The Synaptic Self - How Our Brains Become Who We Are by Joseph LeDoux

Author:Joseph LeDoux [LeDoux, Joseph]
Language: ita
Format: epub
Published: 2011-08-17T22:00:00+00:00

MEMORY MECHANISMS

All forms of gill-reflex learning involve changes in synapses between sensory neurons that receive inputs from the mantle skin and motor neurons that control the gill response. In habituation, for example, the response of the postsynaptic neuron to a presynaptic input weakens, and the gill response gets smaller, because the presynaptic terminal comes to release less glutamate. It simply gets depleted.

In contrast, in sensitization, the gill reacts more to the same stimulus after the tail is shocked than before because the sensory neuron comes to release more glutamate. To understand why more glutamate comes out after the tail is shocked requires that we consider the way the shock pathway interacts with the synapses that connect the sensory and motor neurons.

The shock pathway forms synapses on the terminals of the sensory neurons. These are called axoaxonic synapses, since the axon terminals of the shock pathway make synapses with other axon terminals, in this case, terminals of the sensory pathway. This contrasts with the situation we’ve considered most so far, in which axon terminals contact dendrites. The tail shock pathway thus ends on the presynaptic terminal of the sensory neuron and causes more transmitter to be released. Because the increase in the efficiency of transmission between the sensory and motor neuron is due entirely to alterations in the sensory neuron terminal, it is referred to as presynaptic facilitation. Because the state of activity of the postsynaptic neuron is irrelevant, sensitization by definition is a form of non-Hebbian plasticity (recall that Hebbian plasticity requires presynaptic and postsynaptic activity).

How does the tail shock cause presynaptic facilitation? The tail shock pathway releases the modulator serotonin at the sensory terminal. When serotonin binds to its receptors on the terminal, it activates second messengers there that ultimately lead to the activation of a protein kinase, namely PKA, which is also involved in LTP.

PKA in turn leads to other changes that cause action potentials to last a little longer than usual. As a result, more glutamate is released from the terminal after the shock than before. This causes a bigger response in the motor neuron, and therefore behaviors controlled by motor neurons, like gill withdrawal, are more strongly expressed.

The sensitizing effects of shock are short-lived unless the shock is given repeatedly. When a repeated shock is administered, additional processes are activated, and the effects of sensitization can last for days. In particular, PKA is activated in a special way that allows it to enter the cell nucleus. In addition, a second protein kinase, MAP

kinase (which is involved in hippocampal and amygdala plasticity), is also activated by repeated shocks and moves inside the nucleus. PKA and MAP kinase then phosphorylate the gene transcription factor, CREB, which we also encountered earlier in our survey of LTP.

CREB-activated genes make new proteins that end up facilitating transmission between the sensory and motor neuron in various ways. One effect of these proteins is that PKA becomes persistently activated, which means that the short-term sensitizing effects of PKA are lengthened, continuing the effects on transmitter release described above.

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