Monoamine modulation of tonic GABAA inhibition

Crunelli, Vincenzo; Giovanni, Giuseppe Di

doi:10.1515/revneuro-2013-0059

Cited by 13 publications

(9 citation statements)

References 120 publications

(148 reference statements)

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“…NE increases both the frequency and the amplitude of sIPSC in TRN neurons. Such results are similar to former research (32) indicating that the augment of sIPSC results from actions of NE on both presynaptic transmitter release and postsynaptic receptors. Underlying mechanisms may involve depolarization of neurons by an NE-induced decrease in a K + conductance (33) or a stimulation of b-adrenergic receptors and modulate GABA A -receptor function (34,35).…”

Section: Discussionsupporting

confidence: 93%

Activation of noradrenergic terminals in the reticular thalamus delays arousal from propofol anesthesia in mice

Zhang

Liu

et al. 2019

FASEB j.

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Electroencephalogram monitoring during propofol (PRO) anesthesia typically features low‐frequency oscillations, which may be involved with thalamic reticular nucleus (TRN) modulation. TRN receives noradrenergic inputs from the locus coeruleus (LC). We hypothesized that specific noradrenergic connections in the TRN may contribute to the emergence from PRO anesthesia. Intranuclei norepinephrine (NE) injections (n = 10) and designer receptors exclusively activated by designer drugs (DREADDs) (n = 10) were used to investigate the role of noradrenergic inputs from the LC to the TRN during PRO anesthesia. Whole‐cell recording in acute brain slice preparations was used to identify the type of adrenoceptor that regulates noradrenergic innervation in the TRN. An intracerebral injection of NE into the TRN delays arousal in mice recovering from PRO anesthesia (means ± sd; 486.6 ± 57.32 s for the NE injection group vs. 422.4 ± 48.19 s for the control group; P = 0.0143) and increases the cortical‐δ (0.1–4 Hz, 25.4 ± 2.9 for the NE injection group vs. 21.0 ± 1.7 for the control group; P = 0.0094) oscillation. An intra‐TRN injection of NE also decreased the EC50 of PRO‐induced unconsciousness (57.05 ± 1.78 mg/kg for the NE injection group vs. 72.44 ± 3.23 mg/kg for the control group; P = 0.0096). Moreover, the activation of LC‐noradrenergic nerve terminals in the TRN using DREADDs increased the recovery time [466.1 ± 44.57 s for the clozapine N‐oxide (CNO) injection group vs. 426.1 ± 38.75 s for the control group; P = 0.0033], decreased the EC50 of PRO‐induced unconsciousness (64.77 ± 3.40 mg/kg for the CNO injection group vs. 74.00 ± 2.08 mg/kg for the control group; P = 0.0081), and increased the cortical‐δ oscillation during PRO anesthesia (23.29 ± 2.58 for the CNO injection group vs. 19.56 ± 1.9 for the control group; P = 0.0213). In addition, whole‐cell recording revealed that NE augmented the inhibitory postsynaptic currents in the TRN neurons via the α1‐adrenoceptor. Our data indicated that enhanced NE signaling at the noradrenergic terminals of the LC‐TRN projection delays arousal from general anesthesia, which is likely mediated by the α1‐adrenoceptor activation. Our findings open a door for further understanding of the functions of various LC targets in both anesthesia and arousal.—Zhang, Y., Fu, B., Liu, C., Yu, S., Luo, T., Zhang, L., Zhou, W., Yu, T. Activation of noradrenergic terminals in the reticular thalamus delays arousal from propofol anesthesia in mice. FASEB J. 33, 7252–7260 (2019). http://www.fasebj.org

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Section: Discussionsupporting

confidence: 93%

Activation of noradrenergic terminals in the reticular thalamus delays arousal from propofol anesthesia in mice

Zhang

Liu

et al. 2019

FASEB j.

