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High and asymmetric somato-dendritic coupling of V1 layer 5 neurons independent of visual stimulation and locomotion.

ABSTRACT: Active dendrites impact sensory processing and behaviour. However, it remains unclear how active dendritic integration relates to somatic output in vivo. We imaged semi-simultaneously GCaMP6s signals in the soma, trunk and distal tuft dendrites of layer 5 pyramidal neurons in the awake mouse primary visual cortex. We found that apical tuft signals were dominated by widespread, highly correlated calcium transients throughout the tuft. While these signals were highly coupled to trunk and somatic transients, the frequency of calcium transients was found to decrease in a distance-dependent manner from soma to tuft. Ex vivo recordings suggest that low-frequency back-propagating action potentials underlie the distance-dependent loss of signals, while coupled somato-dendritic signals can be triggered by high-frequency somatic bursts or strong apical tuft depolarization. Visual stimulation and locomotion increased neuronal activity without affecting somato-dendritic coupling. High, asymmetric somato-dendritic coupling is therefore a widespread feature of layer 5 neurons activity in vivo.

SUBMITTER: Francioni V

PROVIDER: S-EPMC6974354 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature

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High and asymmetric somato-dendritic coupling of V1 layer 5 neurons independent of visual stimulation and locomotion.

Francioni Valerio V Padamsey Zahid Z Rochefort Nathalie L NL

eLife 20191227

Active dendrites impact sensory processing and behaviour. However, it remains unclear how active dendritic integration relates to somatic output in vivo. We imaged semi-simultaneously GCaMP6s signals in the soma, trunk and distal tuft dendrites of layer 5 pyramidal neurons in the awake mouse primary visual cortex. We found that apical tuft signals were dominated by widespread, highly correlated calcium transients throughout the tuft. While these signals were highly coupled to trunk and somatic t ...[more]

PMID: 31880536

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Project description:Several lines of evidence implicate serotonin (5-hydroxytryptamine, 5-HT)in regulating personality traits and mood control. Serotonergic neurons are classically thought to be tonic regular-firing, "clock-like" neurons. Neurotransmission by serotonin is tightly regulated by the serotonin transporter (SERT) and by autoreceptors (serotonin receptors expressed by serotonin neurons) through negative feedback inhibition at the cell bodies and dendrites (5-HT1A receptors) of the dorsal raphe nuclei or at the axon terminals (5-HT1B receptors). In dorsal raphe neurons, the release of serotonin from vesicles in the soma, dendrites, and/or axonal varicosities is independent of classical synapses and can be induced by neuron depolarization, by the stimulation of L-type calcium channels, by activation of glutamatergic receptors, and/or by activation of 5-HT2 receptors. The resulting serotonin release displays a slow kinetic and a large diffusion. This process called volume transmission may ultimately affect the rate of discharge of serotonergic neurons, and their tonic activity. The therapeutic effects induced by serotonin-selective reuptake inhibitor (SSRI) antidepressants are initially triggered by blocking SERT but rely on consequences of chronic exposure, i.e., a selective desensitization of somatodendritic 5-HT1A autoreceptors. Agonist stimulation of 5-HT2B receptors mimicked behavioral and neurogenic SSRI actions, and increased extracellular serotonin in dorsal raphe. By contrast, a lack of effects of SSRIs was observed in the absence of 5-HT2B receptors (knockout-KO), even restricted to serotonergic neurons (Htr2b5-HTKO mice). The absence of 5-HT2B receptors in serotonergic neurons is associated with a higher 5-HT1A-autoreceptor reactivity and thus a lower firing activity of these neurons. In agreement, mice with overexpression of 5-HT1A autoreceptor show decreased neuronal activity and increased depression-like behavior that is resistant to SSRI treatment. We propose thus that the serotonergic tone results from the opposite control exerted by somatodendritic (Gi-coupled) 5-HT1A and (Gq-coupled) 5-HT2B receptors on dorsal raphe neurons. Therefore, 5-HT2B receptors may contribute to SSRI therapeutic effects by their positive regulation of adult raphe serotonergic neurons. Deciphering the molecular mechanism controlling extrasynaptic release of serotonin, and how autoreceptors interact in regulating the tonic activity of serotonergic neurons, is critical to fully understand the therapeutic effect of SSRIs.

Dataset Information

High and asymmetric somato-dendritic coupling of V1 layer 5 neurons independent of visual stimulation and locomotion.

Publications

High and asymmetric somato-dendritic coupling of V1 layer 5 neurons independent of visual stimulation and locomotion.

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