Transcript fleming_Oct

SYNAPSES
WITHOUT
NEURONS COULD NOT
‘TALK’ TO ONE ANOTHER AND WE WOULD HAVE NO
Sensory neuron
BEHAVIOR
SYNAPSES on
interneuron
Interneuron
SYNAPSES on motor
neuron
Receptor
SYNAPSES
on sensory neuron
Motor neuron
SYNAPSES on muscle
Fig 2.9
A simple sensory-motor (reflex) arc. A
simple reflex is set in motion by a stimulus
to the skin (or other part of the body). The
nerve impulse travels to the spinal cord
and then back out to a muscle, which
contracts. Reflexes provide an “automatic”
protective device for the body.
Figure 3.4 Temporal and spatial summation
SYNAPSES
1. Structure of the synapse
A. Presynaptic cell
1.Terminal button
2. Synaptic vesicles
3. Reuptake mechanisms
B. Synaptic cleft
C. Post-synaptic cell
Postsynaptic membranes and receptors
SYNAPTIC TRANSMISSION
2. Types of synapses
A. axonal-dendritic (axon to dentrite)
B. axonal-somatic (axon to soma)
C. axonal-axonal (axon to axon –usually inhib)
*****
SYNAPTIC TRANSMISSION
3. Effects of presynaptic action potentials on
polarization of post-synaptic cell
A. excitatory post-synaptic potential (EPSP)
B. inhibitory post-synaptic potential (IPSP)
******
PRIOR TO RELEASE OF NT POSTSYNAPTIC CELL IS IN
RESTING STATE AND POLARIZED AT –70mV
W. W. Norton
AFTER RELEASE OF NTs POSTSYNAPTIC CELL BECOMES
DEPOLARIZED (LESS NEGATIVE) AND ONE CAN RECORD
EXCITATORY POSTSYNAPTIC POTENTIALS. WHEN THESE
ADD UP TO AT LEAST 10Mv AND ‘THRESHOLD’ IS REACHED
THE POSTSYNAPTIC CELL WILL FIRE (ALL-OR-NONE)
W. W. Norton
?
W. W. Norton
IF THE NT THAT IS RELEASED IS AN INHIBITORY NT
IT PRODUCES GREATER POLARIZATION IN
POSTSYNAPTIC CELLS AND ONE RECORDS IPSPs
Inhibitory postsynaptic potential
W. W. Norton
SYNAPTIC TRANSMISSION
4. Summation of EPSPs and IPSPs on
pos-synaptic cell by
A. temporal summation
B. spatial summation
******
SYNAPTIC TRANSMISSION
5. Neurons synapse on one another and
produce additive effects of EPSPs and IPSPs
by
A. convergence
B. divergence
***********
Figure 2.1b
An example of a
neuron, or nerve cell,
showing several of its
important features. The
right foreground shows
a nerve cell fiber in
cross section, and the
upper left inset gives a
more realistic picture of
the shape of neurons.
The nerve impulse
usually travels from the
dendrites and soma to
the branching ends of
the axon. The neuron
shown here is a motor
neuron. Motor neurons
originate in the brain or
spinal cord and send
their axons to the
muscles or glands of
the body.
SYNAPTIC TRANSMISSION
5. Neurons synapse on one another and
produce additive effects of EPSPs and IPSPs
by
more than one axon
terminates on a neuron
A. convergence occurs when
B. divergence occurs when
***********
different axon terminals
from a single neuron
terminates on
different neurons
NEUROTRANSMITTERS
• Criteria for existence of neurotransmitter
a. must be mechanisms in presynaptic cell for its
1. synthesis
2. storage
3. release
4. Inactivation
*******
Sequence of Events at a Synapse
Figure 3.8 Some of the major events in transmission at a synapse
Animation
Sequence of Events at a Synapse
1
3
synthesis
vesicles
4
Presynaptic
terminal
5
2
vesicles
?
