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2. Positive reinforcement mediated by midbrain dopamine neurons requires D1 and D2 receptor activation in the nucleus accumbens

Author

Janak, Patricia, Steinberg, EE, Boivin, JR, Saunders, BT, Witten, IB, Deisseroth, K, and Janak, PH

Abstract

The neural basis of positive reinforcement is often studied in the laboratory using intracranial self-stimulation (ICSS), a simple behavioral model in which subjects perform an action in order to obtain exogenous stimulation of a specific brain area. Recen

Published
2014

5. A causal link between prediction errors, dopamine neurons and learning

Author

Janak, Patricia, Steinberg, EE, Keiflin, R, Boivin, JR, Witten, IB, Deisseroth, K, and Janak, PH

Abstract

Situations in which rewards are unexpectedly obtained or withheld represent opportunities for new learning. Often, this learning includes identifying cues that predict reward availability. Unexpected rewards strongly activate midbrain dopamine neurons. Thi

Published
2013

6. Closed-loop optogenetic control of thalamus as a tool for interrupting seizures after cortical injury.

Author

Paz, Jeanne, Paz, JT, Davidson, TJ, Frechette, ES, Delord, B, Parada, I, Peng, K, Deisseroth, K, and Huguenard, JR

Abstract

Cerebrocortical injuries such as stroke are a major source of disability. Maladaptive consequences can result from post-injury local reorganization of cortical circuits. For example, epilepsy is a common sequela of cortical stroke, but the mechanisms respo

Published
2013

18. Sustained rescue of prefrontal circuit dysfunction by antidepressant-induced spine formation

Author

Moda-Sava, R. N., primary, Murdock, M. H., additional, Parekh, P. K., additional, Fetcho, R. N., additional, Huang, B. S., additional, Huynh, T. N., additional, Witztum, J., additional, Shaver, D. C., additional, Rosenthal, D. L., additional, Alway, E. J., additional, Lopez, K., additional, Meng, Y., additional, Nellissen, L., additional, Grosenick, L., additional, Milner, T. A., additional, Deisseroth, K., additional, Bito, H., additional, Kasai, H., additional, and Liston, C., additional

Published
2019
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25. Locus coeruleus and dopaminergic consolidation of everyday memory

Author

Takeuchi, T., Duszkiewicz, A.J., Sonneborn, A., Spooner, P.A., Yamasaki, M., Watanabe, M., Smith, C.C., Fernandez, G.S.E., Deisseroth, K., Greene, R.W., Morris, R.G., Takeuchi, T., Duszkiewicz, A.J., Sonneborn, A., Spooner, P.A., Yamasaki, M., Watanabe, M., Smith, C.C., Fernandez, G.S.E., Deisseroth, K., Greene, R.W., and Morris, R.G.

Abstract

Item does not contain fulltext, The retention of episodic-like memory is enhanced, in humans and animals, when something novel happens shortly before or after encoding. Using an everyday memory task in mice, we sought the neurons mediating this dopamine-dependent novelty effect, previously thought to originate exclusively from the tyrosine-hydroxylase-expressing (TH+) neurons in the ventral tegmental area. Here we report that neuronal firing in the locus coeruleus is especially sensitive to environmental novelty, locus coeruleus TH+ neurons project more profusely than ventral tegmental area TH+ neurons to the hippocampus, optogenetic activation of locus coeruleus TH+ neurons mimics the novelty effect, and this novelty-associated memory enhancement is unaffected by ventral tegmental area inactivation. Surprisingly, two effects of locus coeruleus TH+ photoactivation are sensitive to hippocampal D1/D5 receptor blockade and resistant to adrenoceptor blockade: memory enhancement and long-lasting potentiation of synaptic transmission in CA1 ex vivo. Thus, locus coeruleus TH+ neurons can mediate post-encoding memory enhancement in a manner consistent with possible co-release of dopamine in the hippocampus.

Published
2016

26. Serotonin engages an anxiety and fear-promoting circuit in the extended amygdala

Author

Marcinkiewcz, C.A., Mazzone, C.M., D'Agostino, G., Halladay, L.R., Hardaway, J.A., DiBerto, J.F., Navarro, M., Burnham, N., Cristiano, C., Dorrier, C.E., Tipton, G.J., Ramakrishnan, C., Kozicz, L.T., Deisseroth, K., Thiele, T.E., McElligott, Z.A., Holmes, A., Heisler, L.K., Kash, T.L., Marcinkiewcz, C.A., Mazzone, C.M., D'Agostino, G., Halladay, L.R., Hardaway, J.A., DiBerto, J.F., Navarro, M., Burnham, N., Cristiano, C., Dorrier, C.E., Tipton, G.J., Ramakrishnan, C., Kozicz, L.T., Deisseroth, K., Thiele, T.E., McElligott, Z.A., Holmes, A., Heisler, L.K., and Kash, T.L.

