Synapse

Synaptic Functions of Neurons

Nerve impulse may be:

1) Blocked in its transmission from one neuron to the next ( inhibitory)

2) Changed from single to repetitive impulse (excitatory)
3) Integrated w/ impulses from other neurons to create a highly intricate patterns of successive impulses in successive
neurons.

Types of Synapses:

1) Chemical - use of neurotransmitters

2) Electrical - direct open fluid channels that conduct electricity from one cell to the next cell (gap junctions)-
from one muscle to other muscle; conduct electricity

Principle of one way conduction of neurons (for chemical only)

Presynaptic terminalsynaptic cleftpostsynaptic membrane

Voltage Gated Calcium Channels

1. Action Potential depolarize the presynaptic terminal (Na++channel open & change charges)
2. Voltage gated calcium channels open (Ca goes in and binds the release sites)
*Amount of Ca goes in = Amount of neurotransmitter release
3. Release sites open = synaptic vesicle release neurotransmitter into synaptic cleft

Action Transmitter Substance on the Presynaptic Neuron- Function of Receptor Proteins

Components of the Receptor Proteins:

1) Binding Component -protrudes outward, towards synaptic cleft

2) Ionophore Component -penetrates the membrane towards interior of postsynaptic mem.
a. Ion channel - cation and anion channel
nd
b. 2 Messenger Activator
-composed of: Alpha, Beta, Gamma Protein
 Excitatory - Sodium Cation Channel
 Inhibitory - Anion Channel (stops Sodium); Open Potassium channel to go out

Active Membrane enzymes; change in cell metabolism:

- cAMP (Cyclic Adenosine Monophospate)
- cGMP (Cyclic Guanosine Monophospate)

Actions of the alpha protein once it has separated:

1) Opens an ion channel in the membrane of the postsynaptic neuron

2) Activate an enzyme in the postsynaptic membrane
3) Activate an intracellular enzyme system
4) Activation of gene transcription

Excitation of the Postsynaptic Neuron

1) Opening of the sodium channels – Na goes in

2) Depressed conduction thru Chloride or potassium channels or both
3) Changes in the internal metabolism of the postsynaptic neuron to excite cell activity
- Increase in excitatory mem. Receptors
- Decrease in inhibitory mem. Receptors
 -

Inhibition of the Postsynaptic Neuron

1) Open chloride channels

2) Increase conductance of potassium
3) Activation of receptor enzyme
- Decrease in excitatory mem. Receptors
- Increase in inhibitory mem. Receptors

Small Molecule Rapid Acting Growth factor/Slowly Acting

Transmitter Transmitter/Neuropeptide
Rapid Prolonged
Response of the Nervous System
Cytosol of the presynaptic Ribosomes
Synthesis terminal (transport thru axonal streaming)
Conductance of the ions -Closure of Ca channel is
Effect Excitatory- Na increase prolonged
Inhibitory-K or Cl increase -prolong change in cell metab.
-prolong inactivation/acti. Of
genes
-prolong change in numbers of
receptors (excit. & inhib.)
Yes No (autolyzed)
Recycle Vesicle Since method of forming this is
laborious, compensation is that
the neuropeptides are more
potent. (lysosome, compensatory
mechanism)

Small Molecule Rapidly Acting Transmitters

1) Acetylcholine (excit)
2) Norephinephrine (excit) - located in brain stem & hypothalamus
3) Dopamine (inhib) - originate in substantia nigra
4) Serotonin (inhib)
5) Nitrous oxide (inhib)

Neuropeptide Slowly Acting Transmitter or Growth Factors

1) Oxytoxin - Milk gateway

2) Growth Hormone
3) Insulin - pancreas
4) Proicatin - milk production

Fatigue of Synaptic Transmission

- Protective mechanism against neuronal activity

- Due to :
1. Mainly exhaustion of stores of neurotransmitter in presynaptic terminals
2. Progressive inactivation of postsynaptic membrane receptors
3. Slow development of abnormal ion concentration in postsynaptic neuronal cell
Effect of alkalosis and acidosis on Synaptic Transmission

Alkalosis - increase excitability

Acidosis - decrease excitability

Drugs that affect Neuronal Transmission

 Increase excitability:
- Caffeine, theophylline, theobromine = reduce the threshold for excitation
- Strychnine = inhibit action of inhibitory transmitter substances (glycine) –causes spasms
 Inhibitory:
- Anesthetics = increase neuronal membrane threshold for excitation

NEUROMUSCULAR

Motor End Plate

1) Nerve terminal w/ synaptic gutter/trough- contains numerous mitoch. & synaptic vesicle
2) Synaptic space/cleft-contains acetylcholinesterase
3) Muscle fiber w/ subneural clefts in the membrane-posess acetylcholine receptors

Roles of Acetylcholine in neuromuscular transmission:

 At the Nerve Terminal

1) An action potential passes down the nerve
2) The nerve releases Ca that results in the release of Ach thru exocytosis into the synaptic cleft
 At the muscle fiber membrane
1) 2 ACh attach to the ACh receptors (ACh-gated ion channels) and the channels open
2) Na (main ion) goes in the muscle fiber also w/ potassium and calcium
3) Na carries a positive charge so end plate potential is created. Action potential that spread thru out muscle
membranemuscle contraction

Destruction of Released ACh by acetylcholinesterase

Fatigue of the Junction

- Stimulation of the nerve at rates greater than 100 times per second often diminishes the number of ACh
vesicleimpulses fail to pass to the muscle fiber

Some drugs that affect the neuromuscular junction and their actions

1) Block transmission at the neuromuscular junction

- Curare/D-tubocurare= blocks gating potential of Acth by competing w/ the Acth cites on the
receptor(paralysis)
2) Drugs that stimulate muscle by ACh like action
3) Inactivates acetylcholinesterase
- Neostigmine= alleviates the symptoms of myasthenia gravis
- Physostigmine
- Diisopropyl flourophosphate = nerve gas