umich psych 230 exam 2

What Causes Neurotransmitter Reselease?

Action Potentials

Ligand

Molecule that bind to a receptor to activate it, like a "key and lock".
Not just Neurotransmitters, but also drugs (anything that fits the receptor).

Reuptake

Pre-synaptic neuron reabsorbs neurotransmitter by a neurotransmitter transporter (vesicle)

Neurotransmitters in the synaptic cleft

Either destroyed by enzymes or reuptake by presynaptic neuron.
Without these, the effect of NT would be amplified too much.
Also allows the recycling of NTs

Classifying Neurotransmitters

Dozens total, but 5-10 major families with similar structures.
Differentiated by Anatomical location and effect (EPSP and IPSP).
The post synaptic receptors and channels determine the effect.

Glutamate

-Most common/prevalent NT in nervous system
-Excitatory (EPSPs)
-Receptors: AMPA (ionotropic) and NMDA (ionotropic) are grouped together on the same synapse, and mGluR (Metabotropic). Use Na+, K+, and Ca2+ flow.
-Learning and memory (among others). NMDA allows for plasticity.

Metabotropic Receptor

Receptors activate intracellular signaling.
G-protein activates secondary messengers to open ion channels, enter nucleus for gene activation, etc.
Slower opening but longer duration.

Ionotropic Receptor

Causes opening of ion channel.
Faster opening but shorter duration.
Na+ causes EPSP, K+ and Cl- causes IPSP

AMPA Receptor

Ionotropic Glutimate Receptor.
Simple: one Glutimate allows flow of Na+ in or K+ out at same time.

NMDA Receptor

Ionotropic Glutimate Receptor.
More Complicated: Need more depolarization from AMPA channels to occur, but stays open for longer.
Magnesium ions block the channel and are removed with depolarization, allowing Na+/Ca2+ in and K+ out.

GABA (Gamma Amino Butyric Acid)

-Most common inhibitory neurotransmitter (IPSP)
-Found throughout the brain
-Two types of receptors GABA-A and GABA-B: Either opens Cl- or K+ ion channels, hyperpolarizing neuron.

Acetylcholine (ACh)

-Usually EPSPs
-In brain: sensation, action, learning, memory
-In Peripheral NS: Activates muscle movements in peripheral motor neurons (parasympathetic system)
-Released in small, cholinergic neurons in few parts of the brain, but the whole brain has receptors that wait for a signal.

Neuromuscular Junctions

The synapses between a motor neurons and muscle fibers. Acetylcholine is NT that translates the neural signals to muscle movements.

Sarin

Extremely toxic chemical weapon that inhibits Acetylcholinesterase, which is the enzyme that degrades ACh. Causes ACh buildup, preventing muscle relaxation.

Adrenaline (Epinephrine)

-One of the Catecholamines
-Can affect both EPSP and IPSP depending on post-synaptic receptor

Norepinephrine (Noradrenaline)

-Catecholamine, so both EPSP and IPSP
-General function: mobilize brain and body for action in sympathetic nervous system
-Like ACh, produced in small structures, but have widespread effects (Locus Coeruleus in brainstem)

Dopamine

-Catecholamine, so both EPSP and IPSP
-Movement, reward-seeking, motivation
-Produced in Substantia Nigra (death causes Parkinsons) and VTA (both brainstem)
-2 "families of receptors": D1 and D2

Seratonin (5-HT)

-Both EPSP and IPSP
-Happiness, mood, sleep, appetite
-Produced in Raphe Nuclei (brainstem)

Endorphin and Enkephalin (Opiods)

-Both EPSP and IPSP
-Pain reduction, rewards, euphoria. Synthesizes following pain, exercise, laughter
-Bind to opioid receptors

Nitric Oxide (Reverse Neurotransmitter)

-Feedback from post-synaptic neuron to pre-synaptic neuron
-Generated by post-synaptic enzyme after activation, soluble gas leaks out of dendrite and into pre-synaptic neuron
-"Retrograde Signaling"

Most psychoactive drugs work on _

Synapses

Agonist

Turn on neurotransmitter system (EPSP or IPSP)
Presynaptic: release NTs
Postsynaptic: Activate receptors or facilitate binding

Antagonist

Turn off NT system
Presynaptic: prevent release
Postsynaptic: block receptors

Inverse Agonists

Binds to receptors, but initiates opposite effect

L-Dopa (drug)

Presynaptic Agonist.
Brain synthesizes dopamine from L-Dopa, so medication provides it to supplement reduced dopamine levels in Parkinson's Disease

Cocaine (drug)

Presynaptic Agonist.
Inhibits reuptake by blocking dopamine transporter

Amphetamine (drug)

