8 Avenue Rockefeller, 69373 LYON Cedex 08, France.
Abstract
The neuronal network responsible for paradoxical sleep (PS) onset and maintenance has not previously been identified in the rat, unlike the cat. To fill this gap, this study has developed a new technique involving the recording of sleep-wake states in unanaesthetized head-restrained rats whilst locally administering pharmacological agents by microiontophoresis from glass multibarrel micropipettes, into the dorsal pontine tegmentum and combining this with functional neuroanatomy. Pharmacological agents used for iontophoretic administration included carbachol, kainic acid, bicuculline and gabazine. The injection sites and their efferents were then identified by injections of anterograde (phaseolus vulgaris leucoagglutinin) or retrograde (cholera toxin B subunit) tracers through an adjacent barrel of the micropipette assembly and by C-Fos immunostaining. Bicuculline, gabazine and kainic acid ejections specifically into the pontine sublaterodorsal nucleus (SLD) induced within a few minutes a PS-like state characterized by a continuous muscle atonia, low voltage EEG and a lack of reaction to stimuli. In contrast, carbachol ejections into the SLD induced wakefulness. In PHA-L, glycine and C-Fos multiple double-labelling experiments, anterogradely labelled fibres originating from the SLD were seen apposed on glycine and C-Fos positive neurons (labelled after 90 min of pharmacologically induced PS-like state) from the ventral gigantocellular and parvicellular reticular nuclei. Altogether, these data indicate that the SLD nuclei contain a population of neurons playing a crucial role in PS onset and maintenance. Furthermore, they suggest that GABAergic disinhibition and glutamate excitation of these neurons might also play a crucial role in the onset of PS.
PMID: 12453060 [PubMed - indexed for MEDLINE
c) microinjection of the GABA-A muscimol within the vlPAG (ventrolateral periaqueductal gray). (still Pierre Luppi's work:
http://www.ncbi.nlm.nih.g
PLoS One. 2009;4(1):e4272. Epub 2009 Jan 26.
Localization of the brainstem GABAergic neurons controlling paradoxical (REM) sleep.Sapin E, Lapray D, Bérod A, Goutagny R, Léger L, Ravassard P, Clément O, Hanriot L, Fort P, Luppi PH.
Source
CNRS, UMR5167, Physiopathologie des réseaux neuronaux du cycle veille-sommeil, Lyon, France.
Abstract
Paradoxical sleep (PS) is a state characterized by cortical activation, rapid eye movements and muscle atonia. Fifty years after its discovery, the neuronal network responsible for the genesis of PS has been only partially identified. We recently proposed that GABAergic neurons would have a pivotal role in that network. To localize these GABAergic neurons, we combined immunohistochemical detection of Fos with non-radioactive in situ hybridization of GAD67 mRNA (GABA synthesis enzyme) in control rats, rats deprived of PS for 72 h and rats allowed to recover after such deprivation. Here we show that GABAergic neurons gating PS (PS-off neurons) are principally located in the ventrolateral periaqueductal gray (vlPAG) and the dorsal part of the deep mesencephalic reticular nucleus immediately ventral to it (dDpMe). Furthermore, iontophoretic application of muscimol for 20 min in this area in head-restrained rats induced a strong and significant increase in PS quantities compared to saline. In addition, we found a large number of GABAergic PS-on neurons in the vlPAG/dDPMe region and the medullary reticular nuclei known to generate muscle atonia during PS. Finally, we showed that PS-on neurons triggering PS localized in the SLD are not GABAergic. Altogether, our results indicate that multiple populations of PS-on GABAergic neurons are distributed in the brainstem while only one population of PS-off GABAergic neurons localized in the vlPAG/dDpMe region exist. From these results, we propose a revised model for PS control in which GABAergic PS-on and PS-off neurons localized in the vlPAG/dDPMe region play leading roles.
PMID: 19169414 [PubMed - indexed for MEDLINE] PMCID: PMC2629845
It has recently been found by Jun Le et al. that there is a flip-flop switch for control of REM in the mesopontine tegmentum (part of the brain stem) [1]. This means that there are REM-off and REM-on areas that inhibit each other. Each has GABA neurons which heavily innervating the other. The REM-on on area also has two populations of glutamatergic neurons projecting to the basal forbrain and spinal chord (this projection is responsible for the atonia seen during REM).
So if you stimulated the REM-on area of the mesopontine tegmentum presumably you would be able to cause the instant onset of REM.
As a side-note deficits in this area are thought to be responsible for narcolepsy.
[1]http://www.nature.com/
http://www.plosone.org/ar
So if you stimulated the REM-on area of the mesopontine tegmentum presumably you would be able to cause the instant onset of REM.
As a side-note deficits in this area are thought to be responsible for narcolepsy.
[1]http://www.nature.com/
http://www.plosone.org/ar
I know from http://drgominak.com/lect
