IB 132 L8

Why are high frequency/pitch sounds detected at the base of the cochlea?

-lose some high frequency information as travel to end of cochlea

-shape and stiffness of basilar membrane causes high frequency sounds to activate it most near the base

Cordiceps fungi

takes over ant --> controls what it does, gets it to die in specific location, forms fruiting body that infects other ants

Jewel wasp

sting cockroach, drive it over to a corner to host larvae

Toxoplasma gondii

a parasite that alters mammalian fear behavior

Toxoplasmosis

a parasite that is most commonly transmitted from pets to humans by contact with contaminated animal feces

Toxoplasma gondii (toxo) life cycle

-preferred host reproduces in cat

-sheds in feces

-uptake by mouse (intermediate host)

-spread to more cats if feces of mouse eaten

How toxo infection changes rat behavior

-rats infected with toxo spend more time in presence of cat odors

-either they lose fear, lose sense of smell, find odor attractive, etc.

-studies showed that infected rodents still feared other things (loud sounds, etc.)

Toxo effects in humans

-worse drivers

-differences in temperament/personality

-possible risk factors for schizophrenia and suicide (supported in some but not all studies)

-implicated in changes in dopamine/testosterone synthesis, vasopressin signaling, and other pathways

Human toxo host

end-stage intermediate host

Physiology of fear

-heart rate increases (sympathetic)

-heart rate variability decrease (lack of parasympathetic signaling)

-skin T decrease (if any change)

-skin conductance increase (cold and clammy)

-->autonomic NS

Activation of sympathetic NS =

deactivation of parasympathetic NS

-->and vice-versa, can't both be activated at same time

Behavior of fear

-distinctive facial expressions

-wide open eyes

-guarding movements

Changes in attention/learning due to fear

-greater attention to fearful stimuli

-enhanced learning with fear

How can we study fear or other processes in the brain?

Method 1: lesions (damage/tissue loss)

-pro: damage causes a deficit, then we can localize where deficit came from

-con: may damage passing fibers (road analogy) --> may identify region that's not actually important

Rabies mechanism of spread

-host becomes aggressive and bites other animals, putting virus laden saliva into wound

-rabies virus then travels backwards up motor neurons to the brain (retrograde)

Cold virus spread

irritates nerve endings in nasal passages, host sneezes and spritzes viral replicates on neighbors

Limbic circuit

Emotional centers/connections

--> but not the only system involved in fear/emotion

Limbic circuit progression

1) hippocampus

2) hypothalamus

3) anterior nuclei of thalamus (sensory relay)

4) cingulate cortex --> emotional experience

5) neocortex --> emotional coloring

Amygdala

almond at end of hippocampus in limbic system

Amygdala damage: calcification

-no fear conditioning

-no recognition of fearful facial expressions

-don't recognize danger

Amygdala functions

-detects possible threats

-facilitates reactions/behaviors

-enhances memory for strongly emotional negative experiences

-essential for fear conditioning to a cue associated with the negative experience (eg. a sound and a shock)

Amygdala inputs

-sensory inputs

-hippocampal input (memory)

-prefrontal cortex

Amygdala outputs

-cortical outputs

-hormone secretions

-autonomic responses

-emotional behavior

High road amygdala pathway

-activate fear responses by thinking

-can suppress fear responses by thinking

Low road amygdala pathway

you can experience fear before you understand it

Pre-pulse inhibition

If you apply a softer tone before a loud tone, there will be less of a startle response

Another method in understanding fear: functional magnetic resonance imaging (fMRI)

measures brain activity by detecting changes associated with blood flow

What else is amygdala involved in?

-not just involved in fear

-also involved in processing facial expressions, response to animals, etc.

Controllable vs. uncontrollable stressors

control matters, and reduces negative effects of a stressor

Fear, stress, and cortex-amygdala connections

-projections from prefrontal cortex (PFC) inhibit amygdala and other deep structures

-with control, PFC inhibits amygdala in aversive situations (shock)

-without a sense of control/when scared, PFC goes "offline" and stops inhibiting amygdala

-electrically, PFC looks like there is actually too much activity, the rest of the brain stops being influenced by it

Stress inoculation

controlled, safe, or repeated exposures prepare you to deal with future stressors

Cortisol and epinephrine

stress hormones

Emotionally arousing stimulus (eg intense fear) and memory

-cortisol crosses into brain

-epinephrine doesn't cross BBB, but binds to the ascending vagus nerve, promoting release of norepinephrine in the brain

-these affect memory encoding --> vivid/durable memories

Unlearning behavioral approach

repeated exposure without negative consequences (extinction of learned association)

Unlearning pharmacological approach

block effects of epinephrine/norepinephrine around time of memory formation/stressful remembering

Unlearning beta blocker

recall memory in presence of a beta blocker --> block binding of epinephrine/norepinephrine at beta-adrenergic receptors involved in sympathetic response