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75 Cards in this Set

  • Front
  • Back
Franz Gall
Pierre Flourens
Franz Gall: Phrenology!
Pierre Flourens: Extirpation (ablation).
William James (what's the system?)
William James: Functionalism.
John Dewey
John Dewey: Functionalist. Started it with his paper, criticism of the reflex arc.
Paul Broca
Paul Broca: Specific functional impairments are linked to specific brain lesions.

Broca's Area: A language area in the dominant hemisphere.
Phineas Gage
Phineas Gage (1848): Damage to prefrontal cortex changed his personality.
Johannes Muller
Johannes Muller: Identified law of specific nerve energies. Each sensory nerve is excited by only one kind of energy. And the brain interprets stimulation of that nerve as being that kind of energy.

Sensation depends on the part of the brain the nerves stimulate vs. the stimulus that activates the nerves.
Hermann von Helmholtz

Sir Charles Sherrington
Hermann von Helmholtz: Measured speed of nerve impulse in terms of reaction. Helped transition psych into natural sciences.

Sir Charles Sherrington: Inferred the existence of synapses. Though he thought they're transmitted electrically, but it's actually CHEMICAL TRANSMISSION.
CNS and PNS (an overview)
Nervous System

1. Central NS: Brain, Spinal Cord.

2. Peripheral NS
a. Somatic NS
b. Autonomic NS
i. Parasympathetic NS
ii. Sympathetic NS
Nerve Cells (three types: Afferent, Efferent, Interneurons. And the Reflex Arc).
Three types of Nerve Cells:

1. Sensory Neurons (afferent): Transmit sensory information from receptors TO the spinal cord and brain.
Afferent fibers Ascend to the brain.

2. Motor Neurons (efferent): Transmit motor information from brain and spinal cord to the muscles.
NOTE: Efferent fibers Exit the brain.
3. Interneurons: Found between other neurons, the most numerous. Located mostly in the brain and spinal cord and liked to reflexive behavior.

Reflex Arc: Painful stimulus TO spinal cord. Sensory neurons connect with Interneurons in Spinal Cord. Send message to brain. Interneurons in the spine transmit pain info to the motor neurons. The motor neurons tell your foot to move. By now the original sensory information has made it to your brain, but your muscles have already responded to the pain.
Autonomic Subdivisions of the Brain (and function)

Discuss: Forebrain (cerbral cortex, basal ganglia, limbic system, thalamus, hypothalamus)
Autonomic Subdivisions of the Brain (and function)

Forebrain:
1. Cerebral Cortex: Complex perceptual, cognitive, behavioral processes
2. Basal Ganglia: Movement
3. Limbic System: Emotion and Memory
4. Thalamus: Sensory relay station
5. Hypothalmus: Feeding, fleeing, fighting, fucking (all the fun things I'm not doing cause I'm studying for this shit)
Autonomic Subdivisions of the Brain (and function)

Discuss: Midbrain (inferior and superior colliculi)
Autonomic Subdivisions of the Brain (and function)

Midbrain:
1. Inferior and Superior Colliculi: Sensorimotor rel
Autonomic Subdivisions of the Brain (and function)

Discuss: Hindbrain (cerebellum, medulla oblongata, reticular formation)
Autonomic Subdivisions of the Brain (and function)

Hindbrain:
1. Cerebellum: Refined motor movement.
2. Medulla Oblongaga: Vital functioning (breathing, digestion)
3. Reticular Formation: Alertness and arousal
The Hypothalamus (Lateral, Ventromedial, Anterior)
The Hypothalamus
1. Lateral HT: Hunger Center. Tells you when to start eating and drinking. Lesions lead to aphagia: Lacking Hunger.
2. Ventromedial HT: Satiety Center. When to stop eating. Lesions lead to hyperphagia: Very Hungry

3. Anterior HT: Sexual Activity. Lesions lead to Asexuality.
"Sham Rage" (remove what?)
"Sham Rage:" From removing a cat's cerebral cortex and keeping the Hypothalamus. Cats are insanely aggressive.

Remove Cortex and HT: Can't defend themselves or be aggressive. Can't coordinate and organize emotional response.

So: Cerbral Cortex= Controls defensive/ aggressive behavior
HT= Ability to defend self.
The Limbic System (in Forebrain. Define Septum, Amygdala, Hippocampus)
The Limbic System (in the forebrain)

1. Septum: Pleasure center identified by Olds and Milner. Inhibits aggression, lesions produce "sham rage."

2. Amygdala: Defensive and aggressive behavior (studied by Kulver and Bucy). Lesions produce docility and hypersexual states.

