Animal physiology Lecture 7

Learning memory pathway

stimulus(information from environment)→ sensory memory(holds info briefly)→ short term memory(holds info longer)→ if info isn’t rehearsed, encoded, or retrieved, then it is forgotten; If the person does rehearsal, encoding, or retrieval, then info goes to long term memory where its stored for long periods

Neural plasticity

Changes in neural pathways or connections between neurons

There are 3 types:

1. Synaptic plasticity: Ability to change the strength of an existing synapse

2. Synaptogenesis: Formation of new synapses

3. Synaptic pruning: Removal of existing synapses

Habituation(1) vs sensitization(2)

1. Decrease in a response with repeated exposure to an uninformative stimulus

2. Enhancement of a response to an uninformative stimulus when paired with an informative stimulus

Short term habituation in aplysia( what did it involve, what was hypothesis, describe experiment

the experiment involved gill withdrawal reflex. THe hypothesis was repeated, harmless stimulation of the siphon leads to a decreased gill withdrawal response.

Short term habituation in aplysia 2

Habituation is due to reduction in the amount of NT released from presynaptic sensory neuron. The results showed that repeated stimulation leads to habituation. After initial trials, the sensory neuron activity was intense, which caused the motor neuron activity(gill response) to have a strong withdrawal. But after repeated trials, the sensory neuron activity decreased significantly and the motor neuron activity showed weak withdrawal

1. Autoreceptors that inhibit NT release

2. Inhibitory retrograde messengers from postsynaptic cell

3. Use-dependent inactivation of presynaptic Ca2+ channels

4. Depletion of releasable pool of vesicles

5. Depletion of available NT for release

Long term in Habituation Aplysia

The gill withdrawal decreases across blocks and remains low after 6 hours. This is due to changes in postsynaptic cell. This requires of receptors glutamate ionotropic receptors (AMPA & NMDA). And may require activation of metabotropic glutamate receptors which requires activation of protein kinase and VGCa2+ channels

Sensitization

A strong (noxious) skin stimulus produces sensitization a an enhance gill withdrawal response.

•Repeated siphon touches alone à habituation

•A strong skin shock à activates a facilitating interneuron

•Subsequent siphon touches à produce larger EPSPs in the MN and bigger gill withdrawal responses (sensitization)

sensitization vs conditioning in aplysia

Sensitization is a short term increase in NT release due to facilitating neuron action e.g presynaptic neuron changes

Conditioning is a process that results in long term learned association between 2 stimuli. Like strengthening of synapse that involves changes in postsynaptic cell or long lasting strengthening of synapse is called Long Term Potentiation(LTP)

Role of astrocytes in synaptic plasticity 1

HFS triggers Ca2+ elevation in astrocyte. This causes the astrocyte to release D-serine into the synaptic cleft where it binds to NR1. It is involved in opening NMDA receptors

Role for astrocytes in synaptic plasticity 2

Astrocyte Ca2+ rise is prevented by Ca buffer solution. This causes D-serine release to be reduced and without D serine, the NMDA receptor cannot open

Gliotransmitters(slide 12)

glutamate ATP D-serine and GABA

Brain structures involved in memory

frontal lobe: involved in short term memory; prefrontal cortex is involved

Distributed cortex(PARIETAL LOBE): involved in long term memory that lasts up to a lifetime e.g declarative, spatial, prospective, and procedural

Anterior hippocampus: involved in declarative memory like experiences and facts

Posterior hippocampus: spatial memory like info about environment, navigation, etc

Cerebellum: Procedural/motor memory like unconscious skills

Major function of hippocampus

part of limbic system that takes care of emotion, motivation and social behavior. Also is essential for memory consolidation( short term→ long term)

memory consolidation

Is the process that stabilizes newly formed memories into long-lasting memory traces

Stages:

Stage 1: Synaptic consolidation (LTP):

•Occurs within minutes to hours after learning

•Strengthens existing synapses through long-term potentiation (LTP)

