Corrigendum: Gain control of gamma frequency activation by a novel feed forward disinhibitory loop: implications for normal and epileptic neural activity

Birjandian, Zeinab; Narla, Chakravarthi; Poulter, Michael O.

doi:10.3389/fncir.2014.00070

Cited by 4 publications

(10 citation statements)

References 1 publication

(1 reference statement)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As studied in St8sia4 −/− mice, thresholds for pentylenetetrazole-induced seizures were unchanged and the anticonvulsant efficacy of the AMPA antagonist NBQX was even enhanced (Potschka et al, 2008). This effect may depend on the loss of direct modulation of AMPA receptors by polySia (Vaithianathan et al, 2004), but could also be linked to altered network activity such as feed-forward disinhibition, which may play a role in the development of epileptic seizures (Birjandian et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

A crucial role for polysialic acid in developmental interneuron migration and the establishment of interneuron densities in the mouse prefrontal cortex

et al. 2014

View full text Add to dashboard Cite

Polysialic acid ( polySia) is a unique glycan modification of the neural cell adhesion molecule NCAM and a major determinant of brain development. Polysialylation of NCAM is implemented by the two polysialyltransferases ( polySTs) ST8SIA2 and ST8SIA4. Dysregulation of the polySia-NCAM system and variation in ST8SIA2 has been linked to schizophrenia and other psychiatric disorders. Here, we show reduced interneuron densities in the medial prefrontal cortex (mPFC) of mice with either partial or complete loss of polySia synthesizing capacity by ablation of St8sia2, St8sia4, or both. Cells positive for parvalbumin and perineuronal nets as well as somatostatin-positive cells were reduced in the mPFC of all polySTdeficient lines, whereas calretinin-positive cells and the parvalbuminnegative fraction of calbindin-positive cells were unaffected. Reduced interneuron numbers were corroborated by analyzing polyST-deficient GAD67-GFP knock-in mice. The accumulation of precursors in the ganglionic eminences and reduced numbers of tangentially migrating interneurons in the pallium were observed in polyST-deficient embryos. Removal of polySia by endosialidase treatment of organotypic slice cultures led to decreased entry of GAD67-GFP-positive interneurons from the ganglionic eminences into the pallium. Moreover, the acute loss of polySia caused significant reductions in interneuron velocity and leading process length. Thus, attenuation of polySia interferes with the developmental migration of cortical interneurons and causes pathological changes in specific interneuron subtypes. This provides a possible link between genetic variation in polyST genes, neurodevelopmental alterations and interneuron dysfunction in neuropsychiatric disease.

show abstract

Section: Discussionmentioning

confidence: 99%

A crucial role for polysialic acid in developmental interneuron migration and the establishment of interneuron densities in the mouse prefrontal cortex

et al. 2014

View full text Add to dashboard Cite

show abstract

“…The stimulation of each slice was in the range of 160–200 μA, each square pulse was 2.0 ms in length. The electrode was connected to a stimulator (S88X dual output square pulse stimulator, Grass Technologies, Astro-Med, Inc., Brossard, QC, Canada), which controlled the pulse frequency and train duration ( Birjandian et al, 2013 ).…”

Section: Methodsmentioning

confidence: 99%

“…The movies were analyzed using Brain Vision Analyzer (Tokyo, Japan) software. A detailed explanation of the technique is described elsewhere ( Birjandian et al, 2013 ).…”

Section: Methodsmentioning

confidence: 99%

“…The PC is of interest in epilepsy because its circuitry easily supports seizures ( Ekstrand et al, 2001 ). We have recently shown that PC excitability is under the control of feed forward disinhibitory circuit that potentiates excitatory input from the lateral olfactory tract (LOT; Birjandian et al, 2013 ). How CRF and/or 5-HT may modulate this circuit is not known.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Suppression of piriform cortex activity in rat by corticotropin-releasing factor 1 and serotonin 2A/C receptors

Narla

Dunn

Ferguson

et al. 2015

Front. Cell. Neurosci.

Self Cite

View full text Add to dashboard Cite

The piriform cortex (PC) is richly innervated by corticotropin-releasing factor (CRF) and serotonin (5-HT) containing axons arising from central amygdala and Raphe nucleus. CRFR1 and 5-HT2A/2CRs have been shown to interact in manner where CRFR activation subsequently potentiates the activity of 5-HT2A/2CRs. The purpose of this study was to determine how the activation of CRFR1 and/or 5-HT2Rs modulates PC activity at both the circuit and cellular level. Voltage sensitive dye imaging showed that CRF acting through CRFR1 dampened activation of the Layer II of PC and interneurons of endopiriform nucleus. Application of the selective 5-HT2A/CR agonist 2,5-dimethoxy-4-iodoamphetamine (DOI) following CRFR1 activation potentiated this effect. Blocking the interaction between CRFR1 and 5-HT2R with a Tat-CRFR1-CT peptide abolished this potentiation. Application of forskolin did not mimic CRFR1 activity but instead blocked it, while a protein kinase A antagonist had no effect. However, activation and antagonism of protein kinase C (PKC) either mimicked or blocked CRF modulation, respectively. DOI had no effect when applied alone indicating that the prior activation of CRFR1 receptors was critical for DOI to show significant effects similar to CRF. Patch clamp recordings showed that both CRF and DOI reduced the synaptic responsiveness of Layer II pyramidal neurons. CRF had highly variable effects on interneurons within Layer III, both increasing and decreasing their excitability, but DOI had no effect on the excitability of this group of neurons. These data show that CRF and 5-HT, acting through both CRFR1 and 5-HT2A/CRs, reduce the activation of the PC. This modulation may be an important blunting mechanism of stressor behaviors mediated through the olfactory cortex.

