Exam 1 Flashcards
neurons
specialized for temporally and spatially precise communication with other cells
glia
support cells
-hold nervous system together
-provide nutrients, raw materials, protection, and general upkeep
-oligodendrocytes, astrocytes, microglia, Schwann cell
dendrites
input region that receives info from other neurons
-“dendron” = tree
dendritic spines
increase SA and allow for more inputs
soma (cell body)
integrates info coming from the dendrites by summing the electrical signals generates there
-regulates cell function with the genetic info in nucleus
axon (nerve fiber)
-conducts info collected by dendrites and integrates by soma into axon terminals
-axon hillock is the wider initial segment
axon terminals
contacts dendrites and somas of other neurons to communicate
-converts electrical signals into chemical
synapses
connection between axon terminal and the next neuron
presynaptic membrane
part of axon terminal that releases neurotransmitters
postsynaptic membrane
dendrites of target cell
synaptic cleft
space between pre and post synaptic membranes where neurotransmitter goes through
cell theory
all living things are made up of cells
neuron doctrine
the brain is comprised of individual neurons
oligodendrocytes
-create fatty myelin sheath that wraps around axons
-allow action potentials to occur faster and more efficiently
what do Schwann cell do?
insulate axons and cause action potential to be quicker and more efficiently in PNS
astrocytes
-star shaped cells with many arms that contact other cells
-help convey vital nutrients from blood to neurons
-the arms that contact blood vessels make up part of the blood brain barrier
blood brain barrier
separates the brain from circulatory system to regulate what enters and protect against pathogens
microglia
defend brain by scavenging for pathogens, damaged cells, and debris
-the ‘immune system’ of brain and spinal cord
resting state: cell bodies still while branches move around, surveying area
if threat detected –> reactive state: change shape and move to where needed to engulf and destroy debris/invader
anterior/ posterior
facing towards/ away from
superior/ inferior
top/ bottom
medial/lateral
center/ outer
ipsilateral/ contralateral
same side/ opposite
dorsal/ ventral
back/ stomach
what cells are in PNS?
nerves and ganglia
nerves
bundles of axons in PNS
ganglia
clusters of cell bodies in PNS
motor nerves
control muscles in efferernt direction (away from CNS) (output and muscles)
sensory nerves
bring sensory info into CNS in afferent direction
cranial nerves
12 pairs that emerge from base of brain
-convey sensory info about vision, taste, smell, balance, etc into brain
-control muscles of neck and head
spinal nerves
31 pairs that emerge from spinal cord
-sensory info about touch, position of limbs in space, etc
-enter dorsals side of spinal cord
somatic nervous system
PNS
-sensation and action
-nerves connect CNS to sensory systems and skeletal muscle
-spinal and cranial nerves
autonomic nervous system
PNS
-nerves connect CNS to organ systems
-energy balance, smooth muscle
-sympathetic and parasympathetic division
sympathetic division
PNS autonomic NS
-increase metabolic burn
-tells body that energy is needed
-increase heart rate and respiration
-ex: jogging
parasympathetic division
PNS autonomic NS
-when active, tells body to build up and conserve metabolic energy
-“rest and digest”
dorsal root ganglia
-contain cell bodies (ganglia) that send sensory info from PNS to CNS
meninges
multilayered fluid-filled sack holds brain and spinal cord
-CSF layer allows brain to float
-originates in lateral ventricles –> other ventricles –> spinal cord
major brain divisions
forebrain
midbrain
hindbrain
theory of localization
different parts of the brain carry out separate and distinct psychological functions
-Franz Joseph Gall
phrenology
pseudoscience that skull forms around the brain
FALSE
psychological processes are localized to ____
specific systems and circuits of neurons (instead of centers)
neural system
- a population of neurons that communicate across the boundaries between brain regions
-along long distance
neural circuit
-a population of neurons that communicate within a brain region or between immediately adjacent brain regions
-communicate in small area
Cortex
-wrinkly exterior made up of gyri and sulci
-crucial role from perception to decision making
-6 layers (1= most superficial 6= deepest)
-4 main lobes
pyramidal cells
have apical dendrites that span across layers
-allows for more synthesis of info
4 lobes and their functions
frontal: attention, planning, decision making, motor control
parietal: somato-sensation (touch, proprioception)
temporal: hearing
occipital: vision
gray matter
-found throughout brain and spinal cord
-made up of cell bodies, dendrites, and unmyelinated axons (surface of the cortex is gray matter)
white matter
-throughout the brain
-myelinated axons
basal ganglia
-initiation of voluntary motion (ex: parkinsons)
-NUCLEI!!! NOT GANGLIA
limbic system
amygdala: emotion
hippocampus: memory
(in temporal lobe)
thalamus
directs sensory info in cortex
hypothalamus
-energy intake and control of endocrine system via PITUITARY GLAND
-regulates hunger
tegmentum
ventral midbrain
-cell bodies that send axons to basal ganglia and cortex –> release dopamine
tectum
-dorsal midbrain
-processes audio/ visual info and controls orientation responses
post-synaptic potential
local changes in electrical change
resting potential
negative charge inside neuron (-50 to -80 mv)
-different concentrations of ions inside and outside
ion channels
-allow ions to pass through
-selective or semi-selective
-gated- only allow ions through in response to a signal/ event
-rely on diffusion/ electrostatic force
what are the properties of neurons due to?
