VGLUT2 functions as a differential marker for hippocampal output neurons

Wozny, Christian; Beed, Prateep; Nitzan, Noam; Poessnecker, Yona; Rost, Benjamin R.; Schmitz, Dietmar

doi:10.1101/348227

Cited by 10 publications

(17 citation statements)

References 19 publications

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“…10g), but not in baseline firing probability. Thus, light-responsive cells had a stronger tendency to be bursty, consistent with previous in vitro results showing that VGlut2 is a specific marker for bursting cells in the subiculum 59 .…”

Section: Spw-r To Grsc Communication Depends On Brain Statesupporting

confidence: 91%

“…The hippocampus-gRSC functional route likely involves the subiculum, since bursting cells at the distal subiculum 56 give rise to projection to the gRSC 30,57,58 . To examine the involvement of this route, we used the VGlut2-Cre mouse line, which expresses Cre in subicular bursting cells 59 , and shows a proximo-distal expression gradient in the dorsal subiculum 60 . We first employed a ChR2-assisted circuit mapping strategy, by injecting AAV9-SwitchON-mRu-byNLS-ChR2(H134R)-EYFP in the dorsal subiculum of VGlut2-Cre mice.…”

Section: Spw-r To Grsc Communication Depends On Brain Statementioning

confidence: 99%

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Propagation of hippocampal ripples to the neocortex by way of a subiculum-retrosplenial pathway

Nitzan¹,

McKenzie²,

Beed³

et al. 2020

Nat Commun

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Bouts of high frequency activity known as sharp wave ripples (SPW-Rs) facilitate communication between the hippocampus and neocortex. However, the paths and mechanisms by which SPW-Rs broadcast their content are not well understood. Due to its anatomical positioning, the granular retrosplenial cortex (gRSC) may be a bridge for this hippocampocortical dialogue. Using silicon probe recordings in awake, head-fixed mice, we show the existence of SPW-R analogues in gRSC and demonstrate their coupling to hippocampal SPW-Rs. gRSC neurons reliably distinguished different subclasses of hippocampal SPW-Rs according to ensemble activity patterns in CA1. We demonstrate that this coupling is brain state-dependent, and delineate a topographically-organized anatomical pathway via VGlut2expressing, bursty neurons in the subiculum. Optogenetic stimulation or inhibition of bursty subicular cells induced or reduced responses in superficial gRSC, respectively. These results identify a specific path and underlying mechanisms by which the hippocampus can convey neuronal content to the neocortex during SPW-Rs.

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Section: Spw-r To Grsc Communication Depends On Brain Statesupporting

confidence: 91%

Section: Spw-r To Grsc Communication Depends On Brain Statementioning

confidence: 99%

Propagation of hippocampal ripples to the neocortex by way of a subiculum-retrosplenial pathway

Nitzan¹,

McKenzie²,

Beed³

et al. 2020

Nat Commun

Self Cite

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show abstract

“…10g), but not in baseline firing probability (p = 0.093). Thus, lightresponsive cells had a stronger tendency to be bursty, consistent with previous in vitro results showing that VGlut2 is a specific marker for bursting cells in the subiculum 62 .…”

Section: Identification Of Subicular Bursting Cells In Vivosupporting

confidence: 91%

Propagation of Hippocampal Ripples to the Neocortex by Way of a Subiculum-Retrosplenial Pathway

Nitzan

McKenzie

Beed

et al. 2020

Preprint

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SUMMARYBouts of high frequency activity known as sharp wave ripples (SPW-Rs) facilitate communication between the hippocampus and neocortex. However, the paths and mechanisms by which SPW-Rs broadcast their content are not well understood. Due to its anatomical positioning, the granular retrosplenial cortex (gRSC) may be a bridge for this hippocampo-cortical dialogue. Using silicon probe recordings in awake, head-fixed mice, we show the existence of SPW-R analogues in gRSC and demonstrate their coupling to hippocampal SPW-Rs. gRSC neurons reliably distinguished different subclasses of hippocampal SPW-Rs according to ensemble activity patterns in CA1. We demonstrate that this coupling is brain state-dependent, and delineate a topographically-organized anatomical pathway via VGlut2-expressing, bursty neurons in the subiculum. Optogenetic stimulation or inhibition of bursty subicular cells induced or reduced responses in superficial gRSC, respectively. These results identify a specific path and underlying mechanisms by which the hippocampus can convey neuronal content to the neocortex during SPW-Rs.

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“…The injection capillary was then advanced, and a Cre-dependent viral vector was injected into the LHb, the medial dorsal thalamic nucleus (MDT) or the ventral pallidum (VP) at a rate of 25 nL / min using a pressure microinjector (Narishige, Tokyo, Japan). Two different vector solutions were used in this study: one containing a pAAV-EF1α-Switch:NLSmRuby2/ChR2(H134R)-EYFP-HGHpA (Wozny et al, 2018) (titre: 2 x 10 13 infectious particles / mL), an adeno-associated virus containing capsid protein 9 which drives expression of ChR2 and eYFP in Cre-expressing cells, or the red fluorescent protein variant mRuby2 in the absence of Cre; or AAV Ef1α-DIO-hChR2-eYFP (titre: 1.6 x 10 8 infectious particles / mL), a mixture of adeno-associated virus particles of serotypes 1 and 2 containing a 1:1 ratio of capsid proteins type 1 and 2. Parameters for LHb-targeted injections were: coordinates (from Bregma, in mm) AP −1.5, ML −0.4, depth 3; volume 50-100 nL; N = 8 PV-IRES-Cre mice, N = 4 SOM-IRES-Cre mice.…”

Section: Methodsmentioning

confidence: 99%

Disentangling neuronal inhibition and inhibitory pathways in the lateral habenula

Webster

Vroman

Balueva

et al. 2019

Preprint

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22 Phone: +44 (0)141 548 2122 23 24 2 25 Summary: The lateral habenula receives inhibitory input from three distinct sources: 26 from local PV-positive neurons, from PV-positive neurons in the medial dorsal thalamic 27 nucleus (MDT); and from SOM-positive neurons in the ventral pallidum (VP). 28 3 Abstract 29 The lateral habenula (LHb) is hyperactive in depression, and thus potentiating 30 inhibition of this structure makes an interesting target for future antidepressant 31 therapies. However, the circuit mechanisms mediating inhibitory signalling within the 32 LHb are not well-known. We addressed this issue by studying LHb neurons expressing 33 either parvalbumin (PV), neuron-derived neurotrophic factor (Ndnf) or somatostatin 34 (SOM), three markers of particular sub-classes of neocortical inhibitory neurons. While 35 we report that Ndnf is not representative of any particular sub-population of LHb 36 neuron, we find that both PV and SOM are expressed by physiologically distinct sub-37 classes. Furthermore, we describe multiple sources of inhibitory input to the LHb 38 arising from both local PV-positive neurons, and from PV-positive neurons in the 39 medial dorsal thalamic nucleus, and from SOM-positive neurons in the ventral 40 pallidum. These findings hence provide new insight into inhibitory control within the 41 LHb, and highlight that this structure is more neuronally diverse than previously 42 thought. 43 44Significance statement 45 The circuitry by which inhibitory signalling is processed within the lateral habenula is 46 currently not well understood; yet this is an important topic as inhibition of the lateral 47 53We are grateful to Hongkui Zeng from the Allen Brain Institute, Seattle, for kindly 54 sharing the Ai9 reporter mice with us, and we thank Csaba Földy, Brain Research 55

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VGLUT2 functions as a differential marker for hippocampal output neurons

Cited by 10 publications

References 19 publications

Propagation of hippocampal ripples to the neocortex by way of a subiculum-retrosplenial pathway

Propagation of hippocampal ripples to the neocortex by way of a subiculum-retrosplenial pathway

Propagation of Hippocampal Ripples to the Neocortex by Way of a Subiculum-Retrosplenial Pathway

Disentangling neuronal inhibition and inhibitory pathways in the lateral habenula

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