chapter3 power point lecture

Chapter 3Synapses

The Concept of the Synapse

• Neurons communicate by transmitting chemicals at junctions called “synapses”

• In 1906, Charles Scott Sherrington coined the term synapse to describe the specialized gap that existed between neurons.

• Sherrington conducted his research investigating how neurons communicate with each other by studying reflexes (automatic muscular responses to stimuli).

Fig. 3-1, p. 52


• Sherrington observed three important points about reflexes:1. Reflexes are slower than conduction

along an axon.2. Several weak stimuli presented at slightly

different times or slightly different locations produces a stronger reflex than a single stimulus does.

3. As one set of muscles relaxes, another set becomes excited.


• Sherrington observed a difference in the speed of conduction of the reflex arc from that of the speed of an action potential.

• He believed the difference must be accounted for by the time it took for communication between neurons to occur.

• Evidence validated the idea of the synapse.

Fig. 3-2, p. 53


• Sherrington observed that repeated stimuli over a short period of time produced a stronger response.

• Led to the idea of temporal summation or that repeated stimuli can have a cumulative effect and can produce a nerve impulse when a single stimuli is too weak.

Fig. 3-3, p. 54


• Sherrington also noticed that several small stimuli on a similar location produced a reflex when a single stimuli did not.

• This led to the idea of spatial summation or that synaptic input from several locations can have a cumulative effect and trigger a nerve impulse.

Fig. 3-4, p. 54


• Excitatory postsynaptic potential (EPSP) is a graded potential that decays over time and space.

• The cumulative effect of EPSPs are the basis for temporal and spatial summation.


• Sherrington also noticed that during the reflex that occurred, the foot of a dog that was pinched retracted while the other three feet were extended.

• He suggested that an interneuron in the spinal cord sent an excitatory message to the flexor muscles of one leg and an inhibitory message was sent to the other three legs.

Fig. 3-5, p. 55


• This led to the idea of inhibitory postsynaptic potential or the temporary hyperpolarization of a membrane.

• An ISPS occurs when synaptic input selectively opens the gates for positively charged potassium ions to leave the cell or for negatively charged chloride ions to enter the cells.

• Serves as an active “brake”, that suppresses excitation.

Fig. 3-6, p. 55


• Neurons can have thousands of synapses.• Both temporal and spatial summation can

occur within a neuron.• The likelihood of an action potential depends

upon the ratio of IPSPs to EPSPs at a given moment.


• The spontaneous firing rate refers to the periodic production of action potentials despite synaptic input.

• EPSPs increase the number of action potentials above the spontaneous firing rate.

• IPSPs decrease the number of action potentials below the spontaneous firing rate.

Chemical Events at the Synapse

• Transmission of a message across the synapse occurs by chemical means.

• Neurotransmitters are chemicals that travel across the synapse and allow communication between neurons.


• The major sequence of events that allow communication between neurons across the synapse are as follows:

1. The neuron synthesizes chemicals that serve as neurotransmitters.

2. Neurons store neurotransmitters in axon terminals or transport them there.

3. An action potential triggers the release of neurotransmitters into the synaptic cleft.

Chemical Events at the Synapse (cont.)

4. The neurotransmitters travel across the cleft and attach to receptors on the postsynaptic neuron.

5. The neurotransmitters separate from the receptors.

6. The neurotransmitters are taken back into the presynaptic neuron, diffuse away, or are inactivated by chemicals.

7. The postsynaptic cell may send negative feedback to slow the release of further neurotransmitters.

Fig. 3-8, p. 59


• Major categories of neurotransmitters include the following:– Amino acids.– Peptides.– Acetylcholine.– Monoamines.– Purines.– Gases.

Table 3-1, p. 60


• Neurons synthesize neurotransmitters and other chemicals from substances provided by the diet.– Catecholimines are synthesized and

contain a catechol group and an amine group.

– Acetylcholine is synthesized from choline found in milk, eggs, and nuts.

– Tryptophan serves as a precursor for serotonin.

Fig. 3-9, p. 61


• Smaller neurotransmitters are synthesized in the presynaptic terminal and held there for release.– Example: acetylcholine

• Larger neurotransmitters are synthesized in the cell body and transported down the axon.– Example: peptides


• Vesicles are tiny spherical packets located in the presynaptic terminal where neurotransmitters are held for release.

