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87 Cards in this Set

  • Front
  • Back
Biopsych: A._____
Modern Branches of Neuroscience. 1) Molecules, 2) Neurons 3) Neural Circuits 4) Brain 5) Organism 6) Behavior
A. Studying the biol mechanisms that give rise to sensation, perception, thought & behavior.
1) 10^-9 and smaller
2) 10^-5
3) 10^-3 and smaller
4) ~10^-3 to 10^0 5) 10^0 6) 10^3
Where did the Scientific Study of the Brain Begin?
Egyptians as early as
3000 BCE recognized links between the brain and behavior
Hippocrates
(~400 BCE) wrote about the brain: united senses, wisdom, etc. under brain. Plato shared this view, but Aristotle (~320 BCE) abandoned it, believing that the heart and other organs were the source of wisdom and intellect
Lucretius (~55 BCE):
The heart “is the seat of the intellect and mind.”
Galen (~150 CE)
demonstrated experimentally (using live dissection) that the brain was the center of control for physical and mental activity
Experimental evidence overwhelmingly demonstrated that the brain was the organ responsible for behavior and perception
Brain vs. Heart
What Happened?
Medieval scholars were influenced greatly by Aristotle and the writings of the Bible, which place the seat of reason, intellect and emotions in various bodily organs (e.g., heart, liver, kidneys, etc.)
Writings were often metaphorical; the role of the brain was almost universally ignored
Students of early scientists did not bother to continue experimenting
Heart-centeredness”
persisted well into the 16th and 17th centuries
Origins of Physiological Psychology
Thomas Willis (1621-1675)
English physician, argued that the brain receives sensations, stores memories, and is the source of behavior
Reneé Decartes
(1640s)
Thought the Pineal body in the brain was the seat of the soul
Thought behavior resulted from movement of hydraulic fluids, initiated by the soul, through nerves into the muscles
His insistence that the brain and body were distinct split the fields of biology (medicine) and philosophy
Origins of Physiological Psychology
The 17th, 18th and 19th centuries were marked by strong advances in physics, biology and philosophy
Late 1800s saw the emergence of psychology out of the convergence of these disciplines
Important Experiments in Physiological Psychology: 1780-1900
Luigi Galvani (1780s)
Electrical stimulation of a nerve caused contraction of the muscle to which it was attached
Thus, neural activity is electrical in nature, dispelling Descartes’ “hydraulic hypothesis”
However, Galvani attributed the finding to “animal electricity” which he believed to be secreted by the brain as a fluid and distributed to muscles via nerves
Franz Joseph Gall (1801-1828)
Functional Specialization
Phrenology (Cranioscopy): “The skull is molded on the brain”

