Endocannabinoid System and Cannabis Overview

False (B)

Arachidonic acid

<p>fatty acid amide hydrolase (FAAH)</p> Signup and view all the answers

<p>CB1 = Central Nervous System CB2 = Immune System 2-AG = Presynaptic metabolism Anandamide = Postsynaptic metabolism</p> Signup and view all the answers

<p>It increases pleasure from stimulants. (A)</p> Signup and view all the answers

<p>False (B)</p> Signup and view all the answers

<p>Agonist treatments</p> Signup and view all the answers

<p>prefrontal cortex</p> Signup and view all the answers

<p>Methadone = Replace heroin Varenicline = Prevent nicotine withdrawal Naloxone = Block heroin effects Disulfiram = Induce negative reaction to alcohol</p> Signup and view all the answers

<p>Basal Ganglia (A)</p> Signup and view all the answers

<p>False (B)</p> Signup and view all the answers

<p>It is involved in the brain stress systems and contributes to negative mood.</p> Signup and view all the answers

<p>Delta-9-tetrahydrocannabinol (THC) (A)</p> Signup and view all the answers

<p>False (B)</p> Signup and view all the answers

<p>CB1 and CB2</p> Signup and view all the answers

<p>10</p> Signup and view all the answers

<p>Sativex = Analgesia Marinol = Appetite Stimulation Rimonabant = Appetite Suppression Diazepam = Prevent Withdrawal Seizures</p> Signup and view all the answers

<p>Retrograde message (A)</p> Signup and view all the answers

<p>False (B)</p> Signup and view all the answers

<p>NMDA receptors</p> Signup and view all the answers

<p>alcohol dehydrogenase</p> Signup and view all the answers

<p>Disulfiram = Prevent Relapse Naltrexone = Prevent Withdrawal Seizures Diazepam = Treat Comorbid Conditions Topiramate = Prevent Relapse</p> Signup and view all the answers

<p>Cannabidiol (CBD) (A)</p> Signup and view all the answers

<p>True (A)</p> Signup and view all the answers

<p>Preventing relapse and managing withdrawal symptoms</p> Signup and view all the answers

<p>Stage 3-4 (B)</p> Signup and view all the answers

<p>False (B)</p> Signup and view all the answers

<p>histamine</p> Signup and view all the answers

<p>REM rebound</p> Signup and view all the answers

<p>Zolpidem (Ambien) = Z drug Zaleplon (Sonata) = Z drug Ramelton (Rozerem) = Melatonin agonist Suvorexant (Belsomra) = Orexin receptor antagonist</p> Signup and view all the answers

<p>Scopolamine (A)</p> Signup and view all the answers

<p>False (B)</p> Signup and view all the answers

<p>Wakes a person up</p> Signup and view all the answers

<p>To induce seizures and reboot the brain (A)</p> Signup and view all the answers

<p>False (B)</p> Signup and view all the answers

<p>Brain-derived neurotrophic factor (BDNF)</p> Signup and view all the answers

<p>cortisol</p> Signup and view all the answers

<p>Tricyclics = Block reuptake of serotonin and norepinephrine Monoamine Oxidase Inhibitors = Inhibit the activity of MAO Electroconvulsive Therapy = Fast-acting and induces brain reboot Antidepressants = Normalize brain plasticity deficits</p> Signup and view all the answers

<p>Electroconvulsive Therapy (ECT) (D)</p> Signup and view all the answers

<p>True (A)</p> Signup and view all the answers

<p>Dietary restrictions and potential cardiotoxicity</p> Signup and view all the answers

<p>Controlling the release of melatonin (A)</p> Signup and view all the answers

<p>False (B)</p> Signup and view all the answers

<p>Norepinephrine and acetylcholine</p> Signup and view all the answers

<p>adenosine</p> Signup and view all the answers

<p>Narcolepsy = Loss of orexin-producing neurons leading to excessive daytime sleepiness Fatal Familial Insomnia = Severe repression of sleep due to cell loss in the anterior hypothalamus Encephalitis Lethargica = Condition characterized by extreme lethargy and sleepiness Sleep Apnea = Disrupted sleep due to breathing difficulties during sleep</p> Signup and view all the answers

<p>Buprenorphine (A)</p> Signup and view all the answers

<p>False (B)</p> Signup and view all the answers

<p>10 g</p> Signup and view all the answers

<p>adenosine</p> Signup and view all the answers

<p>It suppresses neuronal action (C)</p> Signup and view all the answers

Endocannabinoids regulate various bodily functions, including pain perception, sensory processing, motor skills, memory, cognition, appetite, and the immune system.

Endocannabinoids are made and released as needed, directly from fatty acids, rather than being stored.

Endocannabinoids bind to specific receptors in the brain (CB1) and immune system (CB2).

The body breaks down endocannabinoids using enzymes (FAAH & MGL) after they complete their job as messengers.

Endocannabinoids are released from postsynaptic neurons and travel across the synapse to bind to receptors on presynaptic neurons, influencing their signal transmission.

The process where cues associated with a drug become highly motivating and trigger cravings, even in the absence of the drug itself.

The physiological response to a drug that opposes the initial effects and is responsible for withdrawal symptoms.

This stage involves the activation of the limbic system and stress systems, leading to unpleasant feelings like anxiety, irritability, and depression.

Characterized by intense craving and an inability to stop thinking about the drug, often accompanied by impaired executive function and decision-making.

The decreased activity in the prefrontal cortex due to drug use, leading to impulsive behaviors and impaired decision-making.

Replacing the addictive drug with a similar substance that has milder effects, helping to manage withdrawal symptoms.