• Exocytosis refers to the excretion of the neurotransmitter from the presynaptic terminal into the synaptic cleft.– Triggered by an action potential arriving fro

the axon.

Fig. 3-10, p. 61


• Transmission across the synaptic cleft by a neurotransmitter takes fewer than 10 microseconds.

• Most individual neurons release at least two or more different kinds of neurotransmitters.

• A neuron may respond to more types of neurotransmitters than it releases.


• An ionotropic effect refers to when a neurotransmitter attaches to receptors and immediately opens ion channels.

• Ionotropic effects occur very quickly and are very short lasting.

• Most of the brain’s excitatory ionotropic synapses use glutamate or acetylcholine as a neurotransmitter.

Fig. 3-11, p. 63


• Metabotropic effects refer to when a neurotransmitter attaches to a receptor and initiates a sequence of metabolic reactions that are slower and longer lasting.

• Metabotropic events include such behaviors as hunger, fear, thirst, or anger.

• When neurotransmitters attach to a metabotropic receptor, it bends the rest of the protein .

• Bending allows a portion of the protein inside the neuron to react with other molecules.


• The portion inside the neuron activates a G-protein –one that is coupled to guanosine triphosphate (GTP), an energy storing molecule.

• G-protein increases the concentration of a “second-messenger”.

• The second messenger communicates to areas within the cell.– May open or close ion channels, alter

production of activating proteins, or activate chromosomes.

Fig. 3-12, p. 63


• Metabotropic effects utilize a number of different neurotransmitters and are often called neuromodulators because they do not directly excite or inhibit the postsynaptic cell.

• Instead, neuromodulators:– increase or decrease the release of other

neurotransmitters– alter the response of postsynaptic cells to

various inputs.


• A hormone is a chemical secreted by a gland or other cells that is transported to other organs by the blood where it alters activity.

• Endocrine glands are responsible for the production of hormones.

• Hormones are important for triggering long-lasting changes in multiple parts of the body.

Table 3-2a, p. 64

Table 3-2b, p. 64


• Protein hormones and peptide hormones are composed of chains of amino acids and attach to membrane receptors where they activate second messenger systems.

• Hormones secreted by the brain can control the release of other hormones.

Fig. 3-13, p. 65


• The pituitary gland is attached to the hypothalamus and consists of two distinct glands that each release a different set of hormones:

1. Anterior pituitary- composed of glandular tissue and synthesizes six hormones.

2. Posterior pituitary- composed of neural tissue and can be considered an extension of the hypothalamus

Fig. 3-14, p. 65


• Neurons in the hypothalamus synthesize the hormones oxytocin and vasopressin which migrate down axons to the posterior pituitary.– Also known as antidiuretic hormones

• The hypothalamus secretes releasing hormones which flow through the blood and stimulate the anterior pituitary to release a number of other hormones.

Fig. 3-15, p. 66


• The hypothalamus maintains a fairly constant circulating level of hormones through a negative-feedback system.– Example : TSH- releasing hormone

Fig. 3-16, p. 66


• Neurotransmitters released into the synapse do not remain and are subject to either inactivation or reuptake.

• Reuptake refers to when the presynaptic neuron take sup most of the neurotransmitter molecules intact and reuses the.

• Transporters are special membrane proteins that facilitate reuptake. – Example: Serotonin is taken back up into

the presynaptic terminal.


• Examples of inactivation and reuptake include:– Acetylcholine is broken down by

acetylcholinesterase into acetate and choline.

• Some serotonin and catecholamine molecules are converted into inactive chemicals:– COMT and MAO are enzymes that convert

catecholamine transmitters into inactive chemicals.


• Research has begun to investigate the role of events at the synapse and their effects on personality.

• Research suggests that some dopamine receptors may be related to “pleasure-seeking” and “thrill-seeking” behaviors.

Drugs and the Synapse

• The study of the influence of various kinds of drugs has provided us with knowledge about many aspects of neural communication at the synaptic level.

