Nitrergic Tone Influences Activity of Both Ventral Striatum Projection Neurons and Interneurons

GABAergic neurons in the olfactory cortex projecting to the lateral hypothalamus in mice

10.1101/413328 ◽

2018 ◽

Author(s):

Koshi Murata ◽

Tomoki Kinoshita ◽

Yugo Fukazawa ◽

Kenta Kobayashi ◽

Kazuto Kobayashi ◽

...

Keyword(s):

Olfactory Bulb ◽

Lateral Hypothalamus ◽

Ventral Striatum ◽

Glutamate Transporter ◽

Olfactory Cortex ◽

Acid Decarboxylase ◽

Projection Neurons ◽

Diagonal Band ◽

Glutamate Transporter 1 ◽

Glutamic Acid Decarboxylase 65

AbstractOlfaction guides goal-directed behaviours including feeding. To investigate how central olfactory neural circuits control feeding behaviour in mice, we performed retrograde tracing from the lateral hypothalamus (LH), an important feeding centre. We observed a cluster of retrogradely labelled cells distributed in the posteroventral region of the olfactory peduncle. Histochemical analyses revealed that a majority of these retrogradely labelled projection neurons expressed glutamic acid decarboxylase 65/67 (GAD65/67), but not vesicular glutamate transporter 1 (VGluT1). We named this region with GABAergic projection neurons the ventral olfactory nucleus (VON) to discriminate it from the conventional olfactory peduncle. VON neurons were less immunoreactive for DARPP-32, a striatal neuron marker, in comparison to those in the olfactory tubercle and nucleus accumbens, which distinguished the VON from the ventral striatum. Fluorescent labelling confirmed synaptic contacts between VON neurons and olfactory bulb projection neurons. Rabies-virus-mediated trans-synaptic labelling revealed that VON neurons received synaptic inputs from the olfactory bulb, other olfactory cortices, horizontal limb of the diagonal band, and prefrontal cortex. Collectively, these results identified novel GABAergic projection neurons in the olfactory cortex that can integrate olfactory sensory and top-down inputs and send inhibitory output to the LH, which may contribute to forming odour-guided LH-related behaviours.

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Transitions between sleep and feeding states in rat ventral striatum neurons

Journal of Neurophysiology ◽

10.1152/jn.00394.2012 ◽

2012 ◽

Vol 108 (6) ◽

pp. 1739-1751 ◽

Cited By ~ 13

Author(s):

Luis A. Tellez ◽

Isaac O. Perez ◽

Sidney A. Simon ◽

Ranier Gutierrez

Keyword(s):

Neural Networks ◽

Ventral Striatum ◽

Cell Types ◽

Projection Neurons ◽

Inhibitory Interneurons ◽

Medium Spiny Neurons ◽

Spiny Neurons ◽

Fast Spiking ◽

First Time

Neurons in the nucleus accumbens (NAc) have been shown to participate in several behavioral states, including feeding and sleep. However, it is not known if the same neuron participates in both states and, if so, how similar are the responses. In addition, since the NAc contains several cell types, it is not known if each type participates in the transitions associated with feeding and sleep. Such knowledge is important for understanding the interaction between two different neural networks. For these reasons we recorded ensembles of NAc neurons while individual rats volitionally transitioned between the following states: awake and goal directed, feeding, quiet-awake, and sleeping. We found that during both feeding and sleep states, the same neurons could increase their activity (be activated) or decrease their activity (be inactivated) by feeding and/or during sleep, thus indicating that the vast majority of NAc neurons integrate sleep and feeding signals arising from spatially distinct neural networks. In contrast, a smaller population was modulated by only one of the states. For the majority of neurons in either state, we found that when one population was excited, the other was inhibited, suggesting that they act as a local circuit. Classification of neurons into putative interneurons [fast-spiking interneurons (pFSI) and choline acetyltransferase interneurons (pChAT)] and projection medium spiny neurons (pMSN) showed that all three types are modulated by transitions to and from feeding and sleep states. These results show, for the first time, that in the NAc, those putative inhibitory interneurons respond similarly to pMSN projection neurons and demonstrate interactions between NAc networks involved in sleep and feeding.