3. Hippocampus: Memory, lesions produce anterograde amnesia.
Autonomic NS
NNS (Walter Cannon studied it):

ANS (Part of the Peripheral Nervous System): Regulates heartbeat, respiration, digestion, glandular secretions, body temperature, it's AUTOMATIC (autonomic) functions.

ANS (in the Peripheral Nervous System) has two ANTAGONISTIC subdivisions: Sympathetic NS and Parasympathetic NS.
Sympathetic NS

Parasympathetic NS
Sympathetic NS and Parasympathetic NS (Make up the Autonomic NS, in the Peripheral NS)


1. Sympathetic NS: "fight or flight." Fear and rage reactions, increased heart rate, blood sugar level, respiration, pupils dilate, adrenaline.

2. Parasympathetic NS: Conserve energy. Resting and sleeping states, reduced heart and digestion states, manages digestions, acetylcholine.
The Hindbrain (manages what?)
The Hindbrain: balance, motor coordination, breathing, digestion, general arousal (sleep/ awake). Manages VITAL functions.

Forms the brainstem along with the mindbrain.
The Midbrain (manages what? Receives what info?)
The Midbrain: Manages sensorimotor reflexes.

Midbrain receives sensory and motor information
Evolution of brain features (in order)
Evolution of the brain (in order)

Phelogeny: Evolutionary development in humans.

1. Brainstem
2. Limbic system: A group of neural structures associated with emotion and memory, aggression, fear, pain.
3. Cerebral cortex: The outer covering of the cerebral hemispheres.
Hindbrain (what's the medulla oblongota, pons? Cerebellum? Reticular formation?)
Hindbrain:

1. Medulla Oblongata: Vital functioning (breathing, digestion)
2. Pons: Above medulla. Sensory and motor tracts above medulla and cortex.
3. Cerebellum: Maintaining posture, balance, body movement.
4. Reticular Formation: From hindbrain to midbrain, a ntwork of nerve fibers. Regulates arousal and alertness (sleep/wake). Anesthesia: Depresses reticular formation.
Reticular Formation: Arousal, Alertness, Attention.
Midbrain (Associated with what? What's the Superior and Inferior Colliculi?)
Midbrain: Associated with involuntary REFLEX responses triggered by visual or auditory stimuli.

2 Prominant Midbrain Nuclei:

i. Superior Colliculi: Gets visual input. Superior= Seeing.

ii. Inferior Colliculi: Gets auditory input. Reflexes to sudden noise.
Forebrain (Thalamus, Walter Cannon? Osmoregualtion, Drive Behaviors? Hypothalamus?)
Forebrain: Two cerebral hemispheres.

1. Thalamus: Relay station for incoming SENSORY information (all except smell). Sorts input, transmits it to appropriate areas in the cerebral cortex.

2. Hypothalamus: Lateral, Ventromedial, Anterior: Homeostatic functions, emotional experiences during high emotional states, aggression, sexual behavior, some endocrine functions, ANS.

Hypothalamus: Regulates WATER balance (osmoregulation)

Walter Cannon: Conceptualized homeostasis. HT: Big on DRIVE behaviors: Hunger, thirst, sex.
Basal Ganglia (location, function, extrapyramidal motor system?)
Basal Ganglia: are a group of nuclei in the brain interconnected with the cerebral cortex, thalamus and brainstem.

Function: motor control, cognition, emotions, and learning.

Function: Get info from cortex, coordinate body movement to the brain and spinal cord. Does this with the ...

EXTRAPYRAMIDAL motor system: Gets info re: body position (like the basal ganglia), carries it to brain and spinal cord. Helps make our movements smooth, posture steady.

Disease with Basal Ganglia: PARKINSON'S: Jerky movements, uncontrolled resting tumors. Also, maybe Schizophrenia.
Ventricles
Ventricles: One of a system of communicating cavities within the brain that are continuous with the central canal of the spinal cord.

Ventricles: Have cerebrospinal fluid.

Too large ventricles: Pattern of symptoms re: schizophrenia
Limbic System (Location? Basic funtction? Septum, Amygdala, Hippocampus? Kulver and Bucy Syndrome? Septal Rage? H.M's anterograde amnesia)
Limbic System: Emotions and memory. In the forebrain.

1. Septum: Primary pleasure center. (Olds and Milner: discovered that rats love it).

Septum also inhibits aggression. Without it, there's Septal Rage

2. Amygdala: Defensive and aggressive behavior.

Without it: Aggression and fear reactions are reduced Also, lesions produces docility and hypersexual states.