show abstract

“…In APC, inhibition balances excitation 39,44,45 , narrows synaptic integration windows 20,44-48 , supports oscillatory activity and sharpens odor tuning 23,49-51 . Despite the prominent role inhibition plays in shaping cortical responses, few studies have addressed circuits that modulate inhibition in APC 49,51 . In neocortex, a number of disinhibitory circuits have been implicated in the gating or tuning of cortical responses to sensory stimuli 52-59 .…”

Section: Discussionmentioning

confidence: 99%

Opposing spatial gradients of inhibition and neural activity in mouse olfactory cortex

Large

Vogler

Canto

et al. 2017

Preprint

View full text Add to dashboard Cite

24The spatial representation of stimuli in primary sensory cortices is a convenient scaffold for elucidating 25 the circuit mechanisms underlying sensory processing. In contrast, the anterior piriform cortex (APC) 26 lacks topology for odor identity and appears homogenous in terms of afferent and intracortical 27 excitatory circuitry. Here, we show that an increasing rostral-caudal (RC) gradient of inhibition onto 28 pyramidal cells is commensurate with a decrease in active neurons along the RC axis following 29 exploration of a novel odor environment. This inhibitory gradient is supported by somatostatin 30 interneurons that provide an opposing, rostrally-biased, gradient of inhibition to interneurons. 31Optogenetic or chemogenetic modulation of somatostatin cells neutralizes the inhibitory gradient onto 32 pyramidal cells. This suggests a novel circuit mechanism whereby opposing spatial gradients of 33 inhibition and disinhibition regulate neural activity along the RC-axis. These findings challenge our 34 current understanding of the spatial profiles of neural circuits and odor processing within APC. 35 36 37 38 . CC-BY 4.0 International license peer-reviewed) is the author/funder. It is made available under a The copyright holder for this preprint (which was not . http://dx.doi.org/10.1101/152975 doi: bioRxiv preprint first posted online Jun. 20, 2017; 3 It is well established that the spatial organization of sensory information plays an important role 39 in neocortical sensory processing. The retinotopic, tonotopic and somatotopic maps established at the 40 periphery form the basis of stimulus representation in primary visual, auditory and somatosensory 41 cortices. This spatial organization is perhaps the oldest and best understood feature of sensory codes. 42In the olfactory system, odor components are encoded by individual olfactory receptor neurons 43 (ORNs) that express a single receptor gene. All ORNs expressing the same receptor project axons to 44 ~2 target glomeruli in the olfactory bulb (OB) 1,2 . Within the OB, individual mitral/tufted (M/T) cells 45extend apical dendrites to a single glomerulus 3 and respond selectively to glomerular activation 4,5 . 46This extreme connection specificity produces a discrete spatial organization of odor information within 47 the OB [6][7][8][9] . However, just one synapse away in the anterior piriform cortex (APC), any semblance of 48 spatial representation for odor identity is lost. 49The piriform cortex is a trilaminar cortex that extends along the rostral-caudal (RC) axis of the 50 ventral rodent brain. The two main subdivisions, anterior (APC) and posterior (PPC) piriform cortex, 51 differ with respect to afferent and efferent projections [10][11][12] as well as functional roles in olfactory 52 processing [13][14][15][16] . However, despite the fact that each region comprises ~1-2 mm of the RC axis, odor 53 processing within APC or PPC is considered spatially homogenous. The APC is delineated by the 54 lateral olfactory tract (LOT) that deliver...

show abstract

Corrigendum: Gain control of gamma frequency activation by a novel feed forward disinhibitory loop: implications for normal and epileptic neural activity

Cited by 4 publications

References 1 publication

A crucial role for polysialic acid in developmental interneuron migration and the establishment of interneuron densities in the mouse prefrontal cortex

A crucial role for polysialic acid in developmental interneuron migration and the establishment of interneuron densities in the mouse prefrontal cortex

Suppression of piriform cortex activity in rat by corticotropin-releasing factor 1 and serotonin 2A/C receptors

Opposing spatial gradients of inhibition and neural activity in mouse olfactory cortex

Contact Info

Product

Resources

About