-Presynaptic Agonist.
-Blocks and reverses dopamine transporter to increase concentration of dopamine and norepinephrine.
-Stimulation, euphoria, wakefulness, improved cognition.
-Treatment of ADHD, narcolepsy, depression, and athletic performance enhancer

Adderall (drug)

-Combination of amphetamine and dextroamphetamine

Ritalin

-Not amphetamine, but similar effect

SSRIs (Selective Serotonin Reuptake Inhibitor)

Block reuptake of serotonin; antidepressant.
Common drug is Prozac

Morphine and Heroin

Postynaptic Agonists that block opioid receptors by mimicking endorphins and enkephalin

Synthetic opiods

Fentanil (100x potent than morpine)
Carfentanil (100x potent than fentanil)
Pain reduction, tranquilizers.
Overdose inhibits breathing circuits

Benzodiazepines (Xanax, Vallium, etc.)

Postsynaptic Agonist
Bind to GABA receptors to facilitate effects. Enhances the effect when GABA is present (inhibits more than before).
Sedative, hypnotic, anxiolytic (anti-anxiety)

Postsynaptic Antagonists

-"Typical" antipsychotics for schizophrenia blocks D2 dopamine receptors, blocking dopamine from activating
-"atypical" antipsychotics block both dopamine and seratonin receptors

Blood-Brain Barrier

-Only lets small, hydrophobic, or specific chemicals through. Drugs must cross this to reach the synapse

Routes of Drug Administration

-Oral ingestion: easy, safe, but takes long and metabolized by digestive system
-Injection: quicker but more dangerous
-Inhalation: Shortest route to brain, fast, but only possible with few drugs

Receptor Down-Regulation

Tolerance to drug.
Homeostatic regulation reduces receptors in postsynaptic cell, so normal NTs without drug causes weak response and withdrawl

Neural Sensitization

Hyper-response to drug.
"Wanting/Craving" vs. just "liking" dopamine

Neurotoxitiy

High dose of some drugs kills neurons, and most do not regenerate

Sensory Coding

How the brain detects and processes sensory stimuli.
Quantitative aspects of stimuli correlate with neural activity.

Sensation

The activation of sensory brain pathways by physical stimuli

Perception

The extraction of a mental representation from sensation. Higher level.

Psychophysics

Quantitative aspects of stimuli correlate with perception they evoke
Stimulus intensity to stimulus detection.

Receptor Cells

Convert physical stimuli to neural signals (electrochemically).
Specialized cells that shapes organisms perception of the world.

Intracellular electrophysiological recording

Electrode punctures through membrane, measures, and compares to ground state outside of neuron to generate membrane potential (voltage).
Very hard to do, invasive, but can record EPSP and IPSP

Extracellular electrophysiological recording

Electrode near neuron on the outside. Measures brief reduction in positivity as neuron depolarizes.
Much easier, but can only record spikes, not all membrane potentials.
Also measures Local Field Potential (LFP)

Local Field Potential (LFP)

Aggregate neural activity in the area of an extracellular electrophysiological recording.

Optical Recording of Action Potentials (Calcium Imaging)

Calcium indicators (calcium-sensitive dyes) fluoresce in the presence of calcium.
Ca2+ has most abrupt and obvious conc. change during action potentials, so easiest to measure.
Slower and not the actual spikes compared to electrophysiological, but can record cell-type specific neurons over multiple days

Spontaneous firing

Sensory neuron occasionally fires spikes with no relation to stimulus. Stimulus causes neuron to change firing rate.

Raster plot

Measures the frequency and timing of action potentials from trial to trial of same stimulus to determine what a neuron is specialized to.

Peri-Stimulus Time Histogram (PSTH)

Shows the average spike rate of the trials in spike/second of a neuron to determine what stimulus causes repeated firing.

Receptive Field of a neuron

Region of sensory space in which a stimulus will modify the firing of a neuron.
Shows selectivity in neurons (will fire to some stimuli and not others)

___ gives rise to perception

Spike responses to stimuli

Neural code

Rate (frequency) code vs. temporal code
Rate code quantifies strength of responses by spike rate, while temporal code provides information by the timing of the spikes. Shows how spikes give rise to perception.

Cortical maps (topography)

Touch information from adjacent parts of the body are represented in adjacent parts in the cortex.
Parallel hemispheres: left body -> right brain, vice versa.

Homunculus (tiny man)

Orderly representation of the body in the brain, so more cortical area means more sensitive and larger on homunculus.
Comparing different species' somatosensory cortex reflects differences in sensitivities.

Cortical plasticity

Experience can reshape sensory representation and sensitivities in cortex.
-Experiment where monkeys used specific fingertips more, so enlarged the cortical area for those fingers.
-Face is nearby arm in somatosensory cortex, so stimulating face can elicit "phantom limb" sensations in amputees.

