Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

NEUR3310 Neuroscience > Applications of optogenetics and DREADDS > Flashcards

Applications of optogenetics and DREADDS Flashcards

1
Q

Optogenetics: 4

A
  1. Technique to control neuronal activity using light stimulation.
  2. Involves transducing the expression of light-sensitive opsins on neurons, typically ion channels or pumps.
  3. Offers high spatiotemporal resolution, enabling rapid and reversible responses.
  4. Considered invasive due to the need for genetic manipulation and light delivery systems.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

DREADDs (Designer Receptors Exclusively Activated by Designer Drugs): = 3

A
  1. Method to control neuronal activity by transducing the expression of receptors activated by specific drugs, typically GPCRs.
  2. Provides high spatial resolution but lower temporal resolution compared to optogenetics.
  3. Less invasive than optogenetics as it does not require direct light stimulation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Optogenetics and DREADDs …integration in Behavioral Experiments: 3

A
  1. Both optogenetics and DREADDs can be integrated into behavioural experiments to investigate the neural mechanisms underlying animal behaviour.
  2. Researchers can selectively manipulate neuronal activity during behavioural tasks to assess the causal relationship between neural circuit function and behaviour.
  3. By combining these techniques with sophisticated behavioural paradigms, researchers gain insights into the complex interactions between neural circuits and behaviour, paving the way for a deeper understanding of brain function and dysfunction.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Brain Stimulation for Addiction Treatment = 3

GENERAL

A
  1. Targeting specific brain regions/neurons with stimulation can change addiction or substance-seeking behavior.

2 Example: OPTOGENETICS USED IN COCAINE-SEEKING RATS

  1. HOW - Cocaine binds to the DOPAMINE TRANSPORTER , affecting DOPAMINE LEVELS AT THE SYNAPSE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Dopaminergic Neurons and Addiction = 3

A
  1. Addiction and reward-seeking behavior involve neurons and projections from various brain regions.
  2. Dopaminergic neurons play a crucial role.
  3. ALTERED ACTIVITY AND PLASTICITY IN THESE BRAIN REGIONS OCCUR WITH ADDICTION.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Optogenetics Study on Cocaine-Seeking Rats

METHODOLOGY
= OUTCOMES

= 3

A
  1. Rats self-administered cocaine for 8 weeks, followed by shock sessions.
  2. Shock-resistant and shock-sensitive behaviours observed.
  3. Optogenetic stimulation targeted pre-limbic cortex (in mPFC) pyramidal neurons.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

DREADDS Study on vmPFC Neurons - addiction = 3

A
  1. DREADDS used to examine the influence of vmPFC neurons on cocaine-seeking behavior in rats.
  2. vmPFC neurons project to nucleus accumbens, crucial for extinction of cocaine-seeking behaviors.
  3. High spatial resolution allows targeting of specific neuron populations.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

cocaine addiction -Optogenetic Stimulation to Inhibit PL Neurons = 3

A
  1. AAV-eNpHR3.0–eYFP delivered to bilateral PL pyramidal neurons.
  2. Inhibiting PL neurons during cocaine self-administration in shock-sensitive rats.
  3. Optogenetic stimulation applied during specific sessions.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Activation of vmPFC Neurons with DREADD - ADDICTION = 2

A
  1. Activation of vmPFC neurons with DREADD reduces cue-induced cocaine seeking after extinction.
  2. Extinction training to cue is crucial for vmPFC activity on cocaine seeking.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Importance of vmPFC Neurons Projecting to NA - ADDICTION = 2

A
  1. Activation of vmPFC neurons projecting to NA is required for extinction of cocaine seeking behaviors.
  2. Cre-dependent DREADD injected into vmPFC and retrograde Cre injection into NA used to study this.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the key brain regions and methods used in targeting addiction behaviours? = 2

A

Key brain regions include pre-limbic cortex (mPFC), nucleus accumbens (NA), and ventromedial prefrontal cortex (vmPFC).

Methods involve optogenetics and DREADDS (Designer Receptors Exclusively Activated by Designer Drugs).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

DREADS AND MEMORY…3
Implanting “Fake Memories” Using Optogenetics

A
  1. Optogenetics used to create a “fake memory” in the absence of stimuli.
  2. Olfactory system utilized.
  3. Odor conditioned stimulus (CS) paired with an unconditioned stimulus (US) like a foot shock.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Anatomy of Olfactory System and Memory = 4

A
  1. Olfactory sensory neurons (OSN) in the olfactory epithelium (OE) are randomly distributed.
  2. Each OSN expresses one olfactory receptor.
  3. OSN axons converge onto sensory neurons expressing the same receptor in glomeruli.
  4. OB neurons project to brain targets like the hippocampus and amygdala.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Optogenetics Study on Memory Implantation…METHOD AND OUTCOME? = 3

A
  1. Transgenic mice expressing M72-ChR2-eYFP.
  2. M72 olfactory glomerulus activated during foot shock conditioning.
  3. Mice displayed aversion to acetophenone (smell) post-conditioning.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Role of LHb-VTA Pathway in Aversive Behaviors = 2

A
  1. Previous study showed LHb-VTA pathway mediates aversive behaviors.
  2. AAV-ChR2 injected into the LHb and neurons stimulated in VTA.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How can optogenetics be used to implant false memories, and what brain regions are involved in aversive memory formation?

