Research
Neurons & Glial Cells
Neurotransmitters & Drugs
Action Potentials & Synapses
Neuroanatomy
100
These are the three debates relating to Organology vs. Connectionism discussed in lecture.
What are Restak vs. Caine, Lashley vs. Thompson, and Lichtman vs. O'Keefe?
100
This is the most common type of excitatory neuron in the cortex.
What is a pyramidal neuron?
100
These are the primary excitatory & inhibitory neurotransmitters, accounting for 95% of chemical messages in the brain.
What are:
GABA (inhibition)
Glutamate (excitation)?
100
This causes the generation of an action potential.
What is EPSPs overpowering IPSPs to depolarize the membrane to the activation threshold?
100
These are the three divisions of the brain & associated functions
What are the forebrain (information processing), midbrain (Four F's - Feeding, Fight or Flight, and Fu --- er, Fornication), and hindbrain (autonomic functions)?
200
This is the technique Jeff Lichtman uses to map the connections in the brain & what he calls such a map.
What are Imaging & the Connectome?
200
These are three types of glial cells in the brain.
What are astrocytes, oligodendrocytes, and microglia?
200
Adderall and Ritalin primarily enhance this neurotransmitter. Too little of this neurotransmitter is linked to which disease? Too much?
What is Dopamine? Too little: Parkinson's disease; Too much: Schizophrenia?
200
These are the three necessary components of a synapse, and how you can differentiate them.
What are the presynaptic membrane (containing synaptic vesicles holding neurotransmitters), the synaptic cleft, and the postsynaptic membrane (containing ionotropic receptors & GPCRs)?
200
This is the number of layers of the cortex (in most areas)
What is six?
300
This is the technique O'Keefe used and the type of cell he found.
What are single-cell electrophysiological recordings and hippocampal place cells?
300
These are the primary methods of communication A) Within a Neuron, and B) Between Neurons
What are
A) Action Potentials
B) Neurotransmitters?
300
Too much GABA causes this phenomenon, while too much Glutamate causes another phenomenon (name both).
What are sedation (GABA) and seizures (Glutamate)?
300
What are the terms of the electrical changes caused by GABA and Glutamate?
IPSC/ IPSP; EPSC/ EPSP. (Inhibitory/Excitatory Post-Synaptic Current/Potential)
300
These are the four major lobes of the brain & their associated sensorimotor areas.
What are the frontal lobe (M1 - Primary Motor Cortex), temporal lobe (A1 - Primary Auditory Cortex), parietal lobe (S1 - Primary Somatosensory Cortex), and occipital Lobe (V1 - Primary Visual Cortex)?
400
These are the main beliefs of (A) organologists & (B) connectionists.
What are the beliefs that
(A) specific structures in the brain have specific functions
(B) specific functions are implemented by the connections in the brain, rather than individual structures?
400
This is Ramon y Cajal's "Neuron Doctrine"
Neurons are discrete, highly organized entities with structures relating to their functions.
400
These are the six major neurotransmitters discussed in lecture and a function associated with each.
What are:
GABA (inhibition)
Glutamate (excitation)
Dopamine (Reward, Motor Functioning, Attention, etc.)
Serotonin (Impulse Control)
Norepinephrine (Fight or Flight)
Acetylcholine (Memory, Movement)?
400
These are the two types of neurotransmitter receptors, and the primary mechanism by which they function.
What are ionotropic (opens ion channels & allows ions to flow in or out of the cell through the cell membrane) and metabotropic (AKA GPCR, which cause protein phosphorylation and act as second-messenger systems)?
400
These are the two structures that compose the diencephalon & their functions.
What are the thalamus (the major sensory relay point of the cortex) and the hypothalamus (major mediator of hormones & homeostasis)?
500
Which two researchers had the same hypothesis, what was this hypothesis, what were their experiments and conclusions?
Lashley & Thompson both hypothesized memory is localized in the brain.
Lashley concluded after studying the effects of cortical lesioning in mice that memory was not localized -- maze performance was dependent on the amount of cortex resected, rather than where.
Thompson showed that after lesioning a region in the cerebellum, a rabbit's conditioned response (eye blink triggered by a tone) disappeared, and concluded that memory is localized in the brain.
(Whoops, this is not in the form of a question.)
500
Draw and label all the parts of a typical neuron.
(Thanks Chandini)
500
This is the name for the commercially available opioid antagonist.
What is Narcan (AKA Naloxone)?
500
Draw a synapse & label the four main steps to activation & three main methods of inactivation.
(Thanks Hannah)
500
These are the five subcortical structures in the forebrain that were discussed in lecture & their functions.
What are the basal ganglia (motor functions, reward), amygdala (emotional processing), hippocampus (episodic memory), thalamus (sensory relay point), and hypothalamus (hormones & homeostasis)?