Chandelier cells in rat visual cortex

Peters, Alan; Proskauer, Charmian C.; Ribak, Charles E.

doi:10.1002/cne.902060408

Cited by 243 publications

(91 citation statements)

References 33 publications

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“…8). The functional organization of GABAergic molecules is consistent with previous studies demonstrating the localization of GABA and GAT-1 in presynaptic terminals of cortical and hippocampal axo-axonic cells (Peters et al, 1982;Somogyi et al, 1985;DeFelipe and González-Albo, 1998). The localization of GABA A R␣1 and GABA A R␣2 in the AIS of hippocampal pyramidal cells (Nusser et al, 1996) also support the functional organization seen in our study.…”

Section: Discussionsupporting

confidence: 90%

“…The AIS in cortical pyramidal and granule cells is the target for neuronal excitability modulation by specific GABAergic interneurons, called the axo-axonic or chandelier cells (Somogyi, 1977). At axo-axonic synapses, presynaptic elements contain GABA, the GABA synthetic enzyme glutamic acid decarboxylase (GAD), and the plasmalemmal GABA transporter GAT-1 (Peters et al, 1982;Freund et al, 1983;Somogyi et al, 1985;DeFelipe and González-Albo, 1998). Moreover, postsynaptic membranes express GABA A receptors, particularly those containing the ␣2 subunit (Nusser et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

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Lack of Molecular-Anatomical Evidence for GABAergic Influence on Axon Initial Segment of Cerebellar Purkinje Cells by the Pinceau Formation

Iwakura

Uchigashima²,

Miyazaki³

et al. 2012

Journal of Neuroscience

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The axon initial segment (AIS) of cerebellar Purkinje cells (PCs) is embraced by ramified axons of GABAergic basket cells (BCs) called the pinceau formation. This unique structure has been assumed to be a device for the modulation of PC outputs through electrical and/or GABAergic inhibition. Electrical inhibition is supported by enriched potassium channels, absence of sodium channels, and developed septate-like junctions between BC axons. The neurochemical basis for GABAergic inhibition, however, has not been well investigated. Here we addressed this issue using C56BL/6 mice. First, we confirmed previous observations that typical synaptic contacts were rare and confined to proximal axonal portions, with the remaining portions being mostly covered by astrocytic processes. Then we examined the expression of molecules involved in GABAergic signaling, including GABA synthetic enzyme glutamic acid decarboxylase (GAD), vesicular GABA transporter vesicular inhibitory amino acid transporter (VIAAT), cytomatrix active zone protein bassoon, GABA receptor GABA A R␣1, and cell adhesion molecule neuroligin-2. These molecules were recruited to form a functional assembly at perisomatic BC-PC synapses and along the AIS of hippocampal and neocortical pyramidal cells. GAD and VIAAT immunogold labeling was five times lower in the pinceau formation compared with perisomatic BC terminals and showed no accumulation toward the AIS. Moreover, bassoon, neuroligin-2, and GABA A R␣1 formed no detectable clusters along the ankyrin-G-positive AIS proper. These findings indicate that GABAergic signaling machinery is organized loosely and even incompletely in the pinceau formation. Together, BCs do not appear to exert GABAergic synaptic inhibition on the AIS, although the mode of action of the pinceau formation remains to be explored.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Lack of Molecular-Anatomical Evidence for GABAergic Influence on Axon Initial Segment of Cerebellar Purkinje Cells by the Pinceau Formation

Iwakura

Uchigashima²,

Miyazaki³

et al. 2012

Journal of Neuroscience

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“…Anatomically, the synaptic circuitry of cholinergic prefrontal fibers includes symmetric synapses on pyramidal cells (27); symmetric synaptic morphology is characteristic of inhibitory mechanisms (28)(29)(30). It is unclear, however, why a direct inhibition of right prefrontal activity would be correlated with improved WM performance.…”

Section: Discussionmentioning

confidence: 99%

Cholinergic stimulation alters performance and task-specific regional cerebral blood flow during working memory