A
  1. Optogenetics can implant false memories by replacing conditioned stimuli with optogenetic stimulation, as demonstrated in the olfactory system.
  2. Aversive memory formation involves brain regions like the lateral habenula (LHb) and medial ventral tegmental nucleus (VTA), as shown by stimulating LHb neurons projecting to VTA
14
Q

Investigating Neurogenesis with DREADDs = 3

A
  1. DREADDs used to study adult neurogenesis and its relevance to anxiolytic behaviors.
  2. Hippocampal neurogenesis persists throughout life, primarily in the dentate gyrus (DG).
  3. Rodent studies implicate neurogenesis in cognitive tasks, anxiety, and depression-like behaviors.
15
Q

Functional Regions of the Dentate Gyrus (DG)

A
  1. Dorsal DG associated with cognitive tasks and spatial memory.
  2. Ventral DG associated with emotional memory and mood regulation.
16
Q

Experiment Using DREADDs in Transgenic Mice = 2

A
  1. Transgenic mice expressed inhibitory DREADD in adult-born granule cells (abGCs).
  2. CNO injected into the vDG to alter activity of abGCs during a social defeat paradigm.
17
Q

Neurogenesis and Stress Resilience = 3

A
  1. Study examined whether neurogenesis confers stress resilience.
  2. Increased neurogenesis achieved using transgenic mice with a deletion of proapoptotic Bax gene.
  3. These mice showed reduced anxious behaviors.
18
Q

Neurogenesis and Activity in vDG = 2

A
  1. Increased neurogenesis reduces activity in vDG during stressful stimuli, indicated by lower calcium transients.
  2. DREADDs used to modulate excitatory cell activity in vDG during social defeat sessions.
19
Q

How does the dentate gyrus contribute to cognition and emotional regulation, and what techniques were used to study neurogenesis in relation to stress resilience? = 3

A
  1. The dorsal dentate gyrus is associated with cognitive tasks and spatial memory, while the ventral DG is linked to emotional memory and mood regulation.
  2. Techniques such as DREADDs were used to investigate adult neurogenesis in relation to stress resilience,
  3. including studies using transgenic mice with altered neurogenesis and manipulation of excitatory cell activity in the ventral DG during stress sessions.
20
Q

Glaucoma as a Leading Cause of Irreversible Blindness = 3

A
  1. Glaucoma is characterized by progressive damage to retinal ganglion cells, leading to vision loss.
  2. It is the primary cause of irreversible blindness globally.
  3. Can occur as a primary disease or secondary to factors like trauma, inflammation, or tumors.
21
Q

Therapeutic Approach TO GLAUCOMA by OPTOGENETICS AND DREADS = 2

A
  1. Injected the superior colliculus (SC) with a virus to induce expression of an SSFO ChR2 virus in excitatory SC neurons.
  2. Glaucoma induced in mice by cauterizing limbal and episcleral veins, preventing drainage of aqueous humor.
22
Q

Experimental Protocol for Glaucoma Treatment = 3

A
  1. AAV2/7-CaMKII-SSFO virus used for inducing expression.
  2. Glaucoma induced by preventing drainage of aqueous humor.
  3. Continuous light stimulation for 2 seconds, twice a day for 14 days.
23
Q

Outcome Measurement: Neurotrophin Protein Levels …GLAUCOMA = 2

A
  1. Neurotrophin protein levels likely assessed as part of the study’s outcome.
  2. Neurotrophins are essential for the survival and function of neurons, including retinal ganglion cells.
24
Q

What is the therapeutic approach for treating glaucoma described by Wilks et al. (2012), and what outcome measure related to neurotrophins might be relevant in this context? = 3

A
  1. Wilks et al. (2012) used a therapeutic approach involving induction of SSFO ChR2 virus expression in excitatory SC neurons to treat glaucoma in mice.
  2. They induced glaucoma by preventing drainage of aqueous humour and applied continuous light stimulation for 14 days.
  3. In this context, assessment of neurotrophin protein levels could be relevant as neurotrophins play a crucial role in the survival and function of retinal ganglion cells affected by glaucoma.
25
Q

Optogenetics in Retinitis Pigmentosa = 3

A
  1. Retinitis pigmentosa is a neurodegenerative eye disease causing photoreceptor loss and blindness.
  2. Currently, there is no cure or effective treatment.
  3. Potential treatments include stem cell therapy or gene therapy.
26
Q

Study on Optogenetics in Humans = 4

A
  1. report on outcomes from a patient who lost vision two years prior to the study.
  2. Optogenetic approach involves intravitreal injection of AAV2.7m8-CAG-ChrimsonR-tdTomato virus.
  3. ChrimsonR is a light-gated cation channel activating neurons in 590nm light.
  4. Foveal ganglion cell expression stabilizes for approximately 2-6 months.
27
Q

humans - mechanism of Optogenetic Stimulation = 2

A
  1. Light-stimulating goggles capture environmental images and transform them into monochromatic images.
  2. Monochromatic images are projected onto the retina as 595nm pulses.
28
Q

Mechanism of Optogenetic Stimulation…experimental protocol = 3

A
  1. The study conducted 15 visits over 84 weeks.
  2. Objectives included assessing safety and retaining light perception.
  3. Visual training provided for seven months alongside the treatment.
29
Q

What is the optogenetic approach used in treating retinitis pigmentosa in humans, and what are the key findings from the study?

= 3

A
  1. the optogenetic approach involves intravitreal injection of a virus expressing a light-gated cation channel (ChrimsonR) into foveal ganglion cells.
  2. This allows activation of neurons in response to specific light wavelengths.
  3. The study reported retention of light perception and safety outcomes over 84 weeks, with visual training provided alongside the treatment.

NEUR3310 Neuroscience (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions