BIOS 286: Exam III

Neural projections coming out of the retina starting with the optic nerve

Crossing of some information from the nasal retinae to the opposite side of the brain

Partial crossing of information

Lateral geniculate nucleus

LGN, hypothalamus, pretectum, and superior colliculus

Sense of smell

Sense of taste

Area in nasal cavity of olfactory receptor neurons

GPCRs with different detection thresholds

Olfactory epithelium

1. Olfactory receptor neurons

2. Basal cells

3. Supporting cells

Give rise to ORNs

Metabolic support for the OE

Thin protrusions from dendrites of ORNs, contains odorant receptors

Olfactory receptor neurons

Bony structure with openings for axons of ORNs to pass through

One

Yes, affinity overlap

1. Odorants bind to GCPRs, activates adenylyl cyclase

2. Adenylyl cyclase activates cAMP

3. cAMP binds cation channels

4. Na+ and Ca2+ enter

5. Membrane depolarizes

Yes

Extension of the brain above the olfactory epithelium, processes olfactory information

Formed from all axons from the ORNs, layered structure

Cluster of axons from mitral cells, sends information to olfactory bulb, only receives input from ORNs that express the same ORGs

Excitatory

Send their dendrite to only one glomerulus, do not interact with each other

Amygdala and hippocampus

Memory processing, learning

Attention, fear, aggression

Sensory perception, sleep, memory, cognition

Orbitofrontal cortex

First point of convergence, origin of flavor

1. Piriform cortex

2. Olfactory tubercle

3. Amygdala

4. Entorhinal cortex

Prolonged exposure to an odor causes less recognition

1. Ca2+ enters

2. Ca2+ binds to receptor

3. cAMP affinity is reduced

1. Ca2+ enters

2. Ca2+ activates CaMK

3. CaMK reduces adenylyl cyclase activity

4. cAMP is not produced

Inability to smell

Synapse strength can be altered

Long term potentiation

Long term depression

Synapses are strengthened by increased activity

Synapses are weakened by decrease in activity

Entorhinal cortex

Major input to the hippocampus from the temporal, orbital, and amygdala

Requires 2 events: glutamate must bind and the cell membrane must depolarize so the Mg2+ ion can be ejected, permeable to Ca2+

Brief burst of strong stimulation

Normal glutamate binding receptor, glutamate will bind even if Mg2+ is not ejected.

1. Glutamate must bind to AMPARs

2. Na+ ions flow in

3. Membrane is depolarized enough to eject Mg2+ from NMDRs

4. NMDARs enter, Ca2+ flow in

More AMPA receptors are inserted into the membrane, does not require new protein synthesis, lasts a few hours

Requires new protein synthesis and new signaling pathways, lasts 24+ hours

Protein kinase C

Activated by Ca2+

Enhances activity, strengthens postsynaptic response

New growth of dendritic spines due to LTP, increases connectivity between axons and dendrites

Only synapses that receive strong inputs will be strengthened

Synapses can receive inputs to be enhanced or weakened

Depends on amount of Ca2+ that flows into the synapse

1. Low frequency stimulus leads to depolarization

2. Ca2+ enters, Mg2+ is NOT ejected

3. Protein phosphatases are activated by Ca2+

4. Dephosphorylation of AMPARs

5. Less membrane depolarization

1. High frequency stimulus leads to depolarization

2. Ca2+ enters, Mg2+ is ejected

3. Protein kinases are activated by Ca2+

4. Phosphorylation of AMPARs

5. Increased membrane depolarization

Acquisition of new information

Retention of information

Decrease in strength of a behavioral response due to repeated mild stimulus

Increase in strength of a behavioral response due to a strong stimulus

Facts and events, conscious recollection of explicit memories

Skills that are hard to put into words

Transformation of short term memory into long term memory

Retention of information through repetition, but only lasts a short time

Forms declarative memories

Cortical association areas → parahippocampal areas → hippocampus → cortical areas

Loss of memories BEFORE onset

Inability to form new memories AFTER onset

Retina → optic nerve → optic chiasm → optic tract → LGN → primary visual cortex (V1)