Furey

Pietrini

Haxby

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

139

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Modulation of the cholinergic neurotransmitter system results in changes in memory performance, including working memory (WM), in animals and in patients with Alzheimer disease. To identify associated changes in the functional brain response, we studied performance measures and regional cerebral blood f low (rCBF) using positron emission tomography (PET) in healthy subjects during performance of a WM task. Eight control subjects received an infusion of saline throughout the study and 13 experimental subjects received a saline infusion for the first 2 scans followed by a continuous infusion of physostigmine, an acetylcholinesterase inhibitor, for the subsequent 8 scans. rCBF was measured using H 2 15 O and PET in a sequence of 10 PET scans that alternated between rest and task scans. During task scans, subjects performed the WM task for faces. Physostigmine both improved WM efficiency, as indicated by faster reaction times, and reduced WM task-related activity in anterior and posterior regions of right midfrontal gyrus, a region shown previously to be associated with WM. Furthermore, the magnitudes of physostigmine-induced change in reaction time and right midfrontal rCBF correlated. These results suggest that enhancement of cholinergic function can improve processing efficiency and thus reduce the effort required to perform a WM task, and that activation of right prefrontal cortex is associated with task effort.Working memory (WM) refers to processes that maintain temporary, active representations of information so that they are available for further processing or recall (1, 2). The cholinergic neurotransmitter system is associated with WM, insofar as cholinergic agonists improve performance (3-5) and antagonists impair performance (6, 7) on WM tasks. Physostigmine, an acetylcholinesterase inhibitor that increases the duration of action of acetylcholine at the synapse, also improves performance on WM tasks in animals and in patients with Alzheimer disease (3-5, 8, 9). Functional brain imaging studies of humans have identified brain regions involved in the performance of object and spatial WM tasks, including occipital, temporal, parietal, and prefrontal cortical areas (10 -13). On object WM tasks, functional imaging studies in humans, as well as lesion and single neuron recording studies in nonhuman primates, indicate that posterior occipitotemporal cortex is associated more with perceptual processing, whereas prefrontal cortex is associated more with maintaining an active representation of the stimulus after it has been removed from view (10, 14 -17). Although it has been shown that cholinergic modulation alters WM performance, the site of modulation in the distributed neural system that mediates WM has yet to be determined. Therefore, we decided to investigate changes in regional cerebral blood f low (rCBF) and behavioral performance (reaction time) associated with cholinergic stimulation during a WM task. MATERIALS AND METHODSTwenty-one right-handed healthy volunteers participated in the study. Each p...

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“…The axon initial segment of layer 5 pyramidal neurons receives GABAergic inputs from chandelier cells (Peters et al, 1982;Freund et al, 1983). To test whether activation of these inhibitory inputs alters the site of AP initiation, we locally applied GABA (100 M) to the axon initial segment.…”

Section: Impact Of Axonal Inhibitionmentioning

confidence: 99%

Site of Action Potential Initiation in Layer 5 Pyramidal Neurons

2006

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Fundamental to an understanding of how neurons integrate synaptic input is the knowledge of where within a neuron this information is converted into an output signal, the action potential. Although it has been known for some time that action potential initiation occurs within the axon of neurons, the precise location has remained elusive. Here, we provide direct evidence using voltage-sensitive dyes that the site of action potential initiation in cortical layer 5 pyramidal neurons is ϳ35 m from the axon hillock. This was the case during action potential generation under a variety of conditions, after axonal inhibition, and at different stages of development. Once initiated action potentials propagated down the axon in a saltatory manner. Experiments using local application of low-sodium solution and TTX, as well as an investigation of the influence of axonal length on action potential properties, provided evidence that the initial 40 m of the axon is essential for action potential generation. To morphologically identify the relationship between the site of action potential initiation and axonal myelination, we labeled oligodendrocytes supplying processes to the proximal region of the axon. These experiments indicated that the axon initial segment was ϳ40 m in length, and the first node of Ranvier was ϳ90 m from the axon hillock. Experiments targeting the first node of Ranvier suggested it was not involved in action potential initiation. In conclusion, these results indicate that, in layer 5 pyramidal neurons, action potentials are generated in the distal region of the axon initial segment.

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Chandelier cells in rat visual cortex

Cited by 243 publications

References 33 publications

Lack of Molecular-Anatomical Evidence for GABAergic Influence on Axon Initial Segment of Cerebellar Purkinje Cells by the Pinceau Formation

Lack of Molecular-Anatomical Evidence for GABAergic Influence on Axon Initial Segment of Cerebellar Purkinje Cells by the Pinceau Formation

Cholinergic stimulation alters performance and task-specific regional cerebral blood flow during working memory

Site of Action Potential Initiation in Layer 5 Pyramidal Neurons

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