(Kulver and Bucy Syndrome: Changes in animals resulting from removal of amygdala)

3. Hippocamus: Memory, learning. HM: removed his hippocampus, intelligence intact, but couldn't remember anything new (Anterograde amnesia)
Amnesia (antergorade, retrograde)
Amnesia:

1. Anterograde: Can't make new long term memories (H.M., Brenda Milner studied him)

2. Retrograde: Memory loss for events that happened BEFORE injury.
Cerebral Cortex (where is it? What's a convolution? What's the F-POT? Describe the Frontal Lobe, its two basic regions. What's an association area? Damage to prefrontal cortex? Prefrontal lobotomies for what? Motor Cortex, and Broca's Area- where, function?)
Cerebral Coretex (in the forebrain) aka neocortex: The outer surface of the brain.
CC has convolutions: bumps and folds. Helps with increased cellular mass.

2 Cerebral Hemispheres and Four Lobes (the F-POT)!

1. Frontal Lobe (of CC, Forebrain):
i. Prefrontal lobes: An executive functioner, supervises the operations of other brain regions. Supervises perception, memory, emotion, impulse control, L. Term planning.

NOTE: the prefrontal cortex doesn't actually DO like, emotions and memory. It rather delegates the functions by communicating and reminding.

The Prefrontal Cortex is an ASSOCIATION area

Damage to Prefrontal Cortex: Impairs supervisory function. Person's less in control, depressed. Vulgar comments or apathetic.

Prefrontal Lobotomies: Used to treat schizophrenia, but no longer.

ii. Motor Cortex (Location: The Frontal Lobe of the Cerebral Cortex, in the Forebrain): Initiates VOLUNTARY motor movements by sending a neural impulse down the spinal cord toward the muscles.

Motor cortex is a projection area.

iii. Broca's Area (in the FRONTAL lobe). For speech production. Usually in the "dominant" hemisphere (left for most people)
Association vs. Projection Areas
1. Association Area: Combines input from different brain regions
Humans: Have more space for association areas.

2. Projection Area: Receive incoming sensory information or send out motor- impulse commands. ex/ Visual Cortex, Motor Cortex.
Motor Cortex (where? Function? A projection area?)
MOTOR CORTEX:

Location: The Frontal Lobe of the Cerebral Cortex, in the Forebrain.

Initiates VOLUNTARY motor movements by sending a neural impulse down the spinal cord toward the muscles.

Motor cortex is a projection area.

The neurons in the MC are arranged systematically. Top: Genitals, toes, feet, leg, hip, trunk, shoulder head neck, arm, elbow, wrist, fingers (little to thumb), eye, nose, face, lips, teeth, tongue, pharynx, intra-abdominal).

Because certain sets of muscles need more control than others, they get more space in the motor cortex.
F-POT (of the Cerebral Cortex):
The Pareital Lobe:
(What's the somatosensory cortex? The Sensorimotor Cortex? Spatial Processing)
Parietal Lobe (of Cerebral Cortex's F-POT):

Rear of frontal lobe. Somatosensory Cortex: Projection area for all INCOMING sensory signals for touch, pressure, temp, pain.


Somatosensory Cortex: Related to motor cortex, together called SENSORIMOTOR CORTEX.

Central Region of Parietal Lobe: Spatial Process, manipulation, maps, orientations, block in space.
F-POT (of CC): The Occipital Lobe (the visual cortex, Hubel and Wiesel's work, other functions?)
The Occipital Lobe (in the F-POT of CC):

At the rear of the brain. Has the Visual Cortex (aka Striate Cortex): Hubel and Wisel worked on this.

Also, Occipital lob plays role in learning, motor control.
F-POT (of CC in Forebrain): The Temporal Lobe
The Temporal Lobe (in CC):

1. Auditory Cortex
2. Wernicke's Area= language reception, comprehension. Understand spoken language)
3. Temporal Lobe: Memory processing, emotional control, language.

Stimulate temporal lobe: Evoke memories for past. Why? The hippocampus is INSIDE the temporal lobe.

NOTE: The lobes (F-POT inside the Cerebral Cortex, Forebrain) are NOT independent.
Cerebral Hemispheres' Communication (contralateral, ipsilateral)
Cerebral Hemispheres Communication

1. Contraleteral communication: When one side of the brain talks to the opposite side of the body.
2. Ipsilateral communication: Like in smell, the hemespheres communicate with the SAME side of the body.
Cerebral Hemispheres (dominant and nondominant)

What does nondom do? What's Wernicke's and Broca's? Where are they? What's the nondom do?)
Cerebral Hemisphere:

1. Dominant: Usually opposite of your writing hand, so left.
Function: Analytical, details. Language, logic, math,

1. Broca's area: Lang. production. Articulation center of brain, controlled speech muscles

2. Wernicke's area: Lang comprehension for written, spoken language. Gets input from auditory cortex [in temporal lobe] and visual cortex [in occipital lobe].

2. Nondominant Hemisphere: Sensitive to emotional tone in spoken language. Also, intuition and creativity, music, spatial processing, helps process and assemble a stimulus into a holistic image.
Roger Sperry and Michael Gazzinga
Roger Sperry and Michael Gazzinga: Found that severing the Corpus Collosum (fibers that connect the 2 hemespheres), creating a Split Brain, you'll stop the sharing of information between the hemispheres. It created specialization.
Dominant vs. Dominant: Rough function overview
1. Dominant Hemisphere: Letters, words, language-related sounds, speech, writing, reading, arithmetic, complex voluntary movement.

2. Right Hemisphere (Nondominant): Faces, emotions, music, geometry, sense of direciton.
Neurons Anatomy (what's the cell body, dendrite, axon, and terminal buttons?) What energy does the neuron transform?
Neurons Anatomy:

4 basic parts:
1. Cell body (soma): neuron's energy center.
2. Dendrites: Get sensory information from other neurons through Postsynaptic receptors. If you stimulate the dendrites, they'll fire = generate an electrical impulse.
3. Axon:
4. Terminal Buttons: The end of an axon. The TB's have sacs (vesicles) with neurotransmitters: Chemical substances released when the neuron fires.

When the neuron "fires," nt's are released into the synapse by the vesicle (the synapse= space separating the terminal buttons of one neurons from the dendrites of another).

So, the neuron transforms chemical energy into electrical energy and vice versa.
Glial Cells (function? what's a myelin sheath? What's it do?)
Glial Cells: Supporters and caretakers of neurons. Glial cells: Insulate axons with a myelin sheath: Insulates nerve fibers from one another. Helps speed up conduction velocity.

Myelin Sheath: Myelinated and ummyelinated areas. Allow an impulse to transmit down the axon in a saltatory manner (it's faster)
Dendrites (vs. axons)
Dendrites (vs axons)

1. Most axons are mylenated (dendrites are not)
2. Dendrites can regenerate and change branching patterns, and axons can't.
3. Function: Dendrites are RECEPTORS and axons are a communication avenue.
Neural Transmission (when's it electrical? When's it chemical?)
1. Neural conduciont: WITHIN the neuron, it's an ELECTRICAL process (it's among the dendrites, cell body, axon).

2. Neural transmission BETWEEN neurons is a CHEMICAL process that's always at the synapse.
Neural Transmission: (resting potential, What's an ion, what's polarized?)
Neural Transmission: resting
potential, action potential, neurotransmitter release).

1. Resting Potential (aka membrane potential): Slight, negative electrical charge stored in the cell membrane.

Cell membrane: Thin layer of fatty molecules separating the inside of the neuron from the outside. It's semipermeable.

ION: A small, electrically charged particle. Big IONS are trapped, can't pass though cell membrane.

Many big ions INSIDE the C.M are NEGATIVELY charged, and there's a net negative charge INSIDE the neuron = the neuron is POLARIZED.
Neural Transmission: Sodium-Potassium Pump
Neural Transmission: Sodium-Potassium Pump.

* Both sodim and potassium are positively charged ions.
* Potassium ions are usually INSIDE the cell and Sodium ions are OUTSIDE.
*They want to move the other way (sodium wants in, potassium wants out).
*To maintain the resting potential, the cell membrane has to "pump" the positively charged sodium ions back outside, and keep the potassium ions in.. That's the Sodium-Potassium Pump!
The Firing Cycle of the Neuron (resting potential, depolarization, action potential spike, hyperpolarization)
The 4 step firing cycle of the neuron:

1. Resting Potential: When a neuron's polarized at -70mV.

2. Depolarization: When a stimulus is big enough to make the membrane's potential INCREASE the threshold potential, usually to -50mV.
"Depolarizaion" = FIRING the neuron.

3. Action Potential Spike: At reaching the threshold, the membrane makes an Action Potential Spike (when the cell membrane's charge becomes negative for a tiny while).

How? At threshold, the membrane lets sodium ions in, cell membrane charge becomes positive.

4. Repolarization: Cell membrane goes back to being negative charged (by letting positively charged potassium ions out of membrane)

4. Hyperpolarization: the restoration of the membrane's negative charge happens very fast, and the membrane overshoots its original charge, causing HYPERPOLARIZATION.

Here the cell membrane is resistant to inflow of positive sodium ions, and its internal voltage is gradually restored to original value.
Refractory Period (of neuron)

What's Absolute and Relative Refractory Period, and which firing cycle stage do they correspond to??
1. Neuron's Refractory Period: After the Action Potential's been triggered, the neuron can't fire again until the AP's finished the firing cycle.

Refractory Period's Stages
i. Absolute RP: Neuron is totally unresponsive to additional stimulation. It's the depolarization period.
ii. Relative Refr. Period: After the action potential spike,during repolarization. When the membrane's hyperpolarized, you need a stronger stimulation to reach threshold potential.
All-or-nothing law (re: depolarization's critical prd, re: action potential voltage)
All or Nothing Law: The neuron fires each time depolarization's at critical threshold (-50mV).

When action potential begins, its voltage always peaks at same intensity (+35mv), regardless of trigger stiumulus' intensity
Axon Hillock (location? What happens there? What's converted?)
Axon Hillock: Where the action potential originates. It's a small elevation on a neuron where axon meets cell body.

At the Axon Hillock, the graded potential in cell body becomes the all-or-nothing porential of the axon.

Then the action potential is transmitted as an electrical impulse along the axon to the terminal buttons.
Myelin (what's saltatory conduction? What happens at node of Ranvier? Where does depolarization happen? Why regenerate action potential at nodes?)
Myelin:

1. Saltatory conduction: Fast conduction along a myelinated axon.

* Depolarization happens at the nodes.
2. Myelin Sheath has gaps along axon called nodes of Ranvier (where axon is uncovered). When action potential reaches a node, it makes a new action potential in the node next to it.

Action potential skips from node to node (this is faster, and node travel REGENERATES the action potential without losing INTENSITY)
Chemical Neural Transmission (presynaptic membrane? Postsynaptic membrane?)
Chemical Neural Transmission:

The space between terminal button and dendrite is the Synaptic Cleft. The TB facing the SC = Presynaptic Membrane. It has VESICLES with neurotransmitters.

The Dendrite facing Synaptic Cleft = postsynaptic membrane. It has RECEPTORS.
What can happen to the neurotransmitter in the synapse? (3 things) What's binding? After binding?
What can happen to the neurotransmitter in the synapse?

1. The NT's can attach themselves to receptor sites.
2. The NT's can stay in the synapse, where they're destroyed, washed away.
3. The NT's can be drawn back to the vesicles in the terminal buttons= Reuptake.

BINDING: When a neurotransmitter actually fits, attaches itself to, the receptor sites, and communication between nerve cells occurs.

After binding, the neurotransmitter is eliminated from the synapse though reuptake or destruction.

The synapses is where some drugs act to change behavior.
Postsynaptic Potential (IPSP, EPSP, Graded Potentials)
Postsynaptic Potential:

After binding, the nt generates a PSP (Postsynaptic Potential): a tiny electrical charge.

Two things can happen:

1. EPSP (Excitatory PSP): Makes it more likely a neuron will fire
2. IPSP (Inhibitory PSP): Makes it less likely a neuron will fire.

PSP's are GRADED Potentials: Their voltage can vary in intensity. Depends of number of nt's binding to receptor sites.

Graded Potentials
1. Can be weak or strong
2. GP: Spread out from the original site, so their voltage gradually weakens.
Eric Kandel's Sea Snails
Eric Kandel's Sea Snails: Aplysia are those sea snails. Learned habituation: to not withdraw their gills with harmless stimulation.

In this case, habituation meant the aplysia were releasing smaller amounts of nt's into their neurons that controlled the gill-withdrawing reflex.

It's a change in synaptic transmission.
Neurotransmitter:
Acetylcholine
Neurotransmitter:
Acetylcholine: nt's found in CNS and PNS.

Parasymp. NS: Ach transmits nerve impulses to muscles.

CNS: AcH linked to Alzheimer's (memory loss, loss of AcH in neurons connected with hippocampus)
Monoanime Neurotransmitters (noepinephrine and depression mania, dopamine and schizo- dopamine Hypothesis, amphetamines. Dopamine and Parkinson's, and SEROTONIN,Monoamine Theory of Depression)
Monoanime Neurotransmitter
(aka Catecholmines aka Biogenic Amines)

1. Norepinephrine (noradrenaline): Alertness, wakefulness. Implicated in depression [so's serotonin], mania

2. Dopamine: A neurotransmitter associated with movement and posture. Lots of dopamine in the basal ganglia (makes our movements smooth and steady posture).
Dopamine Hypothesis of Schizophrenia: Delusions, hallucinations, and agitation come from either too much dopamine or too much sensitivity to dopamine.

Evidence for Dop. Hyp:

1. Amphetamine: Enhance action of dopamine at synapse, too much of this drug created Amphetamine Psychosis (looks like schizo)
2. Phenothiazines (an antipsychotic drug): Reduce sensitivity of dopamine receptors.

Dopamine and Parkinson's: From a loss of dopamine-sensitive neurons in the basal ganglia.

3. Serotonin: Regulates mood, eating, sleeping, arousal, plays a role in depression and mania.

So: Serotonin Selective Reuptake Inhibitors: ex/ Prozac.

Monoamine Theory of Depression: Theories linking noepinephrine/ serotonin to mania and depression (depending on over or undersupply).
Dopamine and Parkinson's (why? What's relation to schizophrenia? What's L-Dopa?)
Dopamine and Parkinson's: From a loss of dopamine-sensitive neurons in the basal ganglia's substantia nigra. No dopamine= resting tumors and jerky motor movements).

Also:
Tradive Dyskinesia: When schizophrenic patients take antipsychotic meds too long and develop Parkinson's-like symptoms

L-Dopa: Increases dopamine levels in the brain. Real dopamine doesn't pass the blood-brain barrier. BUT: When L-Dopa makes too much dopamine, it can make psychotic symptoms.
GABA (what's it do to neuron? Which type of PSP?)
GABA: Produces Inhibitory PSP, stabilizes neural activity in brain. Causes hyperpolarization in the postsynaptic membrane.
Peptides
Peptides (two or more amino acids joined together).

1. Neuromodulators (neuropeptides): Their synaptic action is slow and has a longer effect on the postsynaptic cell.

ex/ Endorphines and Enkephalins (act like morphine): Peptides.
What behaviors and disorders are linked to neurotransmitters?

1. Acetylcholine
2. Epinephrine (adrenaline)
3. Norepinephrine (noradrenaline)
4. Dopamine
5. Serotonin
6. GABA
7. Endorphin (a peptide)
What behaviors and disorders are linked to neurotransmitters?

1. Acetylcholine: Voluntary muscle control. Linked to Alzheimer's.

2. Epinephrine (adrenaline): "fight or flight."

3. Norepinephrine (noradrenaline): Wakefulness, alertness. Linked to depression and mania.

4. Dopamine: Smooth movement and steady posture. Linked to Schizophrenia, Parkinson's

5. Serotonin: Mood, sleeping, eating, dreaming. Linked to depression and Mania.

6. GABA: Brain "stabilizer." Linked to anxiety disorders.

7. Endorphin (a peptide): A natural pain killer.
Psychopharmacology: Sedative- Hypnotic Drugs
Psychopharmacology: Sedative- Hypnotic Drugs

Depressants: Slow down the CNS. Low dose: Reduce anxiety. Med: Sedation. High dose: Anesthesia or coma.

Sedative-Hypnotic Drugs: Synergistic (additive in effect) ex. alcohol and barbituates.

ex. Benzodizepines (tranquilizers for sedatives ex. Valium) and barbiturates (sedatives for less anxiety): Facilitate GABA action (stabalizes body).

Alcohol: Can result in memory disturbances.
Korsakoff's Syndrome: Anterograde amnesia for chronic alcoholics, also trained to malnutrition.
Behavioral Stimulants
Behavioral Stimulants: Drugs that increase behavioral activity by increasing motor activity/ counteracting fatigue. Stimulate: Dopamine, Noepinephrine, Serotonin.

Antidepressants : Elevate mood and increase activity level, better sleep patterns and appetite.

i. Tricyclic antidepressant: Helps transmissions of norepinephrine or serotonin at the synapse. Block reuptake of monoamines.
ii. MAO inhibitors: Increase supply of norepinephrine and serotonin (b/c MAO is an enzyme that breaks them down).

Prozac: Selective Serotonin Reuptake Inhibitor (SSRI).: Inhibits serotonin reuptake, increases its supply in synapse.

Methylphenidate (Ritalin): Amphetamine for ad. Increases alrertness, decreases motor activity.
Antipsychotic Drugs
Antipsychotic Drugs:

Anti-schizophrenia: Thorazine, Chlorpromazine, Phenothiazine, Haloperidol (Haldol): Reduce delusional thinking, hallucinations, agitation.

They (?): Block receptor sites for dopamine, can't bind, reduce sensitivity to dopamine.

Lithium Carbonate: Treats bipolar (marked mood swings from manic highs to depressive lows). Eliminates 70-90% of symptoms, ex/ mood swings and manic symptoms.
Narcotics
Narcotics: Opium, heroin, morphine. Many bind directly to opiate receptors (normally respond to endorphins).

Psychadelics: Alter sensory perception.
Major Psychoactive Drugs (affects? Medical uses?)

1. sedative-hypnotics: Benzodiazepines (Valium)
2. Barbituates
3. Behavioral-Stimulants: i.Amphetamines
ii. Tricyclics and MAO Inhibitors
iii. Methylphenidate (Ritalin)

4. Antipsychotic Drugs:

i. Chlorpromazine:
ii. Haloperidol (Haldol)
iii. Lithium

5. Narcotics (Opiates):
i.. Heroin and morphine
Major Psychactive Drugs:

1. Sedative-Hypnotics: Benzodiazepines (Valium): Affects GABA. Used as tranquilizers (anxiety)

2. Barbituates: Affects GABA. Sedatives.
3. Behavioral-Stimulants:

i.Amphetamines: Affects norepinephrine, dopamine. Used for narcolepsy.
ii. Tricyclics and MAO Inhibitors: Noerpinephrine, serotonin (used for depression).
iii. Methylphenidate (Ritalin): Affects dopamine. Used for ADD.

4. Antipsychotic Drugs:

i. Chlorpromazine: Affects dopamine. Used for Schizo.
ii. Haloperidol (Haldol): Affects dopamine. Used for schizo.
iii. Lithium: Unknown system affected. Used for bipolar.

5. Narcotics (Opiates):
i.. Heroin and morphine: Affect opiate receptors. Used for pain killing.
The Endocrine System (messenger is? Travels though? Makes what- both hormone and nt?
The Endocrine System communicated with chemical messengers called hormones.

It's slower b/c message is through the bloodstream.

Involved in: Slow, continuous body processes, but responds fast to life-threatening situations.

ES makes adrenaline = epinephrine (both a nt and a hormone).

Also endocrine system: Regulates sexual arousal, reproduction.
Glands and Hormones (Pituitary Gland: Work with what? Anterior P and Posterior P do what?)
Glands and Hormones: The Hypothalamus works directly with the PITUITARY Gland: the End. System's "master gland."

P.Gland:
i. Anterior pituitary: Master, releases hormones.(HT controls it)
ii. Posterior: Secreted hormones into bloodstream that travel to other endocrine glands, activates other glands to make hormones. Those hormones tell certain organs to change functioning.
Sexual Development (controlled by what glands? Dad gives what? Androgens? Androgen insensitivity?)
Sexual Development: Hormones regulated by HT and Pituitary initiate, control, halt development of Primary Sex Char. [present at birth] and Secondary Sex Characteristics [at puberty].

Dad: Gives X or Y. XY: Male!

Male development: Androgens (in fetal development). #1 androgen is testosterone. Y chromosome initiates it.

Androgen-insensitivity syndrome: When a fetus can't make/use androgen, it follows a female pattern regardless of chromosomal genetic sex.
Main endocrine glands and their function:

1. Hypothalamus:
2. Pituitary
3. Thyroid:
4. Adrenal Medulla:
5. Ovaries:
6. Testes:
Main endocrine glands and their function:

1. Hypothalamus: Controls release of pituitary hormones

2. Pituitary: "The master gland," Triggers hormone secretions in other endocrine glands

3. Thyroid: Affects metabolism rate; growth and development

4. Adrenal Medulla: Makes adrenaline (epinephrine), increases sugar output of liver. Also increases heart rate "fight or flight" response.

5. Ovaries: Estrogen stimulates female sex characteristics. Progesterone prepares uterus for implantation of embryo.

6. Testes: Testosterone makes male sex charac, relevant to sexual arousal.
Puberty (gonadoptropic hormones)
Puberty:

1. At puberty the pituitary gland produces gonadotropic hormone: Make a dramatic increase of hormones by testes/ ovaries.

Males: Gonadotropins make facial hair, deeper voice.
Females: Stimulate ovaries to secrete estrogen, accelerates development of female genitalia.
Menstruation
Menstruation:

Estrus: Female reproductive cycle in animals.

Menstrual: 1. Pituitary gland secretes FSH (follicle stimulating hormone), stimulates growth of ovarian follicle (sphere protecting egg).
2. LH (Luteinizing Hormone): Associated with ovulation, release of egg from ovaries.
*Ovaries: Make Estrogen (maturation and release of egg from ovum) and Progesterone (Prepare uterus for implantation).
3. Ovum is fertilized? It divides, attaches itself to the uterine wall. If not, est. and proges. will go down, you'll have a period!
Neuropsychology Research Methods
(ablation, electrically stimulating/recording brain activity, electrodes, rCBF, and CAT,MRI,PET)
Neuropsychology Research Methods:

1. Ablation (extirpation): Induced brain lesions. By electrode, then intense heat, cold, electricity. The Stereotaxic instrument: Finds brain areas for electrode.