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“…This is due to its distinctive regulatory properties, such as constitutive activity and RNA‐editing in vivo and especially the scarcity of subtype‐selective drugs . Nevertheless, 5‐HT 2C R has been shown by experimental and clinical observation to represent a possible therapeutic target for the development of drugs for a range of CNS disorders such as schizophrenia, depression, drug abuse, eating disorders, and Parkinson's disease to name but a few . As activation of 5‐HT 2C Rs suppresses neural network hyperexcitability in different brain areas , it might play a similar role in the hippocampus.…”

Section: Introductionmentioning

confidence: 99%

“…Nevertheless, 5‐HT 2C R has been shown by experimental and clinical observation to represent a possible therapeutic target for the development of drugs for a range of CNS disorders such as schizophrenia, depression, drug abuse, eating disorders, and Parkinson's disease to name but a few . As activation of 5‐HT 2C Rs suppresses neural network hyperexcitability in different brain areas , it might play a similar role in the hippocampus. This hypothesis is corroborated by the high 5‐HT 2C R mRNA and protein hippocampal expression with immunoreactivity for the 5‐HT 2C R, wildly located in the polymorphic cell layer of the dentate gyrus (DG), in the pyramidal cell layer of hippocampus proper (CA1, CA2, and CA3 fields), in the mossy fibers of CA3 and in the subiculum .…”

Section: Introductionmentioning

confidence: 99%

Role(s) of the 5‐HT2C Receptor in the Development of Maximal Dentate Activation in the Hippocampus of Anesthetized Rats

et al. 2014

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“…Since we have recently shown that an aberrant eGABA function in VB neurons is a necessary factor in the expression of SWDs associated with typical absence epilepsy ( Cope et al, 2009 ; Di Giovanni et al, 2011 ; Errington et al, 2011 , 2014 ), it is conceivable that some of the systemically injected 5-HT ligand effects on ASs ( Danober et al, 1998 ; Isaac, 2005 ; Bagdy et al, 2007 ; Bercovici et al, 2007 ; Ohno et al, 2010 ) occur via a modulation of tonic GABA A inhibition. This hypothesis is based also on the evidence that DA and especially the activation of D 2 -Rs decreases both ASs ( Deransart et al, 2000 ) and eGABA current in GAERS VB neurons ( Yague et al, 2013 ; Crunelli and Di Giovanni, 2014 ). Indeed, our preliminary results show that 5-HT 2A -R ligands lack any effect on phasic synaptic GABA A inhibition in VB thalamocortical neurons of Wistar rats ( Cavaccini et al, 2012 ), while 5-HT 2A -R selective agonists significantly enhanced the tonic eGABA A conductance.…”

Section: The 5-ht 2a -Rs In the Regulation Of Epilmentioning

confidence: 99%

Central serotonin-2A (5-HT2A) receptor dysfunction in depression and epilepsy: the missing link?

2015

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5-Hydroxytryptamine 2A receptors (5-HT2A-Rs) are G-protein coupled receptors. In agreement with their location in the brain, they have been implicated not only in various central physiological functions including memory, sleep, nociception, eating and reward behaviors, but also in many neuropsychiatric disorders. Interestingly, a bidirectional link between depression and epilepsy is suspected since patients with depression and especially suicide attempters have an increased seizure risk, while a significant percentage of epileptic patients suffer from depression. Such epidemiological data led us to hypothesize that both pathologies may share common anatomical and neurobiological alteration of the 5-HT2A signaling. After a brief presentation of the pharmacological properties of the 5-HT2A-Rs, this review illustrates how these receptors may directly or indirectly control neuronal excitability in most networks involved in depression and epilepsy through interactions with the monoaminergic, GABAergic and glutamatergic neurotransmissions. It also synthetizes the preclinical and clinical evidence demonstrating the role of these receptors in antidepressant and antiepileptic responses.

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Monoamine modulation of tonic GABAA inhibition

Cited by 13 publications

References 120 publications

Activation of noradrenergic terminals in the reticular thalamus delays arousal from propofol anesthesia in mice

Activation of noradrenergic terminals in the reticular thalamus delays arousal from propofol anesthesia in mice

Role(s) of the 5‐HT2C Receptor in the Development of Maximal Dentate Activation in the Hippocampus of Anesthetized Rats

Central serotonin-2A (5-HT2A) receptor dysfunction in depression and epilepsy: the missing link?

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