GABAergic and non-GABAergic thalamic, hypothalamic and basal forebrain projections to the ventral oral pontine reticular nucleus: Their implication in REM sleep modulation

Rodrigo-Angulo, Margarita L.; Heredero, Susana; Rodríguez‐Veiga, Elisia; Reinoso‐Suárez, Fernando

doi:10.1016/j.brainres.2008.02.095

Cited by 36 publications

(27 citation statements)

References 58 publications

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“…GABA-containing neurons, terminals (de la Roza and Reinoso-Suarez, 2006; Rodrigo-Angulo et al, 2008; Liang and Marks, 2009), and GABA A receptors (Pirker et al, 2000; Heldt and Ressler, 2007) are present within the pontine reticular formation. When administered directly into the pontine reticular formation, GABA A receptor agonists or drugs that increase extracellular GABA levels cause an increase in wakefulness and a decrease in sleep (Camacho-Arroyo et al, 1991; Xi et al, 1999, 2001; Watson et al, 2008; Flint et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Endogenous GABA Levels in the Pontine Reticular Formation Are Greater during Wakefulness than during Rapid Eye Movement Sleep

Vanini¹,

Wathen²,

Lydic³

et al. 2011

J. Neurosci.

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Section: Discussionmentioning

confidence: 99%

Endogenous GABA Levels in the Pontine Reticular Formation Are Greater during Wakefulness than during Rapid Eye Movement Sleep

Vanini¹,

Wathen²,

Lydic³

et al. 2011

J. Neurosci.

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“…Synaptic terminals from local and distant gamma-aminobutyric acid (GABA) containing neurons4,5 as well as GABA type A (GABA A ) receptors6-8 are present in the pontine reticular formation and modulate behavioral arousal. For example, microinjecting the GABA A receptor agonist muscimol into the pontine reticular formation increases wakefulness 9,10.…”

Section: Introductionmentioning

confidence: 99%

γ-Aminobutyric Acid–mediated Neurotransmission in the Pontine Reticular Formation Modulates Hypnosis, Immobility, and Breathing during Isoflurane Anesthesia

et al. 2008

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Background Many general anesthetics are thought to produce a loss of wakefulness, in part, by enhancing gamma-aminobutyric acid (GABA) neurotransmission. However, GABAergic neurotransmission in the pontine reticular formation promotes wakefulness. This study tested the hypotheses that: 1) relative to wakefulness, isoflurane decreases GABA levels in the pontine reticular formation; and 2) pontine reticular formation administration of drugs that increase or decrease GABA levels increases or decreases, respectively, isoflurane induction time. Methods To test hypothesis 1, cats (n = 5) received a craniotomy and permanent electrodes for recording the electroencephalogram and electromyogram. Dialysis samples were collected from the pontine reticular formation during isoflurane anesthesia and wakefulness. GABA levels were quantified using high performance liquid chromatography. For hypothesis 2, rats (n = 10) were implanted with a guide cannula aimed for the pontine reticular formation. Each rat received microinjections of Ringer’s (vehicle control), the GABA uptake inhibitor nipecotic acid, and the GABA synthesis inhibitor 3-mercaptopropionic acid. Rats were then anesthetized with isoflurane and induction time was quantified as loss of righting reflex. Breathing rate was also measured. Results Relative to wakefulness, GABA levels were significantly decreased by isoflurane. Increased power in the electroencephalogram and decreased activity in the electromyogram caused by isoflurane co-varied with pontine reticular formation GABA levels. Nipecotic acid and 3-mercaptopropionic acid significantly increased and decreased, respectively, isoflurane induction time. Nipecotic acid also increased breathing rate. Conclusion Decreasing pontine reticular formation GABA levels comprises one mechanism by which isoflurane causes loss of consciousness, altered cortical excitability, muscular hypotonia, and decreased respiratory rate.

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“…In fact, Rodrigo-Angulo et al, (2008) demonstrated GABAergic projection from the postero-lateral hypothalamus towards the NPO of the cat. Sapin et al, (2010) found that a large number of GABAergic neurons in the tuberal region of the rat hypothalamus express c-fos during the rebound of REM sleep that follows a long-term (3 days) REM sleep deprivation protocol.…”

Section: Discussionmentioning

confidence: 96%

Hypocretinergic and non-hypocretinergic projections from the hypothalamus to the REM sleep executive area of the pons

Torterolo

Sampogna²,

Chase

2013

Brain Research

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Within the postero-lateral hypothalamus neurons that utilize hypocretin or melanin-concentrating hormone (MCH) as neuromodulators are co-distributed. These neurons have been involved in the control of behavioral states, and a deficit in the hypocretinergic system is the pathogenic basis of narcolespy with cataplexy. In this report, utilizing immunohistochemistry and retrograde tracing techniques, we examined the hypocretinergic innervation of the nucleus pontis oralis (NPO), which is the executive site that is responsible for the generation of REM sleep in the cat. The retrograde tracer cholera toxin subunit B (CTb) was administered in pontine regions where carbachol microinjections induced REM sleep. Utilizing immunohistochemical techniques, we found that approximately 1% of hypocretinergic neurons in the tuberal area of the hypothalamus project to the NPO. In addition, approximately 6% of all CTb+ neurons in this region were hypocretinergic. The hypocretinergic innervation of the NPO was also compared with the innervation of the same site by MCH-containing neurons. More than three times as many MCHergic neurons were found to project to the NPO compared with hypocretinergic cells; both neuronal types exhibited bilateral projections. We also identified a group of non-hypocretinergic non-MCHergic neuronal group of neurons that were intermingled with both hypocretinergic and MCHergic neurons that also projected to this same brainstem region. These neurons were grater in number that either hypocretin or MCH containing neurons; their soma size was also smaller and their projections were mainly ipsilateral. The present anatomical data suggest that hypocretinergic, MCHergic and an unidentified companion group of neurons of the postero-lateral hypothalamus participate in the regulation of the neuronal activity of NPO neurons, and therefore, are likely to participate in the control of wakefulness and REM sleep.

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GABAergic and non-GABAergic thalamic, hypothalamic and basal forebrain projections to the ventral oral pontine reticular nucleus: Their implication in REM sleep modulation

Cited by 36 publications

References 58 publications

Endogenous GABA Levels in the Pontine Reticular Formation Are Greater during Wakefulness than during Rapid Eye Movement Sleep

Endogenous GABA Levels in the Pontine Reticular Formation Are Greater during Wakefulness than during Rapid Eye Movement Sleep

γ-Aminobutyric Acid–mediated Neurotransmission in the Pontine Reticular Formation Modulates Hypnosis, Immobility, and Breathing during Isoflurane Anesthesia

Hypocretinergic and non-hypocretinergic projections from the hypothalamus to the REM sleep executive area of the pons

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