Right about functional specialization
Wrong about phrenology
Johannes Müller (1826)
Publishes the Doctrine of Specific Nerve Energies:
A nerve that is activated carries only a single type of information
Prove it to yourself! By pressing on your eyeballs, you activate neurons in the retina, and you see flashes of light
(Note: This effect really has more to do with how your brain interprets the message, rather than how the nerves carry the information. It is more a demonstration of where neurons travel in the brain than of “nerve energies.”
Hermann von Helmholtz (1840s)
“Founder of physiological psychology”
Found that neural impulses did not travel at the speed of light, but rather at a much slower 50 m/s.
(more recent calculations: 0.5 m/s to over 120 m/s; that’s still about 270 miles/hour!)
Fritsch & Hitzig (1888)
Origins of Physiological Psychology
Electrical stimulation of the brain caused movement in the body. //
The roots of Physiological Psychology are in physics, biology and philosophy
Modern neuroscientists remain true to these roots, using techniques from electrophysiology and genetics to computer modeling
Some Current Fields in Neuroscience
Psychopharmacology
Psychoneuroimmunology
Behavioral Genetics
Comparative Neuroanatomy
Evolutionary Psychology
Developmental Psychobiology
Neurophysiology
Computational Modeling
Human Nervous sys
CNS (brain, spinal cord, interneurons) PNS (everything else, sensory & motor neurons)
PNS = Somatic and Autonomic Nervous System
Somatic (voluntary, input from sense organs, output to skeletal muscles) Auto (involuntary, input from internal receptors, output to smooth muscles and glands)
Autonomic Nervous sys = __ & __
sympathetic nervous system (fight or flight response, adrenaline and noradrenaline) parasympathetic nervous system (conserves energy as it slows the heart rate, increases intestinal and gland activity, and relaxes muscles in gastrointestinal tract.)
Cells of the Nervous System
Neurons
Each person has 10^11 to 10^12 neurons
Many specialized types
“Principal” neuron
Interneuron
Receptors
Glia
Other
Neuronal Diversity. Shape indicates specialized function.
A) Retinal ganglion cell (dendrites flat) B) Retinal amacrine cell (no axon, communic through dendritic tree) C) Cortical pyramidal cell (branched axon) D) Cerebellar Purkinje cells (boxlike dendrites)
Soma
Cell Body”
Nucleus
Cytoplasm (travels into dendrites, axons)
Organelles
Golgi Apparatus (packaging proteins)
Mitochondria (energy surce) ER, etc/
Dendrites
Primary target for input from other neurons
Up to 100,000 inputs on a cell’s dendritic tree
Some have specialized structures (Spines)
Axon
Long (up to 5 meters!)
Carries electrical signals from the Soma to the boutons
The electrical signal is called an Action Potential
The action potential is converted into a chemical signal at the terminal boutons
Types of Neurons
Multipolar
Multi: Extending dendrites in all directions from soma. Bipolar: Relatively unbranched, one direction. Uni: All processes from one end of soma; usu receptor cells (ex. auditory sys) Pseudounipolar (usu in spinal area)
The Neuron Doctrine
- The Golgi Method
Reticular Hypothesis
Camillo Golgi vs Santiago Ramon y Cajal
- From camera film w/ silver grains and the fixative to prevent overexposure) Labels an entire neuron
Stains ~5% of neurons
Why? Nobody knows!
RH: Continuous neurons
Electrical transmission
Unitary Hypothesis (Cajal)
The Neuron Doctrine
Individual neurons
Chemical transmission
Electron Microscope confirmed the latter 50 yrs later. Neurons are unitary and communicate with each other across a synapse (chemically)
Signals travel in one direction: from the dendrites to the soma and from the soma to the axon terminals
Exceptions!
Some neurons are connected to each other electrically
Information sometimes travels back into the dendrites or is exclusively carried by dendrites
Glia; types
Neuroglia = “nerve glue” (“Nervenkitt”) Outnumber neurons x10.
Three types:
Astrocytes
Microglia
Oligodendrocytes/Schwann Cells
Astrocytes
Much smaller than a neuron (1/2 or 1/3 as big as soma) Have multiple “end feet”
Some contact blood vessles, some contact neurons.
Hold neurons in place
Control chemical environment surrounding neurons
Provide nourishment for neurons
Microglia
Smallest glial cells
Perform phagocytosis
Principle immune system component within the brain
Oligodendroglia/Schwann Cells
Wrap axons in a sheath of myelin
Oligodendrocytes
Wrap multiple axons
Found within the Central Nervous System (CNS)
Schwann Cells
Wrap only a single axon
Found in the Peripheral Nervous System
Myelination
Increases the speed of communication
“Saltatory Conduction”
Not all neurons are myelinated (at birth only 5-10% are; takes 20-30 yrs to complete)
Myelin is destroyed in Multiple Sclerosis
The Blood-Brain Barrier (BBB)
Blood vessels throughout the body are “leaky” (glucose, poisons, etc)
Capillaries in the brain have specialized structure (less leaky)
Astrocytic “end feet” and capillary “tight junctions” (endothelial cells connecting w/ itself)
blood-brain barrier
Lipophilic compounds vs hydrophilic
Unlike other organs and tissues, brain capillaries show no fenestrations or pinocytotic vesicles and have "tight junctions" that almost fuse adjacent cells. This anatomy creates the blood-brain barrier (BBB). Astrocytic foot processes surround brain capillaries and, during development, induce brain endothelial cells to develop in this special leak-proof fashion.
The ability to exclude certain substances from brain interstitial space has to do not only with the vascular anatomy, but also with lipid solubility and selective transcellular transport by endothelial cells. Lipophilic compounds cross the BBB easier than hydrophilic ones; small lipophilic molecules such as O2 and CO2 diffuse freely. Some hydrophilic compounds, including glucose and amino acids, enter the brain with the help of transporters, and larger molecules enter via receptor-mediated endocytosis. The BBB protects the brain from toxic substances but impedes the entry of drugs.
Fun Facts!
1) The adult human brain weighs about
2) The human brain uses about
3) The elephant brain weighs about
4) Mass of a single large neuron
1) 3 pounds, or about 2% of total body weight. 2) 20% of the body’s oxygen intake
3)6,000 g.
4) = 10-6 gram
Fun Facts!
5) The human brain has about
6) Estimated ___ connections in brain.
7) Neurons multiply at a rate
5) 100,000,000,000 (100 billion) neurons 6) 60 Trillion connections 7)250,000 neurons/minute during prenatal development.
More Facts (Fun!)
Over half of all neurons generated in the nervous system ... During the first month of life, the number of connections between neurons increases from
are lost before birth
2) 50 trillion to over 1 quadrillion
Equivalent of growing from 8 lbs to over 170 lbs in one month!
Fun Facts O’ the Day
In 1 microliter of cerebral cortex there are:
1 shot glass = 40 ml
10^6 neurons
10^9 synapses
48 km of axons

