section 11.8 Flashcards
Hebb’s hypothesis
enduring facilitations of synaptic transmission are the neural bases of learning and memory.
Bliss and Lømø
showed that there is a facilitation of synaptic transmission following high-frequency electrical stimulation applied to presynaptic neurons. Termed long-term potentiation (LTP).
LTP has two key properties that Hebb proposed as characteristics of the physiological mechanisms of learning and memory:
- LTP can last for a long time – for several months after multiple stimulations.
- LTP develops only if the firing of the presynaptic neuron is followed by the firing of the postsynaptic neuron; it does not develop when either neuron fires and the other does not.
The co-occurrence of firing in presynaptic and postsynaptic cells is now recognized as
the critical factor in LTP.
Hebb’s postulate for learning
assumption that co-occurrence is a physiological necessity for learning and memory.
Additional support for the idea that LTP is related to the neural mechanisms of learning and memory has come from several observations:
- LTP can be elicited by low levels of stimulation that mimic normal neural activity.
- LTP effects are most prominent in structures that have been implicated in learning and memory, such as the hippocampus.
- Behavioral conditioning can produce LTP-like changes in the hippocampus.
- Any drugs that influence learning and memory have parallel effects on LTP.
- The induction of maximal LTP blocks the learning of a Morris water maze until the LTP has subsided.
- Mutant mice that display little hippocampal LTP have difficulty learning the Morris water maze.
- LTP occurs at specific synapses that have been shown to participate in learning and memory in simple invertebrate nervous systems.
LTP is a three part process:
induction, maintenance, and expression – that is, the processes by which high-frequency stimulations induce LTP (learning), the changes responsible for storing LTP (memory), and the changes that allow it to be expressed during the test (recall).
NMDA receptor
prominent at the synapses at which LTP is commonly studied; a receptor for glutamate.
An NMDA receptor does not respond maximally unless two events occur simultaneously:
glutamate must bind to it, and the postsynaptic neuron must already be partially depolarized.
This dual requirement stems from the fact that the calcium channels associated with NMDA receptors allow only
small numbers of calcium to enter the neuron unless the neuron is already depolarized when glutamate binds to the receptors; it is the influx of calcium ions that triggers action potentials and the cascade of events in the postsynaptic neuron that induces LTP.
The requirement for the postsynaptic neurons to be partially depolarized when the glutamate binds to them is an
extremely important characteristic of conventional LTP because it permits neural networks to learn associations.
The requirement for co-occurrence and the dependence of NMDA receptors on simultaneous binding and partial depolarization mean that
under natural conditions, synaptic facilitation records the fact that there has been simultaneous activity in at least two converging inputs to the postsynaptic neuron.
Dendritic spines
the calcium ions that enter a dendritic spine do not readily pass out of it, and thus they exert their effect locally.
LTP causes structural changes and many changes have been described including
increases in number and size of synapses, increases in number and size of postsynaptic spines, changes in presynaptic and postsynaptic membranes, and changes in dendritic branching.
transcription factors
intracellular proteins that bind to DNA and influence the operation of particular genes; activated by neural activity.