ion gradient and movement of ions across membrane
what determines if ion channels allow ions to enter/exit neuron?
1) Diffusion- aka chemical pressure
-particles move from more [] to less []
2) electrostatic- ions move away from similar charge towards opposite charge (opposites attract)
Na+ / K+ pump
-doesn’t rely on diffusion/ electrostatic force
-constantly active because distribution/ gradient of ions across the cell membrane is vital for electrical comm.
resting potential
- K+ gradient is at equilibrium
-Na+/K+ pump and electrostatic force keep K+ inside cell
-diffusion will push K+ back out through K+ selective ion channel
depolarization
making inside of neuron more positive
Ionotropic receptors
-ion channels that open when NT bind to them
-cause IPSP and EPSP
-convert chemical signal into electric
ex: Nicotinic Acetylcholine Receptor:
-opens when acetylcholine binds to it
-depolarizes cell (Na+ and Ca2+ in neuron)
postsynaptic potentials (PSP)
graded changes
1- Excitatory: ionotropic receptors allow + ions into neuron (depolarization around synapse)
2- Inhibitory: ionotropic receptors allow - ions into neuron (hyperpolarization)
post-synaptic and temporal summation
combining EPSP and IPSP influence
spatial: across space
temporal: over time
action potential
-happens when spatial and temporal summation of PSP depolarizes axon hillock to its threshold
-never bigger or smaller. same every time
-rapid depolarization followed by hyperpolarization
what happens if there is more intense excitatory input?
more individual action potentials are fired
-NOT: more intense action potentials
what causes depolarization
voltage-gated Na+ channels open and let Na+ in
what causes hyperpolarization?
K+ flow out of axon through K+ channels that are alway open
Cell becomes more negative
what does a wider axon mean for action potential?
action potential will be faster
fatty sheath myelin
-speeds up action potentials
-in myelinated axon=
1.) AP generated at Nodes of Ranvier
2.) everything is equally negative
saltatory conduction
-how AP jumps from node to node of a myelinated axon
what happens when there is myelin damage?
without insulation -> Na+ diffusion less efficient -> slowing AP or eliminating it completely
ex: MS -> immune system attacks myelin (disrupts AP) because misinterprets myelin for invader
local anesthetics
-sensations dulled because drug prevents Na+ from working
-prevent AP from happening and silence sensory nerves
-names end in “-caine”
ex: Tetrodotoxin in puffer fish very toxic because potent
what happens once action potential reaches axon terminal?
1.) voltage-gated Ca2+ channels open and Ca2+ goes in
2.) once Ca2+ detected, vesicles rupture and eject neurotransmitters into synaptic cleft
neurotransmitters
chemical signals that get converted to electrical signals (EPSP & IPSP) by ionotropic receptors
what are 3 ways to study the electrical activity of the nervous system?
1.) electrophysiology
2.) in vitro & in vivo (ex: electrode implanted in rat to listen to action potentials)
3.) EEG in humans (record brain waves of neurons oscillating together)
what was Otto Loewi’s experiment?
-stimulated the vagus nerve and collected the fluid around it
-added the fluid to second heart and second heart had the same response as the first
neurotransmitters
-synthesized and stored in axon terminals
-released when action potentials arrive at axon terminals
Botulinum toxin
-produced by Clostridium botulinum
-toxin incorporates in synaptic vesicles, preventing them from docking with postsynaptic membrane (preventing NT release)
Botox
-a dilute injection of Botulinum toxin
-prevents nerve endings from communicating w muscles
Metabolic receptors
-activate G proteins (secondary messengers) inside of post-synaptic cell, which can open ion channels and/or trigger a cascade of intracellular events
how can neurotransmitters be inactivated once released?