40 billion neurons 40,000,000,000
40 trillion synapses 40,000,000,000,000
1,920,000 km or 1.2 million miles of axons
From here to the moon FIVE TIMES!
Bioelectricity: Membrane Potentials
All neurons have an electrical charge
((Info from dendrites to terminals: law of dynamic polarization))
Inside is more negative than outside
Charge comes from a difference in ionic
concentrations
The charge differential across the membrane is called a Membrane Potential
The membrane potential at rest is called the…

Resting Membrane Potential
Ionic Pressures
Concentration Gradient

Electrostatic Gradient
Ions at high concentration are under diffusion pressure to distribute evenly throughout
- Ions of a particular valence (charge) are attracted to areas of the opposite valence
These pressures are responsible for the free movement of ions across the cell membrane
Pressures on Ions
If the concentration gradient and the electrostatic gradient for a particular ion species are at equal strength and are pushing on opposite sides of the membrane,
the ion is said to be at equilibrium
The membrane voltage (difference in electrical potential between the inside and outside of the neurons) at this point is the Equilibrium Potential for that ion
The Nernst Equation
Equilibrium (mV) = -58 log [ion]out/[ion]in

HUH?
For any given ion, you can figure out the voltage of the membrane at which the concentration gradient and the electrical gradient will be equal and opposite.
The equilibrium potential for a given ion will determine which way it flows across the membrane
The direction an ion flows is critical for knowing how it affects the cell’s voltage
It is important for understanding action potentials... Review of membrance potential:
Produced by membrane impermeability to A- & Na+
Controlled by K+
K+ channels partially open at RMP
Electrical force for K+ is inward
Concentration force for K+ is outward
Electrical force for K+ is balanced by concentration force for K+at RMP (at equilibrium)
What maintains ionic imbalance?
The phospholipid bilayer (membrane) is selectively permeable to certain ions

