Lecture 5: States of Consciousness

Consciousness

Is what we lose when we fall into deep, dreamless sleep, anesthesia, or coma and what we regain when we wake up.

Qualitativeness

A sense that each experience feels something different.

Subjectivity

A sense of the ‘I’ (Or the ‘self’) that is experiencing and acting on the world.

Unity

A sense of experiencing things as a ‘whole’ and not as a collection of parts.

Unconscious Processing “Autopilot”

Processing related to perception, motivation, emotion, certain types of memory movement breathing.

Conscious Processing:

What are we aware of on a moment-to-moment basis (e.g. what we are paying attention to).

Varieties of Consciousness (‘Altered States of Conciseness”)

-Wakefull

-Sleeping

-Dreaming

-Meditative States

-Drug States

Circadian Cycle

-Our sleep-wake cycle has a natural rhythm organized around a 24 hour day.

-The cycle is entrained light coming from the ‘retina’

-This biological clock is located in the hypothalamus

What makes us ‘feel awake?

Multiple neurotransmitters are involved in arousal and wakefulness…

-Acetylcholine

-Norepinephrine

-Dopamine

-Serotonin

What makes us feel ‘Sleepy’ - Adenosine:

Is an inhibitory neurotransmitter that accumulates in the brain throughout the walking period of day.

-By product of the brain metabolic activity.

-Caffeine is the antagonist of adenosine receptors.

The Study of Sleep:

Sleep is studied by measuring the activity of the cerebral cortex and of movements of muscles.

Electroncephalogram (EEG):

Recording of the activity of the neurons of the cortical service.

Electromyogram (EMG):

Recording of muscles and muscle tone of the body.

Electroocugram (EOG):

Recording of muscles involved in eye movements.

‘REM’ Rapid Eye Movement (REM):

-Sleep occurs every 90 minutes throughout the sleep cycle.

-The EEG shows an ‘awake’ pattern:

-High frequency, desynchronized.

REM episodes are characterized by:

-Increased respiration and blood pressure.

-Rapid ‘eye’ movements (REMs)

-Loss of muscle tone (a semi “paralysis”)

-Vivid emotional dreams!

-Sexual Arousal, even if the dreams does not have sexual content.

Psychopharmacology

Is the study of the effects of drugs on the nervous system (and
therefore on the mind & behavior).

Drug:

Is defined as a chemical that:

-is not found in the body

-Is not necessary for normal functioning.

Agonists

Drugs that enhance (boost) the effects of neurotransmitters.

Antagonists:

Drugs that inhibit (block) the effects of neurotransmitters.

Drugs effects on Receptors: Agonists

An Agonists binds to neurotransmitter binding site and leads to the opening of an ion channel.

-e.g., the drugs mimic the effect of the natural neurotransmitter.

Stimulants

Increase excitation in the brain, usually by

1) Binding into glutamate receptors or antagonists or

2) By increasing the levels of classical excitatory neurotransmitters (e.g., dopamine, norepinephrine.

Sedatives (&Tranquilizers):

increase inhibition in the brain, usually by binding to glutamate receptors as antagonists or to GABA receptors as antagonists.

-Sedatives and tranquilizers hyperpolrize neuron

Excitatory Transmitters

Influx of Na+ ions

-ESPS

Excitation Threshold:

The influx of positively charged sodium ions makes the neurons more excited and more likely to reach threshold.

Inhibitory Transmitters (e.g., Gaba)

The influx of negatively charged chloride ions makes the neurons more inhibited and less likely to reach threshold.

Stimulant Drug

That boosts the effects of glutamate would likely make this neuron even more likely to fire an action potential!

Sedative Drug

That boosts the effects of GABA would make this neuron even less likely to fire an action potential!

Stimulants

Dose:

-Concretion and attention

-Wakefulness

-Anxiety

-Too much stimulation = seziures

Sedatives (And Tranquilizers)

Dose:

-Relation

-Sedation

-Sleep

Too much sedation=coma

Classical Stimulants

Block reputake of dopamine and norephrine leading to increased excitation in the brain and the body.

