scholarly journals Decision letter: Three rules govern thalamocortical connectivity of fast-spike inhibitory interneurons in the visual cortex

2020 ◽  
Author(s):  
Barry Connors
eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Yulia Bereshpolova ◽  
Xiaojuan Hei ◽  
Jose-Manuel Alonso ◽  
Harvey A Swadlow

Some cortical neurons receive highly selective thalamocortical (TC) input, but others do not. Here, we examine connectivity of single thalamic neurons (lateral geniculate nucleus, LGN) onto putative fast-spike inhibitory interneurons in layer 4 of rabbit visual cortex. We show that three ‘rules’ regulate this connectivity. These rules concern: (1) the precision of retinotopic alignment, (2) the amplitude of the postsynaptic local field potential elicited near the interneuron by spikes of the LGN neuron, and (3) the interneuron’s response latency to strong, synchronous LGN input. We found that virtually all first-order fast-spike interneurons receive input from nearly all LGN axons that synapse nearby, regardless of their visual response properties. This was not the case for neighboring regular-spiking neurons. We conclude that profuse and highly promiscuous TC inputs to layer-4 fast-spike inhibitory interneurons generate response properties that are well-suited to mediate a fast, sensitive, and broadly tuned feed-forward inhibition of visual cortical excitatory neurons.


2013 ◽  
Vol 33 (28) ◽  
pp. 11372-11389 ◽  
Author(s):  
J. Zhuang ◽  
C. R. Stoelzel ◽  
Y. Bereshpolova ◽  
J. M. Huff ◽  
X. Hei ◽  
...  

2020 ◽  
Vol 30 (8) ◽  
pp. 4662-4676
Author(s):  
Kevin J Monk ◽  
Simon Allard ◽  
Marshall G Hussain Shuler

Abstract The primary sensory cortex has historically been studied as a low-level feature detector, but has more recently been implicated in many higher-level cognitive functions. For instance, after an animal learns that a light predicts water at a fixed delay, neurons in the primary visual cortex (V1) can produce “reward timing activity” (i.e., spike modulation of various forms that relate the interval between the visual stimulus and expected reward). Local manipulations to V1 implicate it as a site of learning reward timing activity (as opposed to simply reporting timing information from another region via feedback input). However, the manner by which V1 then produces these representations is unknown. Here, we combine behavior, in vivo electrophysiology, and optogenetics to investigate the characteristics of and circuit mechanisms underlying V1 reward timing in the head-fixed mouse. We find that reward timing activity is present in mouse V1, that inhibitory interneurons participate in reward timing, and that these representations are consistent with a theorized network architecture. Together, these results deepen our understanding of V1 reward timing and the manner by which it is produced.


2013 ◽  
Vol 110 (4) ◽  
pp. 964-972 ◽  
Author(s):  
Agne Vaiceliunaite ◽  
Sinem Erisken ◽  
Florian Franzen ◽  
Steffen Katzner ◽  
Laura Busse

Responses of many neurons in primary visual cortex (V1) are suppressed by stimuli exceeding the classical receptive field (RF), an important property that might underlie the computation of visual saliency. Traditionally, it has proven difficult to disentangle the underlying neural circuits, including feedforward, horizontal intracortical, and feedback connectivity. Since circuit-level analysis is particularly feasible in the mouse, we asked whether neural signatures of spatial integration in mouse V1 are similar to those of higher-order mammals and investigated the role of parvalbumin-expressing (PV+) inhibitory interneurons. Analogous to what is known from primates and carnivores, we demonstrate that, in awake mice, surround suppression is present in the majority of V1 neurons and is strongest in superficial cortical layers. Anesthesia with isoflurane-urethane, however, profoundly affects spatial integration: it reduces the laminar dependency, decreases overall suppression strength, and alters the temporal dynamics of responses. We show that these effects of brain state can be parsimoniously explained by assuming that anesthesia affects contrast normalization. Hence, the full impact of suppressive influences in mouse V1 cannot be studied under anesthesia with isoflurane-urethane. To assess the neural circuits of spatial integration, we targeted PV+ interneurons using optogenetics. Optogenetic depolarization of PV+ interneurons was associated with increased RF size and decreased suppression in the recorded population, similar to effects of lowering stimulus contrast, suggesting that PV+ interneurons contribute to spatial integration by affecting overall stimulus drive. We conclude that the mouse is a promising model for circuit-level mechanisms of spatial integration, which relies on the combined activity of different types of inhibitory interneurons.