“Gated” Ion Channels
Ionic “pumps”
Ion-specific “leak” channels
Sodium-Potassium Pump
Moves three Na+ ions out of the cell for every two Potassium ions it moves in (3:2)
Requires Energy (ATP)
Does NOT contribute to the RMP
Potassium and the Resting Membrane Potential
(Potassium ions are the most important for resting mem potential) Changing extracellular [K+] changes the resting membrane potential. Equil poten changes across graph (Nernst equation): rel concen changes altered equil (reflecting change).
The Action Potential
A rapid, transient change in voltage (depolarization) within the axon
Initiated proximal to the soma
Progresses all the way to the axon terminals
Ion channel
A specialized protein molecule that permits specific ions to enter or leave the cell.
Voltage-dependent (or “voltage-gated”) ion channel
An ion channel that opens or closes depending on the membrane potential (Vm).
Recap: Ion Concentrations at Rest
Large concen of Na+ outside cell & electrostatic gradient. But selec permeable (cannot pass through at rest) Large k+ inside the cell, but pressure and diffusion makes no net difference. Mem becomes permeable to Na+ (pressures on K+ would have less electrostatic pressure to force k+ out of cell too).
Passive current flow in the axon. SUBTHRESHOLD STIMULATION:
Recording at diff points from stimulus. Depolarizes (from -65 to -60, less neg) mostly nearby, not as great further away. SUBTHRESHOLD STIMULATION: Not to threshold for an action poten called "graded potential." Changes in mem voltage follows rules of passive current flow in axon (cable properties) (like elec wire decay of current)
Suprathreshold stimulation
Leads to an action potential (large, transient depolarization of the membrane potential)
Continues without decrement to axon terminals

Active process!
“All or None”
Voltage Clamp Method
Hold voltage constant and measure current. Certain command voltage: certain nec current. Measure this current, equal to current to get away from (-60 for ex).
Depolarization activates ion currents
Delayed outward current (ions out of cell) and transient inward current (of ions into cell). (Hodgkins and Huxley won Nobel Prize for investigating these currents; proposed ion channels 10 yrs before their discovery.
Pharmacological Characterization
1) Na+ channel blocker (tethrodotoxin) Block inward current, only outward. Therefore inward current from Na+. 2) K+ channel blocker, only blocked outward current.
Depolarization activates ion currents
Na+ rushes in (voltage gated channels), then K+ out (voltage gated k channels).
Dynamics of the Na+v channel
Three states: closed, open, inactivated. Then, closes regardless of mem poten (Refractory Per: before opening again) (Inconsistent; perhaps closed to open and closed) (From inactiv to closed when mem voltage back to resting level).
Dynamics of the K+v channel
Closed-Delay-Open; new more neg outside-want to flow in.
Ionic Basis of the Action Potential
1) Na+ enters cell (channels open; electrostatic & concen; more positive). 2) K+ channels open, K+ leaves cell (b/c of both gradients) 3) Na+ channels become refractory (in addition to inactivated; no more Na+ enters. (REPOL) Mem poten therefore becomes neg b/c): 4) K+ continues to leave. 5) K+ channels close; Na+ channels reset (closed vs inactiv); 6) Extra K+ outside diffuses away after hyperpol (more hyperpol than RMP). 7) K+ requilibrates.
Propagation of the Action Potential
Flows smoothly along length of axon
Active process, but depends on passive spread of electrical potential
- Travels along axon. - Voltage gated Na channels refractory, prevents current from moving backwards. - Conduction in Myelinated Axons (voltage gated Na and K channels not under myelin but only nodes of Ranvier; By pt B t=1.5 vs t=2, faster; same stimulus as for unmy). Action Poten occur w/ stim above threshold voltage. Sequential opening of v-g Na+ channels and influx of Na+. Efflux of K+ ions returns to resting poten. Contin clearing of Na+ from intracell space via Na/K pumps. Saltatory conduc.
Axon terminals and the synapse
Presyn terminal. A) Electronic synapse (rare) Gap junctions; connexon proteins (make pores) Ions flow through pores connecting neurons; one cell to another.
Chemical synapse
More common. No direct ion exchange; neurotrans packets fuse w/ presyn mem and release neurotrans into cleft. Postyn receptors let extracell ions to flow in.
Chemical synapses
Three types:
From axon to dendrite = “axodendritic” (most numerous)
From axon to soma = “axosomatic”
From axon to axon = “axoaxonic” (least numerous)
Presynaptic cell = “sending”
Postsynaptic cell = “receiving”
Discovery of Chemical Synapses
Early 1900s debate: “Soups” vs. “Sparks”
Otto Loewi (1873-1961)
The first discovered neurotransmitter: “Vagusstoff” (Acetylcholine)
Nobel Prize to Loewi in 1936 (with Henry Dale). If electrical/direct, fluid can move to Heart 2 w/ no effect. Unless chem. (Delay, but chem in nature)
Criteria for new Neurotransmitters
The substance must be present in the presynaptic terminal
The substance must be released in response to presynaptic depolarization
This depolarization-induced release must be Ca2+ dependent.
Specific receptors for the substance must be present on the postsynaptic cell Ex Amino Acids, carbon monoxide.
Classes of Neurotransmitters
Excitatory
Increase the likelihood that the postsynaptic neuron will fire