Mike May (Case Study)

Blinded by chemical explosion at 3, scarred cornea blocked light. Still lived successful life.
At 46, surgery cleared corneas but still couldn't see because brain pathways interpreting visual information were not functioning.
After years of training, regained partial vision

Mach Band Illusion

Perceive shade gradient where there is none. Proof we pay specific attention to edges

Light

An energy wave, or stream of photons (particles).
Need to know amplitude (magnitude) and wavelength (frequency)

Light entering visual system

Cornea is protective cover, iris is muscle that allows certain amount of light through pupil, a hole into the lens that focuses light to the back of the eye (upside down).
Passes to the back layer of the eye to photoreceptors, then forward through bipolar (and horizontal and amarcrine) cells and is sent to brain by the Retinal Ganglion Cells

Photoreceptors

Rods and Cones.
Transduce light signals. do not fire action potentials (RGCs do first).
Light strikes rhodopsin (light absorbing pigment) in disc of photoreceptor, and breaks rhodopsin into retinal and opsin. Opsin closes Na+ gates, hyperpolarizing the photoreceptor.
This stops the release of glutamate.

Amacrine and Horizontal cells

Lateral interactions within the retina. Facilitate on center-off surround and vice versa (Lateral inhibition).
Horizontal facilitates photoreceptors, Amacrine facilitates RGCs

Bipolar Cells

carry information from the photoreceptors to retinal ganglion cells

Retinal Ganglion Cells (RGCs)

Send information to the brain

Rods

Photoreceptor highly sensitive to light; ideal for dim environments.
Respond similarly to different wavelengths, so like black-white sensors

Cones vs rods

Color vision photoreceptor.
Much less light sensitive; need more light to activate.
3 types, each sensitive to either red, blue, or green wavelength.

Color vision disparities

Color blindness is lack in one or more cone pigment.
Most primates are trichromatic (3 cones-rgb).
Rats, dogs, cats, raccoons, etc. are dichromatic (2 cones-gb)
Honeybees see 300-600 nm light, while humans see 350-750, so their distinction of colors is different.

Fovea

High density of cones, few rods, so the sharpest point of vision in color, but "blind" in low lights.
Non-photoreceptors are pushed aside.

Lateral inhibition

Capacity of an excited neuron to reduce activity of its neighbors
The horizontal cells connect nearby photoreceptors, so if light hits one photoreceptor (focal light), the next one over is inhibited. If both are hit, retains baseline firing rate with equal inhibition (if both are on-cells).
Photoreceptors work best when surrounded by darkness

From photoreceptor to Retinal Ganglion Cell

1. Light causes photoreceptor to hyperpolarize and release less glutamate
2. This excites on-cell bipolar cells, depolarizing and releasing glutamate
3. Glutamate excites RCGs, so these are bipolar "on-cells"

For off cells, light at center stopping glutamate to bipolar causes bipolar to hyperpolarize and inhibit glutamate to RGC, so these bipolar cells are "off-cells"

Receptive fields of RGCs

On-center, off-surround: Light in center excites bipolar cells, light is surround inhibits, so optimal firing is focused light in the center.
Off-center, on-surround: Light in center inhibits bipolar cells, light in surround excites, so optimal firing is darkness in the center and light surrounding.
All light or all dark means RGC does not fire.

On-center, off-surround enhances sensitivity to _.

Edges.
Edges cause the border of luminescence and non-luminescence, so the RGC are inhibited the least, causes strongest signal (more action potentials).

The bionic retina

When photoreceptors have been lesioned, an implant on the back of the retina responds to signals from a camera and converts to impulses that stimulate the RGCs

Optic Nerve

The axons from Retinal Ganglion Cells go through the optic nerve and to the brain.
No photoreceptors here, so causes a "blind spot"

Nasal and Temporal hemiretina

Each retina is divided into two halves, nasal hemiretina (center) and temporal hemiretina (outside).
Nasal hemiretinas cross over in optic chiasm and the two left hemiretinas and two right hemiretinas stick together into the brain.
Right field of view to left brain and vice versa

Lateral Geniculate Nucleus (LGN)

Where the RGC axons reach in the thalamus.
6 Layers:
1-2: Magnocellular (big cells) sense motions and dim light (rods)
3-4: Parvocellular (small cells) sense color and detail resolution (cones)
Retains center-surround receptive field like RGC

From LGN to cortex

Axons from LGN travel to "optic radiation" to primary visual cortex (V1).
Maintains retinotopic organization, so each V1 neuron responds to stimulus in small area of visual field, nearby neurons respond to nearby stimuli.
Almost exclusively in cortical layer 4.
Oriented lines are important, and one LGN neuron can synapse to multiple V1 neurons

Primary Visual Cortex (V1)

Receives information from thalamus (LGN) into cortical layer 4, the least processed visual information (sensation but not perception).
Hubel and Wiesel (1981) cat experiment found V1 neurons respond to oriented lines in different angles and locations.
There are oriented lines of RGCs correspond to LGN neurons, which send to V1 that responds to that particular neuron.

