Synapses

There is bidirectional communication at almost every synapse to maintain or modulate synaptic activity.

 

  1. Na influx during depolarization
  2. Ca influx (how?) at the synapse
  3. vesicle fusion
  4. vesicle recycling

 

Synapse Locations

Synapses are located on the cell body and dendrites.

 

At the Neuromuscular Junction (NMJ) the whole thing is encased by Schwann cells. Each NMJ has about 1000 active zones, and each presynaptic impulse releases 100-200 ACh molecules. This is a large margin of excess to ensure muscular contraction occurs.

ACh esterase is attached to the basal lamina in synaptic invaginations.

 

 

Pre-synaptic terminal

Calcium release induces vesicle fusion with the membrane, mediated by SNARE proteins. Botulinum and tetanus toxins paralyze SNARE proteins, preventing neurotransmitter release.

 

Some synapses have multiple co-localized neurotransmitters. This often occurs with small transmitters in vesicles about 40 nm in diameter, with neuropeptides present in larger dense-core granules 100-200 nm in diameter. In general, low frequency stimulation causes release of only small transmitters, while high frequency signals cause release of both.

 

Presynaptic inhibition (often GABAB receptors) can occur via phosphorylation of calcium channels, preventing vesicle release.

 

 

 

Post-synaptic terminal

The post-synaptic membrane is frequently amplified through invagination or outfolding of the membrane. This significantly increases the receptor surface area.

Opening of ion channels sums together, across dendrites and cell bodies, in attempts to reach threshold.

 

ACh Receptors are affected in the autoimmune disease Myasthenia gravis; curare also affects the AChR.

 

 

 

Neurotransmitter removal

Post-synaptic responses

a fast epsp is 10 ms

There are two basic mechanisms of post-synaptic receptor activation.

 

Ionotropic mechanisms are the fastest (on the order of milliseconds), with the receptor itself being the ion channel. Ionic channels include:

metabotropic mechanisms are coupled to a G protein and any number of signaling mechanisms (typically IP3, cAMP, and the alpha subunit of the G protein). This results in their taking seconds to minutes to mediate their response.

Metabotropic mechanisms allow for amplification, divergent signaling effects, and long-lasting chemical changes that result in learning and memory.

 

Synaptic strength

Most synapses are not strong enough on their own to activate an action potential. Two exceptions to this are the NMJ and the synapse between climbing fibres in the inferior olive and Purkinje cells. Instead, most synapses require summation of other synaptic inputs before an action potential is reached.

 

drugs or toxins that enhance transmission

 

drugs or toxins that depress transmission

 

 

Gap Junctions

6 connexins form a hemichannel, while a hemichannel in each cell form a gap junction channel