Always produce a depolarizing postsynaptic potential

Acetylcholine, Glutamate
Inhibitory
Decrease the likelihood that the postsynaptic neuron will fire
Usually produce a hyperpolarizing postsynaptic potential
y-aminobutyric acid (GABA)
Important Neurotransmitters
1) Acetylcholine
2) Glutamate
Found at junction with skeletal and cardiac musculature
Role in CNS not well understood
2) Most abundant neurotransmitter in the brain
Always excitatory (almost)
Important Neurotransmitters
3)GABA
4) Biogenic Amines
3) Most abundant inhibitory neurotransmitter
Always inhibitory 4)Implicated in many psychiatric disorders
Dopamine, norepinephrine, epinephrine (Catecholamines; all start with Tyrosine)
Serotonin (early antianxiety, dep drugs targeted serotonin)
Histamine
Parkinson’s disease
Loss of dopaminergic cells
Leads to severe motor disabilities (“Awakenings”)
Cognition remains intact until late stages
Neurotransmitter deficiency: dopamine. Tyrosine-dopa-dopamine. Treatment for Ldopa (synthetic version)
Anatomy of a Synapse
1. NT produced and packaged
2. Vesicle “docked”
3. Action potential arrives
4. Voltage-gated Ca2+ channels open
5. Vesicle fuses with membrane
Anatomy of a Synapse
6. NT released into synapse
7. NT binds to postsynaptic receptors
8. Postsynaptic ion channels open, allowing ions into cell
9. Ion flow changes Vm: “Postsynaptic Potential”
Vesicular Neurotransmitter Release
Vesicle “docked” at presynaptic membrane
Vesicular membrane fuses with pre- synaptic membrane
Neurotransmitter is released into the synaptic cleft (“Omega Figure”)
Neurotransmitter effects on postsynaptic cell
- Excitatory
Post-
Synaptic
Potential
Dependent on postsynaptic ion channels, not on NT - Na+ IN ->
Depolarization of
Membrane
Inhibitory
Post-
Synaptic
Potential
K+ OUT ->
Hyperpolarization
of Membrane.
Cl- IN ->
Cancels effects
of EPSPs
Integration of Postsynaptic Potentials
- ESPSs summed in soma; axon hillock reaches threshold of excitation; action poten is triggered in axon (passive). More than a few inputs needed. ISPSs: axon hillock will not reach excit. Axon hillock (eval net result)(aka spike initiating zone) first part w/ voltage gated Na channels.
Two kinds of integration
Temporal summation
A single input fires rapidly, raising the postsynaptic potential above threshold

