- •Signaling in chemical synapses Overview
- •Neurotransmitter release
- •Receptor binding
- •Termination
- •Synaptic strength
- •Receptor desensitization
- •Integration of synaptic inputs
- •Synaptic plasticity
- •Homosynaptic plasticity
- •Heterosynaptic plasticity
- •Volume transmission
- •Relationship to electrical synapses
- •Effects of drugs
- •Intrinsic excitability of a neuron
- •Axonal modulation
- •Shunting
- •High frequency stimulation
- •Effects on brain cell function Spike generation
- •Regulation of synaptic plasticity
- •Higher brain function involved with nonsynaptic plasticity Long-term associative memory Experimental evidence
- •Nonsynaptic processes and memory storage
- •Learning
- •Classical conditioning Evidence of learning-dependent nonsynaptic plasticity in vertebrates
- •Experiments of trace conditioning
- •Nonsynaptic vs synaptic plasticity
- •Current and future research
Receptor binding
Receptors on the opposite side of the synaptic gap bind neurotransmitter molecules. Receptors can respond in either of two general ways. First, the receptors may directly open ligand-gated ion channels in the postsynaptic cell membrane, causing ions to enter or exit the cell and changing the local transmembrane potential. The resulting change in voltage is called a postsynaptic potential. In general, the result is excitatory, in the case ofdepolarizing currents, or inhibitory in the case of hyperpolarizing currents. Whether a synapse is excitatory or inhibitory depends on what type(s) of ion channel conduct the postsynaptic current(s), which in turn is a function of the type of receptors and neurotransmitter employed at the synapse. The second way a receptor can affect membrane potential is by modulating the production of chemical messengers inside the postsynaptic neuron. These second messengers can then amplify the inhibitory or excitatory response to neurotransmitters.
Termination
After a neurotransmitter molecule binds to a receptor molecule, it must be removed to allow for the postsynaptic membrane to continue to relay subsequent EPSPs and/or IPSPs. This removal can happen through one or more processes:
The neurotransmitter may diffuse away due to thermally-induced oscillations of both it and the receptor, making it available to be broken down metabolically outside the neuron or to be reabsorbed.[14]
Enzymes within the subsynaptic membrane may inactivate/metabolize the neurotransmitter.
Reuptake pumps may actively pump the neurotransmitter back into the presynaptic axon terminal for reprocessing and re-release following a later action potential.[14]
The time frame for these "clearing" processes varies greatly for different types of synapses, ranging from a few tenths of a millisecond for the fastest, to several seconds for the slowest.[citation needed]
Synaptic strength
The strength of a synapse is defined by the amplitude of the change in membrane potential as a result of a presynaptic action potential. A "synapse" usually refers to a group of connections (or individual synapses) from the presynaptic neuron to the postsynaptic neuron. The strength of a synapse can be accounted for by the number and size of each of the connections from the presynaptic neuron to the postsynaptic neuron. The amplitude of postsynaptic potentials (PSPs) can be as low as 0.4mV to as high as 20mV.[15] The amplitude of a PSP can be modulated by neuromodulators or can change as a result of previous activity. Changes in synaptic strength can be short-term, lasting seconds to minutes, or long-term (long-term potentiation, or LTP), lasting hours. Learning and memory are believed to result from long-term changes in synaptic strength, via a mechanism known as synaptic plasticity.
Receptor desensitization
Desensitization of the postsynaptic receptors is a decrease in response to the same neurotransmitter stimulus. It means that the strength of a synapse may in effect diminish as a train of action potentials arrive in rapid succession – a phenomenon that gives rise to the so-called frequency dependence of synapses. The nervous system exploits this property for computational purposes, and can tune its synapses through such means asphosphorylation of the proteins involved.