Stage 2: Systems consolidation

•Occurs over days to years

•Memories gradually become less dependent on the hippocampus and are stored in the cerebral cortex

Stage 3: Reconsolidation

•Retrieval makes a memory temporarily unstable

•The memory is restabilized and can be modified before being stored again

What did the taxi driver study prove about the hippocampus

refer to slide 15

Synaptogenesis

method of new synapse formation and memory consolidation- dedritic branching & splitting at strengthened synapses

Axonal branching

another method of new synapse formation and memory consolidation- when the axon essentially grows longer or forms other branches from the original axon

Dendritic filopodia

a new synapse formation and memory consolidation method that gets rid of immature dendrites or damages dendrites

what 3 things are involved in long term memory and learning (refer to slide 19)

synaptic plasticity, synaptogenesis, and synaptic pruning in some

characteristics of sleep

reduced motor activity, decreased responsiveness to stimuli, rapidly reversible state, and distinct body posture

Two process model of sleep regulation (refer to slide 21)

Process S: homeostatic sleep drive

Process C: circadian alerting signal

They interact together to determine when we feel sleepy or alert over 24hr period

Stage 1: Homeostatic sleep drive builds during wakefulness

Stage 2: Sleep reduces sleep drive

Stage 3: Circadian alerting signal masks sleepiness

Stage 4: Circadian alerting signal

Stage 5: Interaction of the two processes

Stage 6: Sleep onset

Regulation of sleep/wake: Hormonal

Hormones involved are:

melatonin: Promotes sleep; released by the pineal gland in darkness

cortisol: Promotes wakefulness; peaks in the early morning

adenosine: Homeostatic sleep factor that accumulates during wakefulness (neuromodulator rather than a hormone)

growth hormone: Primarily secreted during deep (N3) sleep

Regulation of sleep/wake: Neuronal

Alerting centers: in brainstem & hypothalamus

Suprachiasmatic nucleus (SCN): Master circadian clock

Ventrolateral preoptic nucleus (VLPO): Promotes sleep work as sleep switch, produce GABA, galanin

Ascending Reticular Activating System (ARAS): Maintains wakefulness

Orexin (Hypocretin) neurons: Stabilize wakefulness

Sleep assessment in animals

in mammals and birds, we measure brain waves w/ EEG. in other animals we can use fluorescing molecules, reduced responsiveness to external stimuli, body posture, eye movements, and color changes

Awake EEG waves

gamma and beta waves signify the awake state with high freq and low amplitude activity. Gamma waves have very high freq while beta waves have medium freq. Beta waves are associated with normal wakeful state, alertness, concentration. Gamma waves are associated with high level cognitive processing, attention

Sleep cycles in mammals

relaxation: alpha waves; eyes closed, calm, relaxed but awake

non rem sleep: theta waves; slow eye movement, light sleep, early dreams

non rem sleep stage 2: mixed freq; no eye movement, no dreaming, has sleep spindles & K complexes, body temp and heart rate falls

non rem sleep stage 3: Delta waves; deep sleep, dreams occur, parasomnias may occur

sleep cycles: REM

•EEG waves like awake state

•No muscle tone & little movement

•Rapid eye movements

•Central homeostatic mechanisms are suspended

EEG vs EMG vs EOG

Electroencephalogram for brain activity

Electromyogram for muscle activity

Electrooculogram for eye movement

Purpose of sleep

Energy conservation

Development

Immune function

Information processing:

• Sleep deprivation interferes with task learning and memory recall in fruit flies, bees, birds, mice, rats, primates

• Sleep helps memory consolidation: Mice learning a maze: same neurons active during spatial learning tasks are activated during slow wave sleep

Reverse damage (oxidative stress, depletion of energy stores, cell damage, etc.) that occurs while awake

Cleaning the brain of toxins

Microsleeping

very short periods of sleep that last 15 sec or less

lose conscious control of performance

mostly due to sleep deprivation, monotonous tasks like driving