Behavioral Neuroscience

What part of the brain degenerates in Parkinson’s?

Substantia nigra (dopamine-producing neurons die)

Why can’t you just inject dopamine to treat parkinson’s?

Dopamine can’t cross the blood-brain barrier.

What drug can cross the BBB and become dopamine

L-Dopa (Levodopa)

Neurotransmitter systems involved in depression?

Dopamine, norepinephrine, serotonin

MOAI Mechanism

Monoamine oxidase inhibitors prevent breakdown of monoamines —> increases neurotransmitter levels

The “Cheese Effect”

Foods high in tyramine + MOAI —> Norepinephrine rises —> High BP, risk of heart attack/stroke

SSRI Mechanism

Stops reuptake of serotonin —> more in synapse —> downregulates receptors —> helps depression 2-4 weeks

Key SSRI caution

Must taper off slowly, serotonin regulates temperature, heartbeat, and sexual response

GABA

Inhibitory, decreases neuron firing

Glutamate

Excitatory, most common neurotransmitterH

Histamine

Keeps you awake, antihistamines make you drowsy

Nitric Oxide?

Expands blood vessels —> increases neuron activity

Tyrosine

Precursor for dopamin; found in protein foods (chicken, eggs, dairy)

Dendrite versus Axon?

Dendrite = input, Axon = output

Presynaptic vs Postsynaptic

Pre = sending neurons, Post = receiving neuron

Functional Types?

Motor (to muscles), Sensory (from environment), Interneurons (connect neurons)

Classifcation by processes?

Unipolar, Pseudounipolar, Bipolar, Multipolar

Afferent vs Efferent?

Afferent = to brain, Efferent = from brain

Microglia

Immune defense, injury repair

Radial glia

Guides neuron development/layering

Schwann cells

PNS myelination —> speeds up signals

Oligodendrocytes

CNS myelination —> speeds up signals

Myelin Sheath Purpose

faster neuron transmission

what is the blood brain barrier?

semi permeable barrier protecting the brain

Weak spots of Blood Brain Barrier

circumventricular organs, pituitary gland, area postrema

Can nicotine cross the BBB?

Yes

Ionotropic receptors?

Fast, open ion channels (e.g., glutamate, GABA)

Metabotropic receptors?

Slower, second-messenger system, emotions/cognition (e.g., serotonin)

Steps of action potential?

Na* in —> K+ out —> CA2+ in —> neurotransmitter release

Acetylcholine receptors?

Nicotinic (fast) & Muscarinic (slow)

Dopamine?

too much —> schizophrenia, too little —? parkinson’s; 4 pathways

Norepinephrine

focus, arousal, alertness

Serotonin

Emotional regulation, sleep, maybe aggression

Wellbutrin mechanism?

Increase dopamine —> used for depression with low dopamine

Side effect of Wellbutrin?

Some became psychotic if dopamine was already high

Xanax effect?

Increases GABA —> inhibitory —> too much —> euphoria

Glutamate overdose effect?

too much —> excitotoxicity —> neuron death (after injury)

MOAI common use historically?

TB patients become happier —> noticed antidepressant effect

Resting potential?

-70 mV

Depolarization

Na+ rushes in —> neuron becomes positive

Repolarizaiton

K+ rushes out —> neuron returns negative

Hyperpolarization

too negative temporarily —> refractory period

calcium’s role?

triggers neurotransmitter release at synapse

Steps from action potential to neurotransmitter release?

1. AP reaches terminal

   1. Ca2+ influx

   2. Vesicles release neurotransmitters

   3. A neurotransmitter binds receptor

   4. termination (reuptake/degradation)

Presynpatic Vs Postsynaptic

Pre = releases neurotransmitter, Post = receives neurotransmitter

Downregulation?

Too much neurotransmitter —> neuron removes receptors

Acetylcholine (ACh)

Nicotinic —> fast, Muscarinic —> slow

Nicotine effect

Binds nicotinic ACh receptors —> mimics neurotransmitter —> downregulation

dopamine (da)

addiction, movement, reward

norepinephrine (NE)

focus, alertness, arousal

Serotonin (5-HT)

sleep, mood, emotional regulation, aggression

GABA?

Inhibitory —> decreases neuron firing

Glutamate?

Excitatory, neuron firing, too much = toxic

Histamine?

Wakefulness, antihistamines —> drowsy

Nitric oxide?

expands blood vessels —> more neuronal activity

Lesions?

destroy tissue —> see effect on behavior

electrical stimulation?

activate neurons —> observe effects

post-mortem studies?

study structure after death —> brain-behavior mapping

Imaging methods?

fMRI, PET —> activity; MRI —> structure

Rammachandran video key idea?

Phantom limbs —> brain remapping, cortical plasticity

Neurons are discrete units — who discovered?

Santiago Ramon y Cajal

Functional parts of a neuron?

Dendrites = input

Axon = output

Soma = cell body

Motor neurons?

Spinal cord —> muscles

Sensory neurons?

Receptors —> Central Nervous System

Interneurons?

Connect neurons in central nervous system

Types of Glia?

Microglia, radial glia, schwann cells, oligodendrocytes

Blood brain barrier weak spots?

Circumventricular organs, pituitary, area postrema

what is a “phantom limb”?

feeling a limb is still there after its amputated

why do phantom limbs occur?

brain still has a cortical map of the missing limb —> neurons fire —> sensation

Which brain region is involved in phatom limb sensations?

Primary somatosensory cortex (S1)

Cortical remapping?

neighboring brain areas take over the space of the amputated limb —> can cause sensations like touching the face —> feels like missing hand

mirror therapy?

using a mirror to “trick the brain” —> reflection of intact limb —> reduces phantom pain

Ramachandran’s theory about pain?

Phantom pain comes from maladaptive cortical reorganization

Synesthesia connection?

Sometimes people with phantom limbs report weird sensations —> shows brain map is flexible

example of cortical plasticity from book?

touching a face —> activates neurons that used to sense missing hand

why is phantom limb important for neuroscience?

shows the brain is active even without input —> mind is not just the body

takeaway from ramachandran video?

the brain can rewire itself —> therapies can harness plasticity

Pituitary Gland

Monitors the bloodstream for chemicals

Area postrema

the vomiting center, if you eat a poison, hopefully it will get here so it can make u frowup

blood is toxic to?

neuron

Potassium

K+

Sodium

Na++

Calcium

Ca++

Chloride

CL-

concentration gradient

potassium is trying to get in

sodium wants to get out

Electrical gradient

opposites attract, inside is negative, outside is positive

positive ions are trying to go into the cell

membrane at rest -70 inside

more sodium on the outside than on the inside

sodium is positive

vice versa w potassium and some chloride is inside too

novcane

your sodium channels cannot open

aka u cant feel pain

refractory period

a period of time during which a neuron cannot fire again

relative refractory period

sodium channels are open, but potassium is still leaving

edward charles spitzka

doctors who examined the brain of guiteau

can you see insanity in the brain?

main theory: u can see it between neurons

Otto Lowei

he wanted to figure out how neurons communicated

he went to sleep and found out how to test if a neuron was electrical or chemical

neurotransmission is

electrical

adrenaline

fight or flight

synaptic transmission is

chemical

what is sensory?

taking external info and turning it into something your nervous system can understand

what is perception?

our mental model/understanding of sensory info

synesthesia

sensory experience in one domain triggers another (hearing colors)

trephination

ancient brain surgery, drilling hole into skull