Optogenetics and Chemogenetics

Vlasov, Ksenia; Dort, Christa J. Van; Solt, Ken

doi:10.1016/bs.mie.2018.01.022

Cited by 59 publications

(56 citation statements)

References 28 publications

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“…In particular, the novel developments of gene-engineering techniques and biotechnological tools, such as chemogenetics and optogenetics, provide the possibility to activate or inhibit neurons in a time-, type-and region-specific manner [166]. After light-sensitive ion channels, or designer receptors exclusively activated by designer drugs, are expressed in targeted cells, optogenetics allows neuronal depolarization or hyperpolarization with pulses of light while chemogenetics provides the royalsocietypublishing.org/journal/rsfs Interface Focus 10: 20190092 ability to modulate neuronal firing for several hours with the single administration of a designer drug.…”

Section: Can We Overcome Undesired Stress-related Consequences Of Slementioning

confidence: 99%

Sleep deprivation and stress: a reciprocal relationship

2020

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Sleep is highly conserved across evolution, suggesting vital biological functions that are yet to be fully understood. Animals and humans experiencing partial sleep restriction usually exhibit detrimental physiological responses, while total and prolonged sleep loss could lead to death. The perturbation of sleep homeostasis is usually accompanied by an increase in hypothalamic–pituitary–adrenal (HPA) axis activity, leading to a rise in circulating levels of stress hormones (e.g. cortisol in humans, corticosterone in rodents). Such hormones follow a circadian release pattern under undisturbed conditions and participate in the regulation of sleep. The investigation of the consequences of sleep deprivation, from molecular changes to behavioural alterations, has been used to study the fundamental functions of sleep. However, the reciprocal relationship between sleep and the activity of the HPA axis is problematic when investigating sleep using traditional sleep-deprivation protocols that can induce stress per se . This is especially true in studies using rodents in which sleep deprivation is achieved by exogenous, and potentially stressful, sensory–motor stimulations that can undoubtedly confuse their conclusions. While more research is needed to explore the mechanisms underlying sleep loss and health, avoiding stress as a confounding factor in sleep-deprivation studies is therefore crucial. This review examines the evidence of the intricate links between sleep and stress in the context of experimental sleep deprivation, and proposes a more sophisticated research framework for sleep-deprivation procedures that could benefit from recent progress in biotechnological tools for precise neuromodulation, such as chemogenetics and optogenetics, as well as improved automated real-time sleep-scoring algorithms.

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Section: Can We Overcome Undesired Stress-related Consequences Of Slementioning

confidence: 99%

Sleep deprivation and stress: a reciprocal relationship

2020

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“…Since the systemic CNO administration exerts an effect on neuronal activity for hours 31–33 , we wondered whether the bidirectional control of FN-vlPAG pathway on fear memory occurs specifically during the acquisition or during the consolidation phase that immediately followed 34, 35 . To answer this question we compared the effect of activating and inhibiting the FN-vlPAG pathway starting from the acquisition phase or from the consolidation phase.…”

Section: Resultsmentioning

confidence: 99%

Bidirectional control of fear memories by the cerebellum through the ventrolateral periaqueductal grey

Frontera

Aissa

Sala

et al. 2020

Preprint

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10Fear conditioning is a form of associative learning that is known to involve brain areas, notably the 11 amygdala, the prefrontal cortex and the periaqueductal grey (PAG). Here, we describe the functional 12 role of pathways that link the cerebellum with the fear network. We found that the cerebellar 13 fastigial nucleus (FN) sends glutamatergic projections to vlPAG that synapse onto glutamatergic and 14 GABAergic vlPAG neurons. Chemogenetic and optogenetic manipulations revealed that the FN-vlPAG 15 pathway controls bi-directionally the strength of the fear memory, indicating a role in the association 16 of the conditioned and unconditioned stimuli, a function consistent with vlPAG encoding of fear 17 prediction error. In addition, we found that a FN -thalamic parafascicular nucleus pathway, which 18 may relay cerebellar influence to the amygdala, is involved in anxiety and fear expression but not in 19 fear memory. Our results reveal the contributions to the emotional system of the cerebellum, which 20 exerts a potent control on the strength of the fear memory through excitatory FN-vlPAG projections. 21 22 23 Keywords: cerebellum; limbic circuits; fear memory, chemogenetics, electrophysiology 24 vermis, in relation to negative emotions (e.g. during recall of self-generated emotional episodes 20 ). 50 Consistent with this, localized cerebellar lesions, principally in the midline vermis, account in large 51 part for the emotional disturbances, inappropriate behavior and changes in affect, which are 52 collectively termed the "cerebellar cognitive affective syndrome" 21 and reported in cerebellar 53 patients. Several studies have shown that the cerebellum has functional connections from fear-54 related areas including the PAG, the amygdala, and the prefrontal cortex [22][23][24][25] . In accordance with the 55 existence of such connections, Pavlovian fear conditioning affects cerebellar plasticity 26 , post-56 conditioning cerebellar inactivation affects memory consolidation 27 , and cerebellar lesions -or 57 inactivation-modulate freezing 24,28 ; however, the pathways by which the cerebellum participates to 58 fear learning or expression remain undefined. 59. The cerebellar vermis, which is most consistently associated with emotional pathologies and fear 60 expression 20,24,29 , projects to the fastigial nucleus (FN), a deep cerebellar nucleus (DCN) which 61 projects to many targets from the spinal cord to the diencephalon 22 . The purpose of the present 62 study is to study the contribution of specific FN output pathways to fear learning. Using 63 neuroanatomical tracings, chemogenetic modulation of the cerebellar input to the vlPAG and to the 64 BLA during fear conditioning, optogenetics and extracellular electrophysiological recordings in awake 65 freely moving animals, we demonstrate the contribution of the cerebellum to fear learning through 66 its inputs to the vlPAG. 67 68 4 69 70Results 71 Neuroanatomical link between the cerebellum and vlPAG 72In order to examine cerebellar projections to areas involve...

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“…Optogenetics and chemogenetics have made the ability to modulate cell‐type specific neural networks more routine (Vlasov, Van Dort, & Solt, ). Transducing specific subpopulations of cells with light‐sensitive ion channels (opsins), combined with bioluminescence or fluorescence imaging of the circadian system have revealed interactions between molecular, electrical and behavioural rhythms in mice (Jones, Tackenberg, & McMahon, ; Mazuski et al., ).…”

Section: Intersectional Genetics and The Clockmentioning

confidence: 99%

Synchronization and maintenance of circadian timing in the mammalian clockwork

Maywood

2018

Eur J of Neuroscience

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The hypothalamic suprachiasmatic nucleus (SCN) is the principal circadian pacemaker in mammals. Cells in the SCN contain cell‐autonomous transcriptional‐translational feedback loops, which are synchronised to each other and thereby provide a coherent output to direct synchrony of peripheral clocks located in the brain and body. A major difference between these peripheral clocks and the SCN is the requirement for intercellular coupling mechanisms, which confer robustness, stability and amplitude to the system. There has been remarkable progress to our understanding of the intra‐ and inter‐cellular mechanisms of the SCN circuitry over the last ~20 years, which has come hand‐in‐hand with the development of new technologies to measure and manipulate the clock.

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Optogenetics and Chemogenetics

Cited by 59 publications

References 28 publications

Sleep deprivation and stress: a reciprocal relationship

Sleep deprivation and stress: a reciprocal relationship

Bidirectional control of fear memories by the cerebellum through the ventrolateral periaqueductal grey

Synchronization and maintenance of circadian timing in the mammalian clockwork

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