2010 ◽  
Vol 104 (2) ◽  
pp. 840-853 ◽  
Author(s):  
Kwang-Hyun Cho ◽  
Jin Hwa Jang ◽  
Hyun-Jong Jang ◽  
Myung-Jun Kim ◽  
Shin Hee Yoon ◽  
...  

The Ca2+ increase in dendrites that is evoked by the backpropagation of somatic action potentials (APs) is involved in the activity-dependent modulation of dendritic and synaptic functions that are location dependent. In the present study, we investigated dendritic Ca2+ dynamics evoked by backpropagating APs (bAPs) in four subtypes of inhibitory interneurons classified by their spiking patterns: fast spiking (FS), late spiking (LS), burst spiking (BS), and regular-spiking nonpyramidal (RSNP) cells. Cluster analysis, single-cell RT-PCR, and immunohistochemistry confirmed the least-overlapping nature of the grouped cell populations. Somatic APs evoked dendritic Ca2+ transients in all subtypes of inhibitory interneurons with different spatial profiles along the tree: constantly linear in FS and LS cells, increasing to a plateau in BS cells and bell-shaped in RSNP cells. The increases in bAP-evoked dendritic Ca2+ transients brought about by the blocking of A-type K+ channels were similar in whole dendritic trees of each subtype of inhibitory interneurons. However, in RSNP cells, the increases in the distal dendrites were larger than those in the proximal dendrites. On cholinergic activation, nicotinic inhibition of bAP-evoked dendritic Ca2+ transients was observed only in BS cells expressing cholecystokinin and vasoactive intestinal peptide mRNAs, with no muscarinic modulation in all subtypes of inhibitory interneurons. Cell subtype-specific differential spatial profiles and their modulation in bAP-evoked dendritic Ca2+ transients might be important for the domain-specific modulation of segregated inputs in inhibitory interneurons and differential control between the excitatory and inhibitory networks in the visual cortex.


2020 ◽  
Author(s):  
Tyler D. Marks ◽  
Michael J. Goard

ABSTRACTTo produce consistent sensory perception, neurons must maintain stable representations of sensory input. However, neurons in many regions exhibit progressive drift across days. Longitudinal studies have found stable responses to artificial stimuli across sessions in primary sensory areas, but it is unclear whether this stability extends to naturalistic stimuli. We performed chronic 2-photon imaging of mouse V1 populations to directly compare the representational stability of artificial versus naturalistic visual stimuli over weeks. Responses to gratings were highly stable across sessions. However, neural responses to naturalistic movies exhibited progressive representational drift across sessions. Differential drift was present across cortical layers, in inhibitory interneurons, and could not be explained by differential response magnitude or higher order stimulus statistics. However, representational drift was accompanied by similar differential changes in local population correlation structure. These results suggest representational stability in V1 is stimulus-dependent and related to differences in preexisting circuit architecture of co-tuned neurons.


2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Clémence Bernard ◽  
Alain Prochiantz

The ability of the environment to shape cortical function is at its highest during critical periods of postnatal development. In the visual cortex, critical period onset is triggered by the maturation of parvalbumin inhibitory interneurons, which gradually become surrounded by a specialized glycosaminoglycan-rich extracellular matrix: the perineuronal nets. Among the identified factors regulating cortical plasticity in the visual cortex, extracortical homeoprotein Otx2 is transferred specifically into parvalbumin interneurons and this transfer regulates both the onset and the closure of the critical period of plasticity for binocular vision. Here, we review the interaction between the complex sugars of the perineuronal nets and homeoprotein Otx2 and how this interaction regulates cortical plasticity during critical period and in adulthood.


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