Spatial summation
Many inputs fire simultaneously (or nearly so)
(Rapid succession)
Neurotransmitter Inactivation
Two mechanisms
1) Reuptake: by presyn neuron Or glia (astrocyte) usu active transporters. 2) Enzymatic Degradation
From one cell to another: Summary of Synaptic Transmission
Action potential travels down the axon
Neurotransmitter is released into synaptic cleft
Neurotransmitter binds to specific receptors
Postsynaptic ion channels open
Current flows in postsynaptic cell
Integration of postsynaptic potentials
Action potential begins at axon hillock of POST SYN CELL (second action poten) (also known as the “spike initiating zone”)
Neurotransmitter is cleared from synaptic cleft
Neurotransmitter Receptors
***The receptor determines the action of the neurotransmitter
Receptors are highly specific for particular neurotransmitters (“Lock and Key”) (ex. same precursors for catech. but diff receptors)
Receptors are favorite targets for pharmaceutical companies (ex. SSRIs)
Neurotransmitter Receptors
Two types
Ionotropic – receptor is an ion channel (Type of LIGAND-GATED ion channel; NT binds to binding sites-receptors-into intracell space)
Metabotropic – receptor initiates an intermediary process (“second-messenger”) to open separate ion channels (G-protein coupled receptors; NT into cleft, bind to recept, then integ or re-uptake; ions pass through, changing post-syn mem changes).
Autoreceptors
Presynaptic neurotransmitter receptors
Activated by neurotransmitter released from presynaptic neuron
Decrease the amount of neurotransmitter released by the presynaptic cell
e.g., D2 receptor decreases Ca2+ influx to presynaptic terminal; also increases K+ current
Another mechanism of neurotransmitter regulation (with reuptake and degradation)
Major NTs and their receptors


((Agonist: binds to recept site w/ same effect as NT. Angagonist: prevents action/recep from working.))
Acetylcholine (ACh)
Two major receptors
Nicotinic—Ionotropic; first discovered agonist: Nicotine
Muscarinic—Metabotropic; agonist: Muscarine
Inactivated by AChE (Acetate + Choline)
Choline is taken up into presynaptic cell to make more
Major NTs and their receptors
Glutamate (Glu)
Four major receptor types
1. AMPA
2. Kainate
3. NMDA
These receptors are each Ionotropic
These receptors are each Excitatory (always)
4. mGluR
This class of receptors is Metabotropic
Tricky; can be excitatory or inhibitory
Inactivated by reuptake or enzymatically
Major NTs and their receptors
g-aminobutyric acid (GABA)
Three major receptors
GABAa
Ionotropic ? Cl-
GABAb
Metabotropic ? K+
GABAc
Ionotropic ? Cl-
Inactivated by reuptake or glial uptake; broken down by several pathways
Major NTs and their receptors
Dopamine (DA)
Two main types of receptor
D1
Primary postsynaptic receptor, metabotropic
D2
Primary autoreceptor, metabotropic
Axoaxonic Synapses
Unlike axodendritic and axosomatic synapses, these do not contribute directly to neural integration
Instead, these synapses modulate the release of neurotransmitter from presynaptic terminal
Increase NT release ? presynaptic facilitation
Decrease NT release ? presynaptic inhibition
Nonsynaptic communication
Neuromodulators
Released by neurons
Released in larger quantities than NTs
Diffuse over longer distances than NTs
Modulate responses of many neurons in a localized area of the brain
Behavioral effects are general and widespread (e.g., vigilance, sensitivity to pain)
Examples: Substance P, Acetylcholine
Hormones
((Quickest: NT, then neuromod, then hormones in days vs seconds))
Released by endocrine glands or specialized cells in various organs
Released into extracellular space, carried throughout the body by bloodstream
Modulate responses of many cells throughout the body
Effects are generally slower than effects mediated by neuromodulators
Behavioral effects are longer lasting (e.g., testosterone ? aggressiveness)