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Repression of Dlx1/2 Signaling by Nolz-1/Znf503 is Essential for Parcellation of the Striatal Complex into Dorsal and Ventral Striatum

10.1101/463398 ◽

2018 ◽

Author(s):

Kuan-Ming Lu ◽

Shih-Yun Chen ◽

Hsin-An Ko ◽

Ting-Hao Huang ◽

Janice Hsin-Jou Hao ◽

...

Keyword(s):

Transcription Factors ◽

Ventral Striatum ◽

Dorsal Striatum ◽

Clinical Importance ◽

Projection Neurons ◽

Striatal Neurons ◽

Addictive Disorders ◽

Striatal Projection Neurons ◽

Cells Of Origin ◽

Set Up

ABSTRACTThe division of the striatum into dorsal and ventral districts is of central clinical importance. The dorsal striatum is differentially affected in Huntington’s disease, dopamine in the ventral striatum is differentially spared in Parkinson’s disease, and human brain imaging studies implicate the ventral striatum in addictive disorders. If fits that the dorsal striatum contains the cells of origin of the direct and indirect basal ganglia pathways for motor control. The ventral striatum is a node in neural circuits related to motivation and affect. Despite these striking neurobiologic contrasts, there is almost no information about how the dorsal and ventral divisions of the striatum are set up during development. Here, we demonstrate that interactions between the two key transcription factors Nolz-1 and Dlx1/2 control the migratory paths of developing striatal neurons to the dorsal or ventral striatum. Moreover, these same transcription factors control the cell identity of striatal projection neurons in both the dorsal and ventral striatum including the cell origin of the direct and indirect pathways. We show that Nolz-1 suppresses Dlx1/2 expression. Deletion of Nolz-1 or over-expression of Dlx1/2 can produce a striatal phenotype characterized by withered dorsal striatum and a swollen ventral striatum, and that we can rescue this phenotype by manipulating the interactions between Nolz-1 and Dlx1/2 transcription factors. This evidence suggests that the fundamental basis for divisions of the striatum known to be differentially vulnerable at maturity is already encoded by the time embryonic striatal neurons begin their migrations into the developing striatum.

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Parcellation of the striatal complex into dorsal and ventral districts

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1921007117 ◽

2020 ◽

Vol 117 (13) ◽

pp. 7418-7429 ◽

Cited By ~ 1

Author(s):

Shih-Yun Chen ◽

Kuan-Ming Lu ◽

Hsin-An Ko ◽

Ting-Hao Huang ◽

Janice Hsin-Jou Hao ◽

...

Keyword(s):

Transcription Factors ◽

Ventral Striatum ◽

Dorsal Striatum ◽

Clinical Importance ◽

Projection Neurons ◽

Striatal Neurons ◽

Striatal Projection Neurons ◽

Tier System ◽

And Migration ◽

Set Up

The striatal complex of basal ganglia comprises two functionally distinct districts. The dorsal district controls motor and cognitive functions. The ventral district regulates the limbic function of motivation, reward, and emotion. The dorsoventral parcellation of the striatum also is of clinical importance as differential striatal pathophysiologies occur in Huntington’s disease, Parkinson’s disease, and drug addiction disorders. Despite these striking neurobiologic contrasts, it is largely unknown how the dorsal and ventral divisions of the striatum are set up. Here, we demonstrate that interactions between the two key transcription factors Nolz-1 and Dlx1/2 control the migratory paths of striatal neurons to the dorsal or ventral striatum. Moreover, these same transcription factors control the cell identity of striatal projection neurons in both the dorsal and the ventral striata including the D1-direct and D2-indirect pathways. We show that Nolz-1, through the I12b enhancer, represses Dlx1/2, allowing normal migration of striatal neurons to dorsal and ventral locations. We demonstrate that deletion, up-regulation, and down-regulation of Nolz-1 and Dlx1/2 can produce a striatal phenotype characterized by a withered dorsal striatum and an enlarged ventral striatum and that we can rescue this phenotype by manipulating the interactions between Nolz-1 and Dlx1/2 transcription factors. Our study indicates that the two-tier system of striatal complex is built by coupling of cell-type identity and migration and suggests that the fundamental basis for divisions of the striatum known to be differentially vulnerable at maturity is already encoded by the time embryonic striatal neurons begin their migrations into developing striata.

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