Abstract

Contains fulltext : 168138.pdf (publisher's version ) (Closed access), Serotonin (also known as 5-hydroxytryptamine (5-HT)) is a neurotransmitter that has an essential role in the regulation of emotion. However, the precise circuits have not yet been defined through which aversive states are orchestrated by 5-HT. Here we show that 5-HT from the dorsal raphe nucleus (5-HTDRN) enhances fear and anxiety and activates a subpopulation of corticotropin-releasing factor (CRF) neurons in the bed nucleus of the stria terminalis (CRFBNST) in mice. Specifically, 5-HTDRN projections to the BNST, via actions at 5-HT2C receptors (5-HT2CRs), engage a CRFBNST inhibitory microcircuit that silences anxiolytic BNST outputs to the ventral tegmental area and lateral hypothalamus. Furthermore, we demonstrate that this CRFBNST inhibitory circuit underlies aversive behaviour following acute exposure to selective serotonin reuptake inhibitors (SSRIs). This early aversive effect is mediated via the corticotrophin-releasing factor type 1 receptor (CRF1R, also known as CRHR1), given that CRF1R antagonism is sufficient to prevent acute SSRI-induced enhancements in aversive learning. These results reveal an essential 5-HTDRN-->CRFBNST circuit governing fear and anxiety, and provide a potential mechanistic explanation for the clinical observation of early adverse events to SSRI treatment in some patients with anxiety disorders.

Published
2016

27. Optogenetic control of striatal fast-spiking interneurons in Huntington’s diseasemouse models

Author

Galvan, Laurie, Richler, E, Cepeda, C, Deisseroth, K., Andre, V., Levine, M, and GALVAN, LAURIE

Subjects
nervous system, [SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]
Abstract

Huntington's disease (HD), an inherited neurodegenerative disorder caused by a mutation in the IT15 gene, is characterized by massive degeneration of striatal medium-sized spiny neurons (MSNs). MSNs are gamma-aminobutyric acid (GABA) neurons that project, via the direct and the indirect pathways, to the globus pallidus and substantia nigra. They are affected early in HD while striatal interneurons are relatively spared of the degenerative process. In HD models, spontaneous GABA synaptic activity onto MSNs is increased and one possible source of this increased inhibition is from striatal interneurons. Parvalbumin (PV)-expressing interneurons are the most abundant, display fast-firing properties and mediate feed-forward inhibition. In the present study, we examined the response of MSNs to PV interneuron activation or inhibition in the R6/2 mouse model of HD using optogenetics. We used adeno-associated virus type 2 (AAV2) to express channelrhodopsin-2 H134R (ChR2) or enhanced halorhodopsin (eNpHR) in the striatum of one month old R6/2 and Wild Type (WT) mice crossed with PV-CRE mice to express the construct only in PV-positive interneurons. The expression of these proteins was visualized by enhanced yellow fluorescent protein (EYFP) (ChR2-EYFP, eNpHR-EYFP). These constructs have two flox sites that lead to specific expression in PV interneurons by the CRE recombinase sequence. Blue (470 nm) or yellow (590 nm) light was used to activate or inhibit the PV-positive cells. We found that the level of expression of ChrR2-EYFP and eNpHR-EYFP fluorescence intensity and injection size were not significantly different in the R6/2 and WT PV-CRE mice. Electrophysiological recordings in current and voltage clamp modes, one month after injections, from ChR2-and eNpHR-EYFP PV interneurons using light stimulation validated construct expression. Recordings from MSNs demonstrated that activation of PV-positive neurons produced differential kinetics of GABAergic responses of MSNs obtained from R6/2 and WT mice. These findings suggest that PV interneurons may contribute to differential GABAergic responses in MSNs in HD.

