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Home , Chemical synapse, Synapse

synapses are the functional connection between and a few other cells (eg. muscles, glands)

CNS:  neuron

PNS: neuron  neuron neuron  muscle fiber [=] neuron  gland [=neuroglandular junction] each neuron synapses with 1000 – 10,000 axonal terminals 10 Billion Neurons in NS  500 Trillion Synapses presynaptic neuron vs postsynaptic neuron two kinds of synapses: 1. electrical synapses 2. chemical synapses

1. Electrical Synapses

very common in embryonic ,

much less common in adults; get replaced by chemical synapses

cells are directly connected with each other  cytoplasm is continuous

impulses can go in either direction

eg. brain: rapid stereotyped eye movements eg. rhythmic contractions of smooth muscle eg. intercalated discs of cardiac muscle  chambers contract as single cells

2. Chemical Synapses

most common kind of

actual gap or space between cells

one direction only (= unidirectional)

prevents direct transmission of 1 requires release of a chemical messenger =

What Happens at :

1. AP travels down of presynaptic neuron to axonal end bulb

2. AP causes Ca++ gates to open and Ca++ enters presynaptic neuron

3. Ca++ activates enzymes in axonal end bulb which stimulates of neurotransmitter [synaptic vesicles move to surface of and release NT]

4. NT diffuses across synaptic cleft

5. NT binds to specific molecules in membrane of postsynaptic neuron ( or cell body)

6. causes chemical gates to open allowing some ions in can cause partial or hyperpolarization depending on gates

7. termination of NT occurs when: a. it is degraded by enzyme on postsynaptic neuron or in synapse b. it returns to presynaptic neuron and is reabsorbed c. or it diffuses away from synapse

whole process takes 0.3 – 5.0 ms

Kinds of Chemical Synapses

Above is general idea of what happens at a synapse

There are different kinds of chemical synapses: 1. excitatory  produce EPSP’s 2. inhibitory  produce IPSP’s

1. Excitatory Synapses

NT binding causes partial depolarization of post synaptic membrane

Na+ and K+ ions diffuse simultaneously in opposite directions

but more Na+ in than K+ out  depolarization  produces EPSP’s

2 lasts only a few milliseconds

then membrane returns to resting potential

2. Inhibitory Synapses

NT binding induces hyperpolarization of membrane: becomes more permeable to K+ (out) and/or more permeable to Cl- (in) causes hyperpolarization  produces IPSP’s

Synaptic Interactions (Neural Circuits)

Remember, each postsynaptic neuron may synapse with 10,000’s of presynaptic neurons (=neuronal pools)

some of these synapses are excitatory; some are inhibitory

 sum of all EPSP’s and IPSP’s at a particular time determine whether a neuron will generate an action potential or not

Summation: 1. Temporal summation 1 or more neurons transmit impulses in rapid sequence

2. Spatial summation large # of terminals are stimulated at the same time

 axonal hillock acts as a “bean counter” it totals all the effects may or may not trigger AP

Potentiation:

can also get potentiation (facilitation) doesn’t fire but easier to fire next time.

Finally, there are literally 100’s of different kinds of ; some excitatory, some inhibitory bind to specific receptors in specific parts of

can produce a variety of effects on post synaptic neurons

3 also can get various additional modifications of synapse: changes in the amount of NT released changes in excitability of post synaptic neuron presynaptic inhibition etc.

Neurotransmitters

neurotransmitters are the language of the nervous system

NT are released at chemical synapses

100’s have been identified some are excitatory some are inhibitory

the same NT may have different effects in different parts of body eg. excitatory one place, inhibitory another

The effect of a NT on a postsynaptic neuron depends on the properties of the receptor not on the nature of the NT

some neurons produce and release a single NT

most make 2 or more and can release one or all

synapses in PNS release only a few different neurotransmitters esp ACh, Epinephrine, NE

most of the diversity is in the CNS, esp the brain

a variety of different chemicals have been found to act as neurotransmitters: 1. 2. protein & amino acid derivatives biogenic amines amino acids peptides proteins 3. Inorganic gasses 4. ATP

Effects of Drugs on Nervous Transmission 4 Drugs generally interfere with key steps in synaptic transmission: 1. affect NT synthesis 2. alter rate of release 3. prevent binding to receptor 4. prevent NT inactivation

The end result of these actions: 1. drugs mimic specific neurotransmitters 2. enhance the actions of a NT 3. block action of NT