-Stimulants behave as agonists.

Hypothalamus

Critical for life-sustaining drives (thirst, hunger); plays a key role in sexual and aggressive behavior; links the nervous system to the endocrine system.

Hippocampus

Involved in the formation of memories of everyday events (e.g. declarative memories)

Nucleus Accumbens

The “reward center” of the brain; critical for experience of pleasure.

Amygdala

Involved threat detection, fear and for encoding the emotional aspects of memories.

Cocaine and Dopamine Reputake:

-Cocaine ultimately behaves as a dopamine agonists because it increases the amount of dopamine at synapses.

-Cocaine is technically an antagonist of the dopamine reptuake pump.!

How to stimulants Increases SNS Activity:

(By blocking norepinephrine reputake)

-Pupil Dilation

-Bronchial Dilation (increased oxygen availability)

-Heart rate and blood pressure

-Adrenaline release (from the Adeline Glands)

-Digestive Glands Processes (and Hunger)

Norepinephrine

Is the neurotransmitter released by the sympathetic nervous system to activate flight or fight response.

Classical Sedatives and Tranquilizers: Barbiturates

-Agontists of Gaba Receptors

-Increase inhibition in the brain

-Includes Nembutal, Luminal and Seconal

-Overdose protein is very high!

Classical Sedatives and Tranquilizers: Benzodiazpines

-Agonists of GABA receptors

-Increase inhibition in the brain

-Includes inhibition in the brain

-Includes Valium, Xanax, Ativan, Klonopin

-Overdose potential typically low unless combined with other sedatives (e.g. alcohol)l

Classical Sedatives and the GABA receptor:

Classical sedatives and tranquilizers bind to GABA receptors and, when GABA is bound, lead ti increased hyperpolarization.

Ethyl Alcohol:

-’A typical’ sedative.

-Alcohol is an agonists of GABA receptors.

-It also works as an antagonists of glutamate receptors.

-Increases inhibition, relaxation and sedation in the brain.

-Has a mild dopamine (rewarding effect)

Stimulants: Caffeine

Drug Class: Stimulant

Primary Nt(s) Targeted: Adenosine

Mechanism of Action: Antagonist of the adenosine receptor.

Effects: Wakefulness; increased attention and concentration; insomnia. (close dependent)

Stimulants: Amphetamines

Drug class: Stimulant

Primary Nt(s) Targeted: Dopamine, Norepinephrine

Mechanism of Action: Reputake inhibitor (Antagonists of the dopamine and norepinephrine reputake pumps)

Effects: Wakefulness; increased attention and concentration; euphoria; insomnia, anxiety; panoria, mania, and/or psychosis; seizures (dose-dependent in the order)

Stimulants: Cocaine

Drug Class: Stimulant

Primary Nt(s) Targeted: Dopamine, Norepinephrine

Mechanism of Action: Reputake Inhibitor (Antagonists of the dopamine and norepinephrine Reputake pumps)

Effects: Wakefulness; increased attention and concentration; euphoria; insomnia; anxiety; paranoia, mania and/or psychosis; seizures. (Dose dependent and that in order)

Sedatives and Tranquilizers: Barbiturates

Drug Class: Sedative

Primary (NT) System(s) Targeted: GABA

Mechanism of Action: Agonists of the GABA receptor

Effects: Relaxation, sedation, sleep, coma, death. (Dose dependant, in that order)

Benzodiazepines: Tranquilizer

Drug Class: Tranquilizer

Primary (NT) System(s) Targeted: GABA

Mechanism of Action: Agonists of the GABA receptor

Effects: Relaxation; Sedation, sleep, Coma (Dose-dependant in that order)

Antihistamines: Sedative

Drug Class:

Primary (NT) System(s) Targeted: GABA

Mechanism of Action: Agonists of the GABA receptor Antagonists of glutamate receptors

Effects: Disinhibition; mood changes (e.g. Euphoria) impaired coordination; relaxation; sedation, sleep. (Dose-dependant)