Bneuro Ch 12: Learning and Memory (Amnesia)

learning

how experiences change the brain

memory

how changes are stored and subsequently reactivate

categories of responses to the environment

reflexes, fixed action patterns, learning

types of learning

associative and non-associative learning

associative learning

classical conditioning and operant conditioning

non-associative learning

habituation and sensitization

habituation

occurs when an organism reduces its response to unchanging, harmless stimuli

sensitization

occurs when repeated exposure to a strong stimulus increases response to other environmental stimuli

classical conditioning

Organisms learn that stimuli act as signals that predict the occurrence of other important events (Pavlov)

operant conditioning

organisms form connections between a behavior and its consquences that impact the subsequent frequency of that behavior

information processing modles

sensory memory, short term (working) memory, and long term memory

sensory memory

has a large capacity and short duration (few seconds)

short term (working) memory

has a small capacity (5-9 items) and short duration (15-18 seconds)

long term memory

has a large capacity and unlimited duration

types of long term memory

declarative and non-declarative memories

declarative (explicit) memory

contains semantic memory and episodic memory

nondeclarative (implicit) memory

contains procedural memory, classical conditioning, and priming

semantic memory

contains basic knowledge of facts and language (eg. first president)

episodic memory

relates to your own personal experience (eg. your first kiss, a friend’s birthday party)

procedural memory

stores information about motor skills and procedures (eg. learning to play guitar)

frequently studied organisms

fruit flies and sea slugs (aplysia californica)

aplysia

simple neural networks make it an ideal candidate for the study of learning. many learned responses involve neurons in the animal’s abdominal ganglion (P9 is the largest nerve serving the tail). The size and distinctiveness make them ideal for electrical recording

habituation in Aplysia

gill-withdrawal reflex, reduced activity at synapse between sensory and motor neurons, and direct result of decreased neurotransmitter release

sensitization in Aplysia

a stimulus gains the ability to influence more than 1 neural pathway

classical conditioning in Aplysia

by pairing it with a tail shock (US), they conditioned mantle shell touch (CS+) to elicit gill withdrawal (CR). it reflects changes in neurotransmitters released by sensory neurons onto motor neurons controlling the gill withdrawal response

operant conditioning in Aplysia

Aplysia biting behavior increased in frequency when trained with a contingent award of a liquid.

neural pathways involves in operant conditioning

1. direct transcortical connections - one cortex area to another

2. connections via the basal ganglia and thalamus

transcortical pathways

involved in the acquisition of complex behaviors involving deliberation. ex. learning to drive stick shift (slow and awkward, but becomes more automated once transferred down to basal ganglia pathways)

basal ganglia

passive observer when the transcortical pathway is occurring, but this pathways then learns what to do and takes over. the caudate and putamen receive sensory input from cortical areas sends outputs to globus pallidus then to the frontal lobe, then to the premotor cortex and onto the motor cortex.

Hebb’s rule

“any 2 cells or systems of cells that are repeatedly active at the same time will tend to become ‘associated',’ so that activity in one facilitates activity in the other”

long-term potentiation (LTP)

synaptic connections are effectively made stronger by repeated stimulation. Bliss and Lomo (1973). 2 main properties: it can last for many weeks, and it only occurs if presynaptic firing is followed by post synaptic firing. It is only seen in synapses where it was induced, not in surrounding synapses.

Hebb’s postulate for learning

co-occurrence (associativity) is necessary for learning and memory

evidence of LTP

• elicited by levels of stimulation that mimic normal neural activity

• LTP effects are greatest in brain areas involved in learning and memory

• learning can produce LTP-like changes

• drugs that impact learning often have parallel effects on LTP

LTP three-part process

Induction (learning), maintenance (memory), and expression (recall)

Induction

(learning) early phase of LPT, involves calcium flow into post-synaptic resulting in new AMPA-R at the cell surface

maintenance

(memory) late phase of LTP-transcription factors alter gene expression to increase AMPA-R production

expression

recall, last process of LTP

induction of LTP

studied where NMDA Glu receptors are prominent, those receptors do not respond maximally unless 2 things happen: Glu binds to the receptor (NT-dependent), and neuron is already depolarized (voltage-dependent)-AMPA-R