cleft5
6
Postsynaptic cell
Figure 3.8 Some of the major events in transmission at a synapse
Animation
NEUROTRANSMITTERS
1. Criteria for existence of neurotransmitter
b. stimulation of the neuron must result in
its release
c. must have specialized postsynaptic
receptors
d. agonists will mimic and antagonists will
block its effect
NEUROTRANSMITTERS
1. Different Neurotransmitters (and quick
associations)
B. Amines
Dopamine (Parkinsonism, Schizophrenia, Reward)
Norepinephrine (Learning, fear)
Acetylcholine (Motor, memory, Alzheimers)
Serotonin (Depression (SSRIs), aggression)
NEUROTRANSMITTERS
1.Different Neurotransmitters (and quick
associations)
B. Neuropeptides
Opioids, endorphins (pain, addiction)
CCK (satiation, eating)
Oxytocin (milk-letdown, maternal behavior)
GABA, Glutamate (inhibition, learning)
**********
DRUG EFFECTS ON NTS
3. Pharmacology
a.Agonists
b.Antagonists
inhibitors, false transmitters, inhibitors
of inactivation, depleting agents,etc.
**********
Synapses, Abused Drugs, and Behavior
How Drugs Affect Synapses
Agonist-a drug that mimics or increases the effects of a
neurotransmitter
Antagonist-a drug that blocks or takes away from the
effects of the neurotransmitter
Affinity-ability of a drug to bind a receptor
Efficacy-the degree to which the drug activates the
receptor once bound
1.
3
2.
4.
5
Figure 3.15 Events at a dopamine synapse
and how certain drugs affect the process
Drugs can alter any stage of processing at a
1.AGO
3 ANTAG
2. ANTAG
4. ANTAG
5 AGO
Figure 3.15 Events at a dopamine synapse
and how certain drugs affect the process
Drugs can alter any stage of processing at a
Dopamine is a neurotransmitter that excites
postsynaptic neurons. If a drug were injected
into an animal that blocked dopamine from
attaching to its receptors, what would happen
to the postsynaptic neurons?
Dopamine is a neurotransmitter that excites
postsynaptic neurons. If a drug were injected
into an animal that blocked dopamine from
attaching to its receptors, what would happen
to the postsynaptic neurons?
They would be less likely to produce further action potentials.
DISEASE CONDITIONS PRODUCED BY DISRUPTIONS IN
NEUROTRANSMISSION
Parkinson’s Disease
Symptoms-rigidity, muscle tremors, slow movement, difficulty initiating
movement
Brain Changes-Selective loss of cells in substantia nigra and
amygdala/decrease in dopamine
Possible Causes
genetics
exposure to toxins (MPTP)
smoking decreases risks/these data have been questioned
BRAIN STRUCTURES THAT ARE DISRUPTED IN PARKINSON PATIENTS
Figure 8.16 Connections from the substantia nigra: (a) normal and
(b) in Parkinson’s disease
Excitatory paths are shown in green; inhibitory are in red. The substantia nigra’s axons inhibit the
putamen. Axon loss increases excitatory communication to the globus pallidus. The result is increased
inhibition from the globus pallidus to the thalamus and decreased excitation from the thalamus to the
cerebral cortex. People with Parkinson’s disease show decreased initiation of movement, slow and
inaccurate movement, and psychological depression.
DRUG TREATMENTS FOR PARKINSON PATIENTS
Parkinson’s Disease
L-Dopa Treatment IS ONE treatment *
precursor for dopamine
demonstrates individual effectiveness
does not stop progression of the disease
numerous side effects (nausea, restlessness, sleep problems, low
blood pressure, hallucinations, and delusions)
WHY the side effects?
*Therapies Other Than L-Dopa
antioxidants, dopamine receptor stimulants, glutamate blockers,
neurotrophins, drugs that decrease apoptosis, pallidotomy, cell
transplants
BECAUSE
DOPAMINE IS RELEASED AT MANY SYNAPSES
ALL OVER THE BRAIN AND PRODUCES EFFECTS SPECIFIC
TO THESE SITES.
ONE NOTABLE SIDE EFFECT OF L-DOPA (DA AGONIST) IS
PSYCHOSIS
NOTE: SCHIZOPHRENICS WHO EXPERIENCE PSYCHOSIS
ARE GIVEN NEUROLEPTICS WHICH ARE DOPAMINE
ANTAGONISTS
ONE OF THE SIDE EFFECTS OF NEUROLEPTICS IS MOTOