Layer-Specific Noradrenergic Modulation of Inhibition in Cortical Layer II/III

Salgado, Humberto; García-Oscos, Francisco; Patel, Ankur B.; Martinolich, Laura; Nichols, Justin A.; Dinh, Lu; Roychowdhury, Swagata; Tseng, Kuei‐Yuan; Atzori, Marco

doi:10.1093/cercor/bhq081

Cited by 55 publications

(79 citation statements)

References 69 publications

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“…Previous electrophysiological studies have emphasized the role of NA in the modulation of cortical glutamatergic neurotransmission (Nowicky et al, 1992, Dinh et al, 2009, the latter being the main determinant for the coupling between increased cortical activity and hemodynamic alterations (Attwell and Iadecola, 2002). This is consistent with the numerous c-Fos-positive pyramidal-shaped cells found in our study (not quantified) and, to a lesser extent, COX-2-immunopositive pyramids (ϳ20%).…”

Section: Mediators Of the Hemodynamic Responses To Lc Stimulation Glusupporting

confidence: 92%

“…In contrast, no significant CBF changes were observed with the selective COX-1 inhibitor SC-560 [5-(4-chlorophenyl)-1-(4-methoxyphenyl)-3-trifluoromethyl pyrazole] (2.7 Ϯ 2.2%) (Fig. 5C), as found after sensory or basal forebrain stimulation (Niwa et al, 2000;Lecrux et al, 2011Lecrux et al, , 2012.…”

Section: Mediators Of the Hemodynamic Responses To Lc Stimulation Glumentioning

confidence: 93%

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Locus Coeruleus Stimulation Recruits a Broad Cortical Neuronal Network and Increases Cortical Perfusion

et al. 2013

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Section: Mediators Of the Hemodynamic Responses To Lc Stimulation Glusupporting

confidence: 92%

Section: Mediators Of the Hemodynamic Responses To Lc Stimulation Glumentioning

confidence: 93%

Locus Coeruleus Stimulation Recruits a Broad Cortical Neuronal Network and Increases Cortical Perfusion

et al. 2013

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“…In addition to the excitatory inputs, inhibitory inputs to excitatory neurons came largely from the same cortical layer (Katzel et al 2011). Thus the layer-specific modulation of inhibitory transmission by 5-HT in the present study and by norepinephrine (Salgado et al 2011) might be an important factor in pathway-specific information processing. …”

Section: Variable Effects Of 5-ht In the Cortexsupporting

confidence: 47%

“…Layer-specific cholinergic (Cho et al 2008;Gil et al 1997) and adrenergic (Salgado et al 2011) modulation has been reported in layer 2/3 pyramidal neurons, which might be important in the inputspecific modulation of cortical circuits. Thus we investigated the subcellular domain dependence of 5-HT facilitation on IPSC.…”

Section: -Ht 2 Receptor-dependent Facilitation Of Ipscmentioning

confidence: 99%

Layer-specific serotonergic facilitation of IPSC in layer 2/3 pyramidal neurons of the visual cortex

Jang¹,

Cho

Park³

et al. 2012

Journal of Neurophysiology

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Jang HJ, Cho KH, Park SW, Kim MJ, Yoon SH, Rhie DJ. Layer-specific serotonergic facilitation of IPSC in layer 2/3 pyramidal neurons of the visual cortex. J Neurophysiol 107: 407-416, 2012. First published October 19, 2011 doi:10.1152/jn.00535.2011 inhibits the induction of longterm synaptic plasticity in layer 2/3 of the visual cortex at the end of its critical period in rats. However, the cellular and molecular mechanisms remain unclear. Since inhibitory influence is crucial in the induction of synaptic plasticity, the effect of 5-HT on inhibitory transmission was investigated in layer 2/3 pyramidal neurons of the primary visual cortex. The amplitude of inhibitory postsynaptic current (IPSC), but not excitatory postsynaptic current, evoked by stimulation of the underlying layer 4, was increased by ϳ20% with a bath application of 5-HT. The amplitude of miniature IPSC was also increased by the application of 5-HT, while the paired-pulse ratio was not changed. The facilitating effect of 5-HT on IPSC was mediated by the activation of 5-HT 2 receptors. An increase in intracellular Ca 2ϩ via release from inositol 1,4,5-trisphosphate (IP 3 )-sensitive stores, which was confirmed by confocal Ca 2ϩ imaging, and activation of Ca 2ϩ /calmodulin-dependent kinase II (CaMKII) were involved in the facilitation of IPSC by 5-HT. However, 5-HT failed to facilitate IPSC evoked by the stimulation of layer 1. These results suggest that activation of 5-HT 2 receptors releases intracellular Ca 2ϩ via IP 3 -sensitive stores, which facilitates GABA A ergic transmission via the activation of CaMKII in layer 2/3 pyramidal neurons of the visual cortex in a layer-specific manner. Thus facilitation of inhibitory transmission by 5-HT might be involved in regulating the information flow and the induction of long-term synaptic plasticity, in a pathwayspecific manner.␥-aminobutyric acid; inhibitory transmission; 5-HT; CaMKII; IP 3 SEROTONIN (5-hydroxytryptamine, 5-HT), one of the major neuromodulators in the brain, has been implicated in many brain functions, such as memory, mood disorders, sleep, neuroendocrine control, sex behavior, feeding behavior, and epilepsy. The molecular mechanisms of 5-HT functions are diverse because of its multiple receptor subtypes (Barnes and Sharp 1999), and thus the cellular functions might differ depending on the cellular expression of receptor subtypes in different brain areas. In the visual cortex, the expression of 5-HT receptor subtypes also changes during postnatal development in cats (Kojic et al.

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“…NA excites GABAergic interneurons (McCormick 1992a;Kawaguchi and Shindou 1998) and indirectly inhibits principal neuron activity in different CNS areas (Segal et al 1991). On the other hand, NA can increase GABA A IPSCs of interneurons such as, cerebellar stellate cells (Kondo and Marty 1997), frontal cortex (Kawaguchi and Shindou 1998), cerebellum and have opposite effects in GABAergic neurons of different layers of sensory cortices depending on the type of NAR activated (Salgado et al 2011).…”

Section: Nars-egaba a Rs Interactionmentioning

confidence: 99%

GPCR Modulation of Extrasynapitic GABAA Receptors

Connelly

Errington

Yagüe

et al. 2014

Extrasynaptic GABAA Receptors

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γ-Aminobutyric acid type A (GABA A ) receptors (GABA A Rs), the main inhibitory neurotransmitter-gated ion channels in the central nervous system, are finely tuned by other neurotransmitters and endogenous ligands. The regulation of synaptic GABA A Rs (sGABA A Rs) by G protein-coupled receptors (GPCRs) has been well characterized and is known to occur either through the conventional activation of second-messenger signalling cascades by G proteins or directly by protein-protein coupling. In contrast, research on the modulation of extrasynaptic GABA A R (eGABA A Rs) is still in its infancy and it remains to be determined whether both of the above mechanisms are capable of controlling eGABA A R function. In this chapter, we summarize the available literature on eGABA A R modulation by GPCRs, including GABA B , serotonin (5-HT), dopamine (DA), noradrenaline (NA) and metabotropic glutamate (mGlu) receptors. Although at present these GPCRs-eGABA A Rs cross-talks have been investigated in a limited number of brain areas (i.e., thalamus, cerebellum, hippocampus, striatum), it is already evident that eGABA A Rs show a nucleus-and neuronal type-selective regulation by GPCRs that differs from that of sGABA A Rs. This distinct regulation of eGABA A Rs versus sGABA A Rs by GPCRs provides mechanisms for receptor adaptation in response

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Layer-Specific Noradrenergic Modulation of Inhibition in Cortical Layer II/III

Cited by 55 publications

References 69 publications

Locus Coeruleus Stimulation Recruits a Broad Cortical Neuronal Network and Increases Cortical Perfusion

Locus Coeruleus Stimulation Recruits a Broad Cortical Neuronal Network and Increases Cortical Perfusion

Layer-specific serotonergic facilitation of IPSC in layer 2/3 pyramidal neurons of the visual cortex

GPCR Modulation of Extrasynapitic GABAA Receptors

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