• Drugs work by mimicking our own neurochemistry.– Example: receptors in the brain respond to

LSD and cocaine• Drugs alter various stages of synaptic

processing.

Fig. 3-1, p. 52


• Drugs either facilitate or inhibit activity at the synapse.– Antagonistic drugs block the effects of

neurotransmitters.– Agonist drugs mimic or increase the effects

of neurotransmitters.


• Drugs work by doing one or more of the following to neurotransmitters:1. Increasing the synthesis.2. Causing vesicles to leak.3. Increasing release.4. Decreasing reuptake.5. Blocking the breakdown into inactive

chemical.6. Directly stimulating or blocking

postsynaptic receptors.


• A drug has an affinity for a particular type of receptor if it binds to that receptor.– Can vary from strong to weak.

• The efficacy of the drug is its tendency to activate the receptor.

• Drugs can have a high affinity but low efficacy.


• Almost all abused drugs stimulate dopamine release in the nucleus accumbens, – small subcortical area rich in dopamine

receptors– an area responsible for feelings of pleasure

• Sustained bursts of dopamine in the nucleus accumbens inhibit cells that release the inhibitory neurotransmitter GABA

Fig. 3-18, p. 72


• Drugs are categorized according to their predominant action or effect upon behavior

• Stimulant drugs increase excitement, alertness, motor activity and elevate mood.

• Examples: amphetamines, cocaine, methylphenidate (Ritalin), MDMA (Ecstasy), nicotine

• Stimulant drugs directly stimulate dopamine receptor types D2, D3, and D4.

Fig. 3-19, p. 72


• Amphetamine stimulate dopamine synapses by increaseing the release of dopamine from the presynaptic terminal.

• Cocaine blocks the reuptake of dopamine, norepinephrine, and serotonin.

• Methylphenidate (Ritalin) also blocks the reuptake of dopamine but in a more gradual and more controlled rate.– Often prescribed for people with ADD


• Ecstasy increases the release of dopamine at low doses that account for its stimulant properties.

• Ecstasy increases the release of serotonin at higher doses accounting for its hallucinogenic properties.

• Research indicates ecstasy use may contribute to higher incidences of anxiety and depression as well as memory loss and other cognitive deficits.

Fig. 3-20, p. 73


• Nicotine is the active ingredient in tobacco.• Nicotine stimulates one type of acetylcholine

receptor known as the nicotinic receptor. • Nicotinic receptors are found in the central

nervous system, the nerve-muscle junction of skeletal muscles and in the nucleus accumbens.

• Nicotinic receptors are also abundant in the nucleus accumbens and facilitate dopamine release.


• Opiate drugs are those that are derived from (or similar to those derived from) the opium poppy.

• Opiates decrease sensitivity to pain and increase relaxation.

• Examples: morphine, heroin, methadone.


• The brain produces peptides called endorphins.

• Endorphin synapses may contribute to certain kinds of reinforcement by inhibiting the release of GABA indirectly.

• Inhibiting GABA indirectly releases dopamine.

• Endorphins attach to the same receptors to which opiates attach.


• Opiates also block the locus coeruleus.– involved in our response to arousing

stimuli by release of norepinephrine– also involved in memory storage.


• Tetrahydocannabinol (THC) is the active ingredient in marijuana.

• THC attaches to cannabinoid receptors throughout the brain but especially the cerebral cortex, cerebellum, basal ganglia, and hippocampus.

• Anandamide and 2-AG are the endogenous chemicals that attach to these receptors.


• The location of the receptors in the brain may account for the subjective effects of loss of time, an intensification of sensory experience, and also memory impairment.

• The cannabinoid receptors are located on the presynaptic neuron and inhibit the release of glutamate and GABA.


• Hallucinogenic drugs cause distorted perception.

• Many hallucinogenic drugs resemble serotonin in their molecular shape.

• Hallucinogenic drugs stimulate serotonin type 2A receptors (5-HT2A2A) at inappropriate times or for longer duration than usual thus causing their subjective effect.

Fig. 3-21, p. 75

Table 3-3, p. 76

chapter3 power point lecture

Business

synapse neurons

synapse sherrington

synapse transmission

chemical events

release of neurotransmitters

neurotransmitters travel

single stimuli

repeated stimuli