1. Drugs with general effects on Synapses a. Dilantin used to treat epilepsy epilepsy a too rapid firing of certain brain cells subsides only when NT supply runs out dilantin increases effectiveness of Na+ active transport to stabilize resting potential

b. generally lowers threshold at synapses

2. Acetylcholine (ACh) 1st to be identified at all NM jcts also found in autonomic NS at some smooth and cardiac muscles generally has stimulatory effect on skeletal muscles in autonomic NS may have stimulatory or inhibitory effect

in CNS: 1. inadequate amt ACh  correlated with Alzheimer’s 2. ACh receptors destroyed in Myasthenia gravis, an autoimmune disease

in PNS: Acetylcholine at NM Jcts 1. Botulism Toxin blocks release of ACh  paralysis 2. Black Widow Toxin stimulates massive releases of ACh  intense cramping & spasms 3. Nicotine mimics ACh binds to receptor and activates it but no enzyme to remove it

5  prolonged hyper activity 4. atropine, binds to receptor but does not induce since ACh cannot bind to receptors already bound to curare muscle cells cannot be stimulated to contract  paralysis

in most synapses, once ACh binds to receptor and initiates a response it is removed by enzyme

nerve gas, malathion (= inhibitors) blocks breakdown of ACh  extended, extreme contractions

3. Protein & Amino Acid Derivatives broadly distributed in brain affect behavior, moods, sleep, thought

some examples:

a. a synthesized from tyrosine esp in of basal ganglia (midbrain) affects coordination of skeletal muscles also a “feel good” NT

1. Parkinson’s Disease deficiency tremors (no inhibition of basal nuclei) 2. schizophrenia correlated with excess of dopamine 3. enhance its feel good effects 4. blocks its uptake

b. norepinephrin esp in brain stem another “feel good” NT affects mood: arousal, dreaming also released by some neurons in autonomic NS (sympathetic branch)

6 1. generally excess  mania deficiency  depression 2. Cocaine & amphetamines prevents inactivation of norepinephrin enhances its effect amphetamines and cocaine have similar effect as on dopamine c. indolamine syn from tryptophan or histidine in brain stem (reticular system) induces sleep, temp regulation, appetite, affects mood and aggression

1. LSD binds to serotonin receptors prevents its effect or counteracts its function in brainstem (RAS) 2. Prozac prevents its uptake  relieves anxiety and depression 3. linked to migraine headaches d. produced in hypothalamus in immune system is powerful vasodilator e. aspartate amino acid only in CNS excitatory f. glutamate amino acid only in CNS excitatory important in learning and

1. released in large quantities after stroke  increases damage to g. amino acid in spinal cord inhibitory

7 blocks receptors  causes convulsions h. GABA modified amino acid most abundant inhibitory NT in brain (~1/3rd of all) inhibits skeletal movements

1. deficiency: Huntington’s disease  jerky movements 2. enhances its inhibitory effects  slowed reflexes  reduced coordination

also affects mood excess: less anxiety deficiency: more anxiety

1. Valium binds to GABA receptors mimics or enhances its effects  less anxiety i. Substance P peptide (chain of amino acids) mediates transmission in PNS in CNS affects mood also involved in respiratory and cardiovascular control j. & enkephalins peptides in limbic system and related structures natural opiates reduces pain perception “runners high”

1. , heroin, methadone binds to enkephalin receptors  mimicks effecs of endorphins k. cholecystokinin peptide

8 may be related to feeding disorders

4. Inorganic Gasses

a. NO (nitric oxide) toxic gas short lived is synthesized on demand not stored in axonal vesicles in CNS may be involved in learning and memory in PNS causes relaxation of smooth muscle

b. CO (carbon monoxide) in CNS similar physiology as NO

5. ATP now recognized as a major neurotransmitter in both CNS and PNS produces fast excitatory response at certain receptors

Neuromodulators

other chemicals can be released at synapse in addition to neurotransmitters: =neuromodulators

neuromodulators can influence the release of NTs or the post synaptic neuron’s response to the NT

NM are usually peptides =

a chemical may be both a NT and NM

neuromodulators function in 3 different ways: 1. have direct effect on by opening and closing chemical gates 2. have indirect effect on membrane potential thru “second messenger” eg. receptor on cm

adenylate cyclase

cyclic AMP

3. gasses are lipid soluble and diffuse into post-synaptic cell to activate enzymes and second messengers

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