Ca++

channels do not open fully unless both conditions are met, and their influx may activate protein kinases that induces changes in trafficking of AMPAR, causing LTP

protein kinases

may increase the sensitivity of and/or increase the number of glutamate receptors. they may also activate some type of retrograde messenger. inhibitors block LTP

activation of non-NMDA glutamate receptors

causes depolarization of postsynaptic cell membrane

protein synthesis

underlies long-term changes in extracellular Glu levels. Glu levels are increased by LTP.

nitric oxide and endocannabinoids

coordinates presynaptic and postsynaptic changes. they are synthesized in postsynaptic neurons in response to Ca++ influx may diffuse back to presynaptic neurons - cause increase GLU release presynaptically

structural changes (LTP consequence)

increase in number and size of synapses and increase in NMDA and AMPA receptors.

type II calcium-calmodulin kinase

an enzyme that must be activated by Ca++, may play a role in the establishment of LTP by moving AMPA-R

AMPA-R trafficking

controls synaptic development, controls NA channels by releasing GLU to produce EPSPs in the membrane of the dendritic spine. the more AMPA-R, the realse of GLU by the terminal button causes a larger EPSPs, the response of the synapse becomes stronger.

dendritic spine growth

following LTP, changes in the size and shape of dendrite spines occur

LTD

long-term depression

H.M.

an epileptic who had his temporal lobes removed in 1953. his seizures were dramatically reduced, but so was his memory. he had mild retrograde amnesia and severe anterograde amnesia. his short term memory was still intact-he could remember up to 7 digits and he learned rotary-pursit and a drawing task. he also learns responses through classical conditioning-conditioned eye-blink

retrograde amnesia

backward acting, unable to remember the past

anterograde amnesia

forward-acting, unable to form new memories

block-tapping memory-span test

this test demonstrated that HM’s amnesia was global and not limited to one sensory modality

mirror-drawing task

H.m exhibits improvement with practice, able to show skill memory and demonstrating learning.

medial temporal lobe amnesia

we learned from H.M. that they are involved in memory. not all with this form of amnesia are unable to form new explicit long-term memories. semantic memory (general info) may function normally while episodic (events that one has experiences) does not.

explicit memories

conscious memories

implicit memories

unconscious memories

repetition priming test

used to assess implicit memory. performance in identifying word fragments is improved when the words have been seen before. (the incomplete pictures of the elephant and umbrella)

reconsolidation

when a memory is retrieved from LTM, it is temporarily help in STM. memory is susceptible to post-traumatic amnesia until it is reconsolidated.

anisomycin

a protein synthesis inhibitor, prevented reconsolidation of conditioned fear in rats

R.B.

suffered damaged to just one part of the hippocampus and developed amnesia. CA1 cell layer. his case suggests that hippocampal damage alone can produce amnesia

bilateral medial temporal lobe lesions

decreased performance for delays of 15 secs or longer, still had STM but LTM effected, and effect was mirrored in humans

aspiration used to lesion the hippocampus

resulted in additional cortical damage (in monkeys)

bilateral damage to rats (hippocampus, amygdala, rhinal cortex)

produces the same deficits seen in monkeys with hippocampal lesions

bilateral removal of rhinal cortex

consistently results in object-recognition deficits

bilateral removal of the hippocampus

produces moderate or no effects on object recognition. (ischemia-induced lesions to a small part of it leads to severe deficits)

bilateral removal of the amygdala

has no effect on object-recognition

ischemia induced hyperactivity of CA1 pyramidal cells

damages neurons outside the hippocampus

extrahippocampal damage

is not readily detectable and is largely responsible for ischemia-induced object recognition deficits because bilateral hippocamectomy prevents ischemia-induced deficits

hippocampus

plays a key role in memory for spatial location (cognitive map). contains mainly place cells

rhinal cortex

plays important role in object recognition