Lesions to V1

Causes partial or complete blindness (single/both hemispheres)
When asked to detect objects, appear blind, but when forced to guess, are better than chance. Cannot consciously perceive vision, but still have inclinations.
Called Blindsight

Blindsight

Lesions to V1 means when asked to detect objects appear blind, but still has inclination to vision.
Information does not reach primary visual cortex, so not conscious vision, but suggests that stimuli do not need to reach consciousness to influence behavior.

Patient TN (Case study)

Lost V1 in both hemispheres and indicated complete blindness in vision tests.
Walked down crowded corridor and avoided obstacles smoothly. Shows V1 is critical for conscious perception of stimuli, but not detection.

V2 (visual cortex)

Neurons in V2 have similar response properties to V1 but with more complexity and closer to visual perception.
Along with lines, also respond to visual illusions.
First point of different for dorsal and ventral streams

The Ventral "What" Stream

Parvocellular LGN Neurons -> V1 -> V2 -> V4 -> Inferior Temporal Lobe (IT)
Responds to increasingly complex stimuli as pathway continues (V4 responds to geometric shapes and shows attention modulation)

Inferior Temporal Lobe (IT)

End of the Ventral "What" Stream.
Responds to visual objects (e.g. cars) in a position-invariant and size-invariant manner, so still recognize the same object when changing the position and size.

Fusiform Face Area (FFA)

In IT, neurons respond specifically to faces (proposed by Kanwisher).
"Expertise Hypothesis": Argued that FFA is selective to identifying objects of expertise, not just faces. Supported by experiment comparing bird experts to car experts.
Lesions here make it especially difficult to recognize faces, called prosopagnosia (face-blindness).

Lesions of Inferior Temporal Lobe (IT)

Visual agnosia: severe and permanent impairment in learning and recognizing visual stimuli.
Case studies:
-Man who mistook wife for a hat
-41 y/o man with tumor. First resection caused no damage, 2nd cause strong and permanent prosopagnosia (face blindness).

The Dorsal "Where" Stream

Magnocellular LGN Neurons -> V1 -> V2 -> V3 -> V5 (MT) -> Parietal Cortex.
Spacial attention (guiding vision to points of interest) and using vision for guidance of actions (detecting and analyzing movement)

Change Blindness

Inability to detect small changes between two likes (e.g. two photos) because we cannot take in a whole landscape at once.
Saccades (fast eye movements), guided by dorsal "where" stream, focus our fovea on only small areas of interest at a time, so visual attention only focuses on a small area at a time.

Parietal Cortex (visual stream)

The highest level of the dorsal stream.
Shape, size, orientation, movement, visual maps (relation of one object to another).
Unilateral lesions causes neglect syndrome.

Neglect Syndrome

Unilateral lesion of the parietal lobe.
Cannot pay attention to visual information on the field of view opposite to the lesion.
When copying an image, can only copy one side.

Lesions in dorsal vs. ventral streams

Ventral: patient can reach and grab normally, but cannot say what the object is.
Dorsal: Ignores object if in impaired field of view, but if show it on correct side, can still identify the object.

Sound

Vibrations (speed in air/room temp is 340 m/s).
Pressure changes of great to little compression.
Frequency-determines pitch (cycles/sec; Hz), species perceive pitch differently (Humans ~20-20,000 Hz)
Amplitude-determines loudness (dB), above 130 dB causes instant, irreversible hearing loss.

Fourier transformation

Decomposition of a complex sound down to just the pure tone components (sinusoidal waveforms)

Spectogram

Shows the frequencies of sound and how they change over time

The ear

Pinna collects sound and directs down ear canal, where it strikes tympanic membrane (ear drum). Middle ear bones pass vibrations to cochlea.

The cochlea

A coiled tube containing the basilar membrane, which vibrates with the sound wave. Transduces vibrations to electronic signals

Basilar membrane

Decomposes complex sounds into their component functions "tonotopically" with high frequencies causing thicker, basilar side to vibrate and lower frequencies causing thinner, apical end to vibrate.
Contains hair cells that convert sounds to electrical signals.

Hair cells

Convert sounds to electrical signals.
Vibration of basilar membrane causes movement of hair cell stereocilia, opening K+ channels, depolarizing the cell and causing NT release (no action potential).
High K+ conc. outside (opposite to normal), so opening channels causes depolarization.
Membrane potential encodes how fast and wide stereocilia move, so how much NT is released

Receptive field of hair cells

Tonotopic signals means hair cell only responds to the range of frequencies it corresponds to on the basilar membrane