Published
2012

30. Manipulating a "Cocaine Engram" in Mice

Author

Hsiang, H.-L., primary, Epp, J. R., additional, van den Oever, M. C., additional, Yan, C., additional, Rashid, A. J., additional, Insel, N., additional, Ye, L., additional, Niibori, Y., additional, Deisseroth, K., additional, Frankland, P. W., additional, and Josselyn, S. A., additional

Published
2014
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33. Activation of a novel p70 S6 kinase 1-dependent intracellular cascade in the basolateral nucleus of the amygdala is required for the acquisition of extinction memory

Author

Huynh, T N, Santini, E, Mojica, E, Fink, A E, Hall, B S, Fetcho, R N, Grosenick, L, Deisseroth, K, LeDoux, J E, Liston, C, and Klann, E

Abstract

Repeated presentations of a previously conditioned stimulus lead to a new form of learning known as extinction, which temporarily alters the response to the original stimulus. Previous studies have shown that the consolidation of extinction memory requires de novo protein synthesis. However, the role of specific nodes of translational control in extinction is unknown. Using auditory threat conditioning in mice, we investigated the role of mechanistic target of rapamycin complex 1 (mTORC1) and its effector p70 S6 kinase 1 (S6K1) in the extinction of auditory threat conditioning. We found that rapamycin attenuated the consolidation of extinction memory. In contrast, genetic deletion and pharmacological inhibition of S6K1, a downstream effector of mTORC1, blocked within-session extinction, indicating a role for S6K1 independent of protein synthesis. Indeed, the activation of S6K1 during extinction required extracellular signal-regulated kinase (ERK) activation in the basolateral nucleus of the amygdala (BLA) and was necessary for increased phosphorylation of the GluA1 (Thr840) subunit of the AMPA receptor following extinction training. Mice exposed to brief uncontrollable stress showed impaired within-session extinction as well as a downregulation of ERK and S6K1 signaling in the amygdala. Finally, using fiber photometry we were able to record calcium signals in vivo, and we found that inhibition of S6K1 reduces extinction-induced changes in neuronal activity of the BLA. These results implicate a novel ERK-S6K1-GluA1 signaling cascade critically involved in extinction.

Published
2018
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34. Functional Integration of Grafted Neural Stem Cell-Derived Dopaminergic Neurons Monitored by Optogenetics in an In Vitro Parkinson Model

Author

Mattson, M, Tonnesen, J, Parish, CL, Sorensen, AT, Andersson, A, Lundberg, C, Deisseroth, K, Arenas, E, Lindvall, O, Kokaia, M, Mattson, M, Tonnesen, J, Parish, CL, Sorensen, AT, Andersson, A, Lundberg, C, Deisseroth, K, Arenas, E, Lindvall, O, and Kokaia, M

Abstract

Intrastriatal grafts of stem cell-derived dopamine (DA) neurons induce behavioral recovery in animal models of Parkinson's disease (PD), but how they functionally integrate in host neural circuitries is poorly understood. Here, Wnt5a-overexpressing neural stem cells derived from embryonic ventral mesencephalon of tyrosine hydroxylase-GFP transgenic mice were expanded as neurospheres and transplanted into organotypic cultures of wild type mouse striatum. Differentiated GFP-labeled DA neurons in the grafts exhibited mature neuronal properties, including spontaneous firing of action potentials, presence of post-synaptic currents, and functional expression of DA D₂ autoreceptors. These properties resembled those recorded from identical cells in acute slices of intrastriatal grafts in the 6-hydroxy-DA-induced mouse PD model and from DA neurons in intact substantia nigra. Optogenetic activation or inhibition of grafted cells and host neurons using channelrhodopsin-2 (ChR2) and halorhodopsin (NpHR), respectively, revealed complex, bi-directional synaptic interactions between grafted cells and host neurons and extensive synaptic connectivity within the graft. Our data demonstrate for the first time using optogenetics that ectopically grafted stem cell-derived DA neurons become functionally integrated in the DA-denervated striatum. Further optogenetic dissection of the synaptic wiring between grafted and host neurons will be crucial to clarify the cellular and synaptic mechanisms underlying behavioral recovery as well as adverse effects following stem cell-based DA cell replacement strategies in PD.

Published
2011

39. Optogenetic Inhibition of Dorsal Medial Prefrontal Cortex Attenuates Stress-Induced Reinstatement of Palatable Food Seeking in Female Rats

Author

Calu, D. J., primary, Kawa, A. B., additional, Marchant, N. J., additional, Navarre, B. M., additional, Henderson, M. J., additional, Chen, B., additional, Yau, H.-J., additional, Bossert, J. M., additional, Schoenbaum, G., additional, Deisseroth, K., additional, Harvey, B. K., additional, Hope, B. T., additional, and Shaham, Y., additional

Published
2013
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