Scientific Illustration

Origins of synaptic genes. (A) Homologues of genes in the human synaptic complex were identified in the genomes of selected organisms representing key phylogenetic steps in animal evolution. Colors indicate the inferred ancestor of origin for each gene, as indicated in B. (B) Evolutionary relationships among animal phyla. The names of representative species are shown.

infinity-imagined:

This illustration shows a synapse.  When an action potential arrives at a synapse, the positive charge causes the opening of voltage gated calcium channels.  Calcium pours into the synaptic button and binds to several proteins, changing their shape.  The activated proteins dynamically rearrange the blue cytoskeleton to transport green vesicles filled with yellow neurotransmitters to the synaptic cleft, which is filled with red adhesion proteins.  Calcium-activated SNARE proteins bind to both the vesicle and the synaptic membrane, causing the vesicle to fuse with the membrane, turning it inside out and spilling neurotransmitters into the synaptic cleft.  The neurotransmitters then bind to proteins on the receiving cell.  There are several types of yellow-green receptor proteins.  Sodium (Na+) channels (excitatory) respond the the neurotransmitter Glutamate.  Chloride (Cl-) channels (inhibitory) respond to the neurotransmitter GABA.  Dopamine, Serotonin, and Opioids bind to G-Protein Coupled Receptors (GPCRs) which cause complicated phosphorylation cascades that change the metabolism of the cell.

Artwork by David S. Goodsell 

(via srlyll)

tinyhands:

The idealized diagram I (obviously) drew, depticting short-term sensitization of gill withdrawal in Aplysia

As the name implies, this is the mechanism underlying organism-wide increased sensitivity to touch after it has been shocked at just one site. 

Short-term sensitization of gill withdrawal in aplysia occurs when the organism’s tail is subjected to a stimulus shock, thereby activating tail sensory neurons, and by extension, the modulatory interneurons which innervate with presynaptic terminals of the gill sensory neurons. At any one of these synaptic clefts, serotonin is released by the interneuron and received by G-coupled serotonin receptors, which, in the presence of ATP, catalitically releases cAMP, activating protein kinase A (PKA). PKA then mediates phosporylation of the K+ channels, which reduces the probability that it will open, enhancing Ca2­­+ entry through its respective ionic channel and facilitating a greater release of glutamate into the synaptic cleft between the siphon sensory neuron and the gill motor neuron.

aspoonfulofmedicine:

synapse

houseofmind:

The Neuromuscular Junction (NMJ) is a specialized synapse that serves to transmit electrical impulses (action potentials) from the motor neuron nerve terminal to the skeletal muscle. Basically, the NMJ allows for efficient and reliable communication between the motor neuron nerve and the muscles required for contraction and movement. The primary chemical messenger in this synapse, which consists of the presynaptic region (containing the nerve terminal), the synaptic cleft and the postsynaptic surface, is acetylcholine. These regions are defined by the differential localization of specific proteins, which underlie their distinct anatomical features and their physiological roles. 

Now it’s time to briefly sum up what goes on in the NMJ, as shown in the diagram above. 

1. The action potential (or electrical impulse signal) reaches the nerve terminal in the presynaptic region. The hallmark feature of the nerve terminal is that it contains the synaptic vesicles, along with the proteins that help vesicle function. These vesicles are aligned near their release site, called an active zone. 

2. When action potentials reach the nerve terminal they activate calcium channels, which open up and facilitate the influx of calcium into the presynaptic terminal, which in turn commences the process of vesicular release into the synaptic cleft. 

3. The increase in intracellular calcium concentration triggers the fusion of the synaptic vesicles with the nerve terminal membrane. The mechanism of synaptic vesicle fusion involves conformational changes in multiple docking proteins both on the vesicle and the nerve terminal’s plasma membrane. 

4. Once fused with the nerve terminal membrane, the vesicle releases its contents into the extracellular space, also known as the synaptic cleft. The chemical or neurotransmitters (in this case, acetylcholine) released then bind to their corresponding receptors on the postsynaptic surface (also known as the motor end plate in the NMJ). 

5 & 6. Acetylcholine binds to its receptors and opens ligand-gated Na+/K+ channels. These structures are designed to optimize cholinergic neurotransmission in order to produce an end plate potential (EPP). The EPP is simply the net synaptic depolarization caused by the release of acetylcholine triggered by the nerve action potential. The EPP is a function of the miniature endplate potential (MEPP) amplitude, which represents the depolarization of the postsynaptic membrane produced by the contents of a single vesicle, and quantal content (number of transmitter vesicles released by a nerve terminal action potential. The EPP serves to open the voltage-gated Na+ channels in the postsynaptic region, which in turn results in an action potential that triggers muscle fiber contraction. These changes in the postsynaptic region potential result in muscle stimulation and contraction.

7. Acetylcholinesterase degrades acetylcholine so that it (choline) can be re-uptaked and recycled to produce new acetylcholine molecules. It’s activity terminates synaptic transmission. 

Sources:

Hughes, Benjamin W., et. al. 2006. Molecular architecture of the neuromuscular junction. Muscle & Nerve. 33(4): 445-461. DOI 10.1002/mus.20440

Motor Systems: Control of Movement and Behavior. 2008. Available at: http://www.colorado.edu/intphys/Class/IPHY3730/09motorsystems.html

fyeahmedlab:

The transmission of Serotonin across a synapse.