Biological Basis Of Behavoir

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James Lange Theory-

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This is still viable today- you get a stimulus (a bat), there is a physiological arousal (increased heart, etc) and then the emotion (fear) kicks in.

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Cannon-Bard Theory-

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This is now disregarded. You get a stimulus (bat) and then have both emotion and a physiological arousal together.

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Two Factor Theory-

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This is also still viable today. You get the stimulus (a bat) and then you have both physiological arousal (increased heart, etc) and cognitive interpretation (eg, I feel afraid) which leads to the emotion (fear, OMFG there’s a goddamned bat).

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The Limbic system

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the home of emotions. Mostly the amygdala and the hippocampus.

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Amygdala-

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the amygdala is also responsible for determining what memories are stored and where the memories are stored in the brain.

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Phineas Gage-

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He had damage to the orbito-frontal cortex, which led to separation of the frontal lobe from the limbic system. His IQ was intact but his ability to control his emotions was severely disrupted. Animal/childlike behaviors surfaced.
The frontal cortex assigns importance to emotions and helps control emotions.
-Alcohol also shuts down the frontal cortex.

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Frontal Lobotomy-

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-a device inserted into the orbital cavity and directed into the ventral portion of the frontal lobe.
-patients responded with a flattened affect.
-Symptoms resemble Phineas Gage’ post injury behavior.
-If a lobotomy was done right it would give the recipient a zombie-like manner.

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Kluver-Bucy Syndrome= {an emotional disorder}

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cause: bilateral damage to the temporal lobes (amygdala). Monkeys are innately afraid of snakes, monkeys with bilateral damage will not be afraid of snakes.
Symptoms-
-flat affect
-indiscriminate diet
-hypersensitivity and responsiveness to environmental stimuli.
-hypersexuality (auto, homo, hetero)
-explores all objects with mouth
-visual agnosia (have trouble recognizing objects- people with this usually use touch to identify instead).
Frontal lobe damage also frequently causes perseveration (doing things over and over).

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Conditioned Emotional response-

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-a classical conditioned response that occurs when a neutral stimulus is followed by an aversive stimulus.
-foundation of learned emotional responses (eg. phobias).
-does not require consciousness.

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Unconditioned stimulus UCS-

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the stimulus that elicits an unconditioned (unlearned) response. You get a puff of air on your eye = you blink.

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Unconditioned Response UCR-

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The response elicited by an unconditioned stimulus without prior learning.

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Conditioned Stimulus CS-

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A previously neutral stimulus that comes to elicit the conditioned response.

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Conditioned Response CR-

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A response elicited by a previously neutral stimulus that has become associated with the unconditioned stimulus.

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Anatomy of Fear Conditioning-

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-Auditory fear conditioning blocked with medial geniculate nucleus (MGN) lesions- not affected by auditory cortex lesions. What does this mean? The animal does not need to ‘hear’ the tone to respond to it. Not conscious of the tone- but still responds to it.
Subliminal advertisement- subtle stuff in ads you don’t consciously see but you get a response to. May not be that effective.
-Critical pathways: MGN to amygdala.
-Amygdala lesions blocks fear conditioning, so if you wanna be fearless maybe you should just need to lesion the amygdala.

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Cognition and Emotion- High Road-

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slower, requires the cortex (MGN or LGN going to cortex for processing).

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Cognition and Emotion- Low Road-

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direct projections to amygdala, FAST, allows you to respond with conscious interpretations to stimulus.

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Extinction- (not like the dinosaurs).

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-systematic desensitization
-an effective behavioral therapy for conditioned fears phobias.
However, emotional memories are strong (glucose/epi facilitate memory); flashbulb memories.
-Fear memories are permanent.
Therapists calm ppl down, relaxation techniques, move thru steps, exposure to fears until they no longer have “fear response”.

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Extinction of Fear Response-

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Def: the conditioned response goes away/ present the tone w/o the shock.
Does it erase the memory? NO! We know this b/c it comes back.
New learning occurs that inhibits old fear memories.
Requires connections between mPFC (medial pre-frontal cortex) and the amygdala, maybe using endogenous cannabinoids. Our own THC-like animals have them go thru memory again and then manipulate that memory.

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Brain region and biological/physiological responses Lateral Hypothalmus=

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sympathetic activation, increased heart rate and blood pressure. Paleness.

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Brain region and biological/physiological responses Dorsal Motor Nucleus of Vagus=

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Parasympathetic activation, ulcers, urination, defecation.

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Brain region and biological/physiological responses Parabrachial Nucelus=

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increased respiration.

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Brain region and biological/physiological responses Periaquaduct Grey Matter=

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Freezing/behavioral arrest.

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Brain region and biological/physiological responses Trigeminal facial motor nucleus=

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facial expressions of fear

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Contextual Fear conditioning and the Hippocampus-

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-just as fear of an auditory stimulus can be learned, so can fear of the environment.
-hippocampus involved:
-lesion before conditioning prevents development of contextual fear.
-they can’t acquire new fear/ can have old fear
-lesion after conditioning blocks retention of contextual fear response.
-old fear responses still intact.
You would need to lesion the amygdala to make yourself fearless.

