Learning and memory - Storing Information in the Nervous System

we wouldn't call footprints that we leave memories. similarly, when a pattern of activity passes through the brain, it leaves a trace or path of physical change. not every change is a memory
EARLY THEORIES
1. PENFOLD suggested that each neuron held a specific memory, however stimulation elicited memories more like a dream....
2. in the 1960s and 1970s it was proposed that memory is coded as a specific molecule, such as RNA or protein. found that when rats were trained to approach clicking for food and then RNA from their brains put into another brain, the untrained rats will approach the clicking
HEBB - proposed a mechanism for a change at a synapse. he suggested that an axon that had successfully stimulated a cell in the past becomes even more successful in the future.
1. A HEBBIAN SYNAPSE is a synapse that increases in effectiveness because of simultaneous activity in the pre and post synaptic neurons.
  1. such synapses may be critical for associative learning.
  2. simultaneous activity increases effectiveness. axon and cell connection is strengthened. synapse strengthened, increased effectiveness, post synapse more sensitive, more transmitters released.
APLYSIA - animal like a slug, has less neurons and they are large and easy to study. HABITUATION IS A DECREASE IN RESPONSE TO A STIMULUS THAT IS PRESENTED REPEATEDLY. e.g. respond less and less when clock continues to chime.
1. HABITUATION in APLYSIA occurs when serotonin blocks potassium channels in post synaptic neuron, and prolongs neurotransmitter release from that neuron.
LONG-TERM POTENTIATION (LTP)
1. AXONS connected to a DENDRITE, one or more axon bombards a dendrite with stimulation. synapse is 'potentiated' and neuron is MORE RESPONSIVE for minutes / days / weeks. intense stimulation delivered to a neuron, prolongs the release of transmitter from that neuron
  1. three properties, SPECIFICITY - only the active synapses become strengthened. COOPERATIVITY - simultaneous stimulation by axons produces LTP more strongly than repeated stimulation by just one axon. ASSOCIATIVITY - pairing weak with strong input enhances later response to the weak input.
2. BIOCHEMICAL MECHANISMS - LTP depends on changes at glutamate synapses.
  1. GLUTAMATE RECEPTORS
    1. AMPA RECEPTOR - excited by neurotransmitter glutamate and AMPA acid. opens SODIUM channels, depolarisation = excitation.
    2. NMDA RECEPTOR - excited by glutamate and NMDA. SODIUM and CALCIUM channels open, only when membrane is already depolarised.
    3. ** Repeated glutamate excitation of AMPA receptors depolarizes the membrane, depolarisation removes magnesium ions that had been blocking NMDA receptors, GLUTAMATE can then excite the NMDA receptors, opening a channel for calcium ions to enter the neuron ** the entry of calcium is key to maintaining LTP.
    4. drugs that block NMDA synapses prevent the establishment of LTP but don't interfere with the maintenance of LTP
3. LTP reflects increased activity in the presynaptic neuron as well as increased responsiveness by the post synaptic neuron
LONG-TERM DEPRESSION (LTD) - prolonged decrease in response at a synapse for axons that are less active than others, as one synapse strengthens, another one weakens.
CONSOLIDATION
1. short term memory consolidated into a long-term memory. LTP in the hippocampus important for certain types of learning, but as time passes learning becomes less dependent on the hippocampus and more dependent on the CEREBRAL CORTEX. more activity in the hippocampus after 15 minutes, more activity in the cerebral cortex after 24 hours.
IMPROVING MEMORY - understanding the mechanisms of LTP enable researchers to understand what could impair or improve memory. AT THIS POINT IN TIME HOWEVER there are no safe and effective procedures or drugs that improve memory

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Learning and memory - Storing Information in the Nervous System

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