1) enzymatic degradation- enzymes in synaptic cleft break down NT
2) reuptake- transporter molecules on presynaptic cell and glia grab NT and pull out of synaptic cleft back into axon terminal
psychopharmacology and its 2 subsections
science that deals w the uses, effects of drugs that influence thought and behavior by influencing action of NT
1) pharmacokinetics- absorption, distribution, metabolism, and excretion of drugs
2) pharmacodynamics- how drugs exert their effects at site of action
what is a ligand?
molecule that binds to receptors site
endogenous ligands
-produced by body
-exert their effects through receptor bindings (ex: NT)
exogenous ligands
-produced outside the body and bind to receptor sites
-ex: drugs, nicotine
agonist and antagonists
agonists- bind and mimic endogenous ligand
antagonists- bind and block action of exogenous/ agonist ligands
Dose-Response Curve
-relationship between dose and response
-if drug is more fat soluble = can get through membrane faster -> site of action faster -> biger effect at low dosage
-if drug is more attracted to receptor site= bigger effect at low dosage
therapeutic index
range between ED50 and LD50 determines the margin for safety for a drug
effects of repeated drug exposure
1.) sensitization- drug effects get bigger with repeated exposure
- shifts dose-response curve left because needs less to get same effect
2.) tolerance- body used to functioning with drugs reacts with withdrawal symptoms if drug leaves the system (different from addiction)
types of neurotransmitters
1.) classical- made in axon terminal
ex: dopamine, norepinephrine, epinephrine
2.) non-classical- made in cell body and transported to the terminal
- ex: large precursor protein is produced and chopped into neuropeptides
Glutamate
-primary excitatory NT in the brain
-ionotropic glutamate receptors (AMPA & DMDA)
AMPA- Na+ channel, EPSP
NMDA- Ca+ channel, triggers plasticity
GABA
primary inhibitory NT in the brain
ionotropic GABA receptors= GABAa opens Cl- channel
metabolic GABA receptors= GABAb activate G-proteins
GABA antagonists- convulsants (remove inhibitory influence and excitatory will take over)
ketamine
NMDA antagonist
causes dissociative effects but low doses give antidepressant effects (Spravato)
Benzodiazepines
allosteric agonists for GABA- bind to GABAa receptors at different sites than GABA
- increase degree to which GABAa receptor attracts GABA
ex: Diazepam (Valium) & Lorazepam (Ativan)
acetylcholine
in PNS- makes muscles contract at neuromuscular junction
in CNS- send axons throughout cortex and limbic system (influencing attention & memory)
only NT that is removed from synapse entirely (by enzymatic degradation)
Alzheimer’s treatments
many drugs to treat Alzheimer’s inhibit enzymatic degradation of acetylcholine
Sarin- nerve gas that blocks message of acetylcholine
Monoamine neurotransmitters
nuclei are divergent - makes more postsynaptic contacts than usual
ex: dopamine, norepinephrine, serotonin
dopamine
motor control, motivation, reinforcement learning
removed from synapse by dopamine transporter
nigrostriatal pathway and mesolimbic pathway
dopamine receptors
all metabolic
5 types under D1-like and D2-like
parkinson’s disease
disease caused by death of neurons that make up nigrostriatal pathway
what happens when DAT is blocked?
dopamine builds up in synapse –> reinforcing –> habit forming
low doses of drugs that block DAT can help focus (Ritalin = slow Cocaine = fast)
cocaine
agonist of dopamine- facilitate action of dopamine by allowing it to be in synapse longer
Norepinephrine
arousal, wakefulness, alertness
cell bodies in locus coeruleus in hindbrain
axons to
cortex in limbic system
Yerkes-Dodson law
there is an optimal level of arousal for peak performance of complex tasks
receptors are all metabolic (alpha & beta)
serotonin
cell bodies in raphe nuclei in mibrain & hindbrain
axons to
CNS
SSRIs prevent serotonin transporter from clearing serotonin from synapse
neuropeptides
non-classical NT made from a precursor protein in cell body
metabolic receptors include mu, kappa, and delta
ex: endogenous opioids
endogenous opioids
reward and pain relief
ex: endorphin (enkephalin)
in periaqce ductal gray of midbrain- produce natural form of analgesia (ex: battlefield anesthesia)
exogenous opioids
agonists for endogenous opioids
ex: heroin, morphine, codeine
mediated by mu receptors (important for brain stimulation)
naloxone
drug that can reverse the effects of an opioid OD
antagonist for endogenous opioids at mu receptor
outcompetes endogenous ligands and agonist because receptor is more attracted to naloxone
where does CSF originate?
lateral ventricle in the brain