Blocking the effects of the addictive drug by preventing it from binding to receptors.

Inducing the immune system to produce antibodies against the drug, reducing its effectiveness.

A signal sent from a postsynaptic neuron back to a presynaptic neuron, inhibiting the release of neurotransmitters. It acts as a 'brake' on signal transmission.

The primary psychoactive compound in cannabis, responsible for the 'high' associated with marijuana use. It binds to cannabinoid receptors in the brain.

A non-psychoactive compound in cannabis known for its potential therapeutic properties. It does not produce a 'high' and may have anxiolytic and anti-inflammatory effects.

CB1 and CB2. CB1 is primarily found in the brain and is responsible for the psychoactive effects of THC. CB2 is mainly located in the immune system and plays a role in inflammation.

An endogenous cannabinoid, produced naturally by the body, that acts as a neurotransmitter. It binds to the same receptors as THC.

The study of how the body absorbs, distributes, metabolizes, and eliminates THC. It involves its half-life, depot binding, and metabolism into active and inactive metabolites.

The time it takes for the concentration of THC in the blood to reduce by half, which is approximately 30 hours.

THC binds to fat and other tissues, leading to its prolonged presence in the body, contributing to 'reverse tolerance.'

THC has potential medical applications, including pain relief, appetite stimulation, and treatment of certain conditions like cancer or AIDS.

Alcohol readily diffuses through membranes and is rapidly absorbed from the gastrointestinal tract into the bloodstream.

Alcohol easily crosses the blood-brain barrier, reaching the brain quickly and contributing to its psychoactive effects.

The body metabolizes alcohol at a constant rate, regardless of how much is consumed. This means the amount of alcohol metabolized per hour is constant.

Alcohol suppresses NMDA receptor function, reducing glutamate release. Chronic alcohol consumption then increases NMDA receptors.

Alcohol acts as a GABA agonist, increasing GABAergic activity. Chronic alcohol consumption decreases chloride ion influx, reducing GABAergic function.

Alcohol induces opioid release, which in turn stimulates dopamine release. Endogenous opioid release contributes to alcohol's pain-relieving and sedative effects.

As you progress through sleep stages 1-4, brain wave patterns become increasingly rhythmic and synchronized, reflecting a decrease in overall brain activity.

Stages 3 and 4 of sleep are characterized by slow brain waves (delta waves), indicating a state of deep sleep, essential for physical restoration and cognitive function.

REM sleep is associated with an increase in body temperature, while REM deprivation leads to a rebound effect, causing increased REM sleep later on.

Insomnia can affect different aspects of sleep, including sleep onset (difficulty falling asleep), maintenance (difficulty staying asleep), and termination (waking up too early).

Many over-the-counter sleep aids are antihistamines, which have sedative effects and can help promote sleep.

Z drugs like Zolpidem, Zaleplon, and Eszopiclone are prescription sleep medications that enhance GABAergic activity and promote sleep.

Suvorexant is a novel sleep medication that works by blocking orexin receptors, which are involved in regulating sleep and wakefulness.

Scopolamine is an anticholinergic drug that blocks muscarinic acetylcholine receptors, leading to a range of effects, including sedation, amnesia, and even hallucinations at higher doses.

The level of wakefulness is determined by the relative activity of excitatory and inhibitory chemicals in the brain.

A network of neurons in the brainstem that releases glutamate into the forebrain, promoting wakefulness.

A brain region that releases acetylcholine into the forebrain, contributing to wakefulness.

A brain area that releases norepinephrine into the forebrain, promoting wakefulness.

The hypothalamus, particularly the posterior region, plays a crucial role in wakefulness. Damage to this area can lead to excessive sleepiness.

The anterior hypothalamus is important for sleep. Damage to this area can disrupt sleep patterns.

Neurons in the hypothalamus that release orexin, a neurotransmitter essential for wakefulness. Loss of orexin-producing neurons leads to narcolepsy.

The brain's internal clock, located in the hypothalamus. It controls the release of melatonin by the pineal gland, regulating sleep-wake cycles.

Caffeine is an adenosine receptor antagonist, meaning it blocks the effects of adenosine, a neurotransmitter that promotes sleep.

Caffeine is a stimulant that increases alertness, improves mood, and enhances cognitive function. It constricts blood vessels, which may help alleviate headaches.

Major Depressive Disorder (MDD) is characterized by prolonged sadness, hopelessness, worthlessness, impaired sleep and concentration, anhedonia (loss of pleasure), and physical pain. These symptoms must significantly impair daily functioning.

High cortisol levels in depression have negative effects on brain cells, impacting neuronal plasticity. The dexamethasone suppression test measures cortisol response to stress.

Depression is linked to low levels of brain-derived neurotrophic factor (BDNF) in the blood. BDNF is crucial for brain cell growth and survival.

Depression is associated with changes in brain structures like the prefrontal cortex, hippocampus, and amygdala. There is decreased dendritic branching (connections between neurons) and reduced neurogenesis (new brain cell birth).

Electroconvulsive Therapy (ECT) induces seizures by applying electricity to the brain. It's a fast-acting treatment for severe depression.

Tricyclics, like imipramine (Tofranil), block the reuptake of serotonin and norepinephrine, increasing their levels in the synapse.

Monoamine Oxidase Inhibitors (MAOIs) inhibit the enzyme MAO, which breaks down neurotransmitters. They are effective but require dietary restrictions.

Antidepressant treatment aims to normalize brain function by increasing BDNF levels, promoting dendritic branching, and improving neurogenesis, ultimately enhancing plasticity.