2. Electrically stimulating/ recording brain activity (by Wilder Penfield's approach): Leads neurons to fire, activates a relevant behavior/process. The person's awake, and you map out cortical maps.

3. Electrode Uses: i. Study deeper regions of the brain (electrical activity to elicit sleep, sexual arousal...) . ii. Record electrical activity of the brain (even into one individual neuron. ex/ Hubel and Wisel: recording monitors an ongoing activity).
iii. Electrodes: Record electrical activity generated by a large number of neurons (electrodes on top of head: Broad patterns of electrical activity detected by EEG, like in sleep research).

4. rCBF (regional cerebral bloodflow): Detect broad patterns of neural activity based on increased blood flow to certain areas.

5. CAT, MRI, PET: Noninvasive computer scanner to detect radioactivity in bloodstream.
Clinical Disorders (Luria? Apasia? Agnosia? Apraxia? Dementia?)
1. A.R Luria: Wrote about neuropsychological disorders.

2. Apahsia: "No speech."
i. Broca's Aphasia: impairments in producing spoken language.
ii. Wernicke's Aphasia: can't understand spoken language.

3. Agnosia: "not knowing." Perceptual recognition. Like, you can see something, but you don't know what it is you see.
ex. recognition takes place in a projection area close to the visual cortex.
i. Visual agnosia: Can't visually recognize things.
ii. Tactile agnosia: Can't recognize tactile things.

3. Apraxia: Impairment in organized motor action (apraxia= Can't act). Simple actions can become fragmented/ disorganized).
Why? Apraxia, projection areas in the motor cortex (send impulses down to muscles) are intact. The problem's in the association areas near it, which organize simple movement into predictable acts.

4. Dementias: Neurological disorder characterized by a loss in intellectual functioning. Alzheimer's: Progressive memory loss. Huntington's/ Parkinson's Disease: Dementia. Less and slower cognitive deficits.
But: Motor systems in Huntington's (loss of motor control) and Parkinson's (resting tremors, muscles rigid) are worse.
Sleep and Sleep Disorders: Reticular formation.
Sleep and Sleep Disorders
1. Reticular Formation: In the brain stem. Keeps our cortex aware. Disconnected? Person's awake all the time.

2. Circadian Rhythms: Lasts approx. 24hours, without light and dark, it's still 24 maybe a little shorter or longer.
Brain Waves and Sleep Stages (BAT-D)
Brain Waves and Sleep Stages:

1. Mostly we use EEG to study this
Anyway, it's the Bat-D, check it.

1. Awake: Beta waves (Person is awake and alert- fast EEG activity)

Relaxed: Alpha waves: Person is awake, relaxed and with eyes closed, slower EEG activity.

Stage 1: Theta waves (light sleep)

Stage 2: Theta waves (EEG shows "sleep spindles" and k complexes

Stage 3: Delta waves. Person's more deeply asleep. Slower EEG and steeper "sleep spindles"

Stage 4L Delta waves: Deepest sleep, slowest EEG, steepest sleep spindles, relaxed muscle tone, decreased respiration and heart rate.

REM Sleep: Delta waves. "Paradoxical Sleep:" fast but irregular EEG activity, similar to waking state Relaxed muscle tone, eyes dart around, associated with dreaming.

REM sleep is also the phase of sleep in which you dream. This sleep phase begins about 70 to 90 minutes after you fall asleep. The first sleep cycle has a shorter phase of REM sleep. Toward morning, the time spent in REM sleep increases and the deep sleep stages decrease.
Sleep Disorders (Insomnia, narcolepcy, REM rebound)
Sleep Disorders

1. REM rebound: When a person who was deprived of REM sleep spends more time than usual in it.

2. No REM sleep (but other cycles yes): Irritable during waking state.

3. No sleep: Psychotic symptoms.

4. Insomnia: Can't fall asleep or stay asleep
5. Narcolepcy: Can't control when you fall asleep, you suddenly pass out!
6. Sleep Apnea: Inability to breathe during sleep, sometimes wake up for more than a minute.
Perception of Emotion and Physiology (James-Lange, Cannon-Bard, Schachter- Singer).
James-Lange Theory: We recognize emotions based on how our body reacts ("we're sad b/c we cry") Role of PNS.

Cannon-Bard Theory: Emotions reflect physiological arousal of the SNS and specific neural circuits.

Schachter-Singer Theory (two-factor theory): Unspecified physiological arousal will be labeled as different emotions depending on our mental response to environmental stimulation.