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Schacter and Singer Two-Factor Theory:

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gave college students either epinephrine or saline. Split them into positive or negative environment. The environment had no effect on the saline recipients- but it had an effect on the ones with the epinephrine (they felt good after the good envir. bad after the bad envir.)

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Brain Mechanisms in human emotion-

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learned a great deal by studying patients with brain damage.
functional imaging of the healthy subject.
amygdala and prefrtontal cortex clearly play a role and are active in the presence of emotional stimuli.
Human stuff- (recent) years verifies the animal research (less recent).

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Specific brain structures play specific roles in emotion-

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-amygdala- recognition of negative facial expressions.
-right hemisphere is dominant for perception of emotion- facial expressions, emotional prosody (emotional content in voice/sarcasm etc) reaction to emotional words (CANNABALISM< MURDER etc).

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How many emotions do we experience?

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anger, sadness, happiness, fear, disgust, surprise, contempt and embarassment.
these emotions can be detected in facial expressions that are similar across cultures.

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Facial Feedback hypothesis-

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smiling does make you happier, facial muscles may feedback and influence emotional experience.

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-different muscles involved in fake and real smiles

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real smiles involve the orbicularis oculi muscles and the zygomatic muscles.
only the zygomatic muscles can be activated voluntarily, so these are “polite” smiles.

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-volitional facial paresis

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-difficulty in moving the facial muscles voluntarily: caused by damage to the face region of the primary motor cortex.
Fake smiles: No Real smiles: YES

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Emotional facial paresis

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-lack of movement of facial muscles in response to emotions in people who have no difficulty moving their muscles voluntarily, caused by damage to the pre-frontal cortex.
Fake smiles: yes Real Smiles: No

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learning

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a process through which experience produces lasting change in behavior or mental processes (and physiology). Even thinking is a behavior- . Anything that changes your behavior is learning.

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Habituation

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learning not to respond to repeated presentation of a stimulus. (Eg. how Sheila’s house is next to the railroad tracks and they probably don’t hear it anymore).

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Sensitization

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learning to over-respond to a single presentation of a stimulus.
eg- after watching ‘one missed call’ the phone rings and scares Ellie to death.

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Habituation in the sea slug

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1) Following habituation each touch fully activates the sensory neurons, there is no reduction in the number of action potentials.
2) however, less Ca enters the button in response to each action potential.
3) As a result, less NTS is released into the synapse in response to each action potential.
4) consequently, each touch generates fewer action potentials in the motor neurons,
5) ultimately there is less contraction of the gill-retractor muscles in response to each siphon touch.

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Sensitization in the sea slug

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1) a strong shock to the tail activates sensory neurons
2) the tail sensory neurons activated facilitatory interneurons that synapse on the buttons of sensory neurons from the siphon.
3) the barrage of action potentials from the facilitatory interneurons produces other changes in the buttons of the siphon sensory neurons that cause more calcium to enter the button in response to each action potential.
4) the increased influx of calcium into the buttons of siphon sensory neurons causes more neurotransmitter to be released in response to each action potential.
5) this increases the # of action potentials generated in the motor neurons by each siphon touch.
6) and this in turn increases the strength of the gill retraction produced by each siphon touch.

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Hue-

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determined by wavelength

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Brightness-

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determined by the intensity of the electromagnetic radiation

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saturation

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determined by the purity of the light wave.

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Trichromatic theory

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states that the spectrum of color is produced by differentially activating the three types of cones. Activation of all three results in “white”.

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Switch from cones to rods-

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-day vision requires cone activity: night vision utilizes rods (very poor color perception at night).

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Concentric Receptive Fields-

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Two Types:
On center/off surround
off center/on surround
The center and its surround are always antagonistic.

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On center biopolar cells-

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turning on light excites them. They receive less glutamate, which normally inhibits on center cells.

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Off center bipolar cells-

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turning off light in the center of the field excites them. They receive more glutamate and are depolarized.

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Bipolar cells- ganglion cells:

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bipolar cells release glutamate which always depolarizes ganglion cells.
On center bipolar cells excite on center ganglion cells when light is turned on.
off center bipolar cells excite off center ganglion cells when light is turned off.

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LGN cells: Magnocellular-

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Magnocellular-
large receptive fields.
respond with a transient burst of activity (change)
insensitive to wavelength (color)

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LGN cells:
Parvocellular-

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small receptive fields
respond with sustained activity
sensitive to color

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Striate Cortex-

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David Hubel and Torsten Wiesel (1960’s)
-discovered that neurons in the visual cortex did not simply respond to light: they selectively responded to specific features in the visual world.

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Cortical Cell Coding
Simple cortical cells-

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also called bar or edge detectors, respond to an edge or bar of a particular width, orientation and location.

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Cortical Cell Coding
Complex cortical cells-

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also respond to a bar of a particular width and orientation, but may be located anywhere in the visual field.

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Damage to the Occipital Lobe

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-cortical blindness:
-blindness caused by damage to the optic radiations or primary visual cortex.

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Blindsight

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the ability of a person to reach for objects located in his or her “blind” fieldL occurs after damage restricted to the primary visual cortex.

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Agnosia-

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the inability to perceive or identify an object by means of a particular sensory modality.

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Visual Agnosia-

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deficits in visual perception in the absence of blindness.

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Balints Syndrome-

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Optic Ataxia:
-difficulty in reaching for objects under visual guidance
Ocular Apraxia:
-difficulty in visual scanning
Simultanagnosia:
-difficulty in fixating on more than one object at a time.

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Pitch-

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a perceptual dimension of sound: corresponds to the fundamental freq. of the stimulus. Measured in Hertz: cycles per second.

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Loudness-

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a perceptual dimension of sound: corresponds to the intensity of the stimulus. Measured in decibels (dB).

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Timbre-

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a perceptual dimension of sound corresponds to the complexity of the stimulus.

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Transduction {Hair cells-receptor cells-}

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inner- important for hearing. 95% of the synapses are between inner cells and auditory neurons. Outer- function not known.
** hair cells synapses with dendrites of neurons that form the auditory nerve**

Receptor potentials occur when hair cells are deflected due to movement of the basilar membrane and tectorial membrane in response to vibration.

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Place Coding-

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high freq- sounds of different frequencies (f) cause a different area of the basilar membrane to flex. High f sounds cause the membrane closes to the stapes (anterior) to flex and low f sounds cause the posterior end of the membrane to flex. So the firing of a particular neurons located along the basilar membrane will code for the pitch of the sound.

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Rate coding-low frequencies-

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sounds with freq. lower than 200 Hz are not detected with place coding. Neurons at the posterior end of the basilar membrane fire in synchrony with the freq. of low f sounds. So the brain reads the rate of firing to detect real low frequency sounds.

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Detection of Loudness-

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axons of the cochlear nerve code for loudness by changing their rate of firing.
* however, loudness of real low frequency sounds are detected by the number of neurons that are activated, not just the rate of a single neuron firing.

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Detection of Timbre-

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not well known. Different portions of the basilar membrane are stimulated by different types of sounds, so there is a unique pattern of activation in the firing of the cochlear nerve.

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operant conditioning-

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BF Skinner believed that the most powerful influencer of behavior are its consequences.

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Law of Effect-

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behaviors that are reinforced are likely to continue. Behaviors that are ignored or punished will likely discontinue. This is a fundamental practice in behavior modification.

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Positive Reinforcement-

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-Stimulus presented after a response that increases the probability of that response happening again. Something good for the animal/child. This would be the “high” in drug use.

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Negative Reinforcement-

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-Removal of an unpleasant stimulus, contingent on a particular behavior. (take away curfew, chores) . This would be the avoidance of withdrawal in drug use.

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Primary Reinforcer-

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For anyone at anytime. Reinforcers, such as food or sex, have an innate basis because of their biological value to an organism. Physiological needs are satisfied.

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Secondary Reinforcers-

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Stimuli, such as money or tokens, that acquire their reinforcing power by their learned association with primary reinforcers. (IE, you use money to buy primary reinforcers, these aren’t the same from culture to culture)

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Punishment-

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an aversive stimulus which will decrease the likelihood that the response will continue.

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Positive punishment-

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means adding something. The application of an aversive stimulus after a response (eg hitting)

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Negative Punishment-

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the removal of an attractive stimulus after a response (to take away something, eg tv, games, time out).

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Sensory Registers-

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all sensory information that is being perceived at a given moment.

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Short term memory-
Long term memory-

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immediate memory for events, which may or may not be consolidated into long term memory (lasts maybe 30 seconds)
relatively stable memory of events that occur in the more distant past.

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Short term memory/working memory-

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Short term memory/working memory-

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Delayed matching to sample task/ or delayed non matching to task sample-

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a task that requires the subject to indicate which of several stimuli has just been perceived.

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Declarative Memory, 2 types:
Semantic memory
episodic memory

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includes memories for language, facts, general knowledge

- includes memory for events, personal experiences

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procedural memory-

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includes memory for motor skills, operant and classical conditioning.

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Amnesia,

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a selective disruption of the processes underlying long-term memory. Short term and sensory memory are usually functional. Other cognitive functions are not impaired (intelligence and attention). retrograde- before brain damage can’t remember anterograde- can’t form new memories after brain damage.

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HM

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Bilateral temporal lobe seizures due to head trauma at age 9.
underwent bilateral removal of the medial temporal lobe that included parts of the hippocampus, amygdala and association cortex.
result= anterograde amnesia.
LTM= okay
STM= okay
consolidation lost so no STM-LTM processing for declarative memories.

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Korsakoff’s Syndrome-

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permanent anterograde amnesia caused by damage to the thalamus.
resulting from chronic alcoholism or malnutrition. Thiamine deficiency (vitamin B). characterized by confabulations. Symptoms- typically unaware of memory problems. You often see symptoms that are acute.

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Spatial learning-

Place cell-

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damage to hippocampus impairs spatial memory.

a neuron that becomes active when the animal is in a particular location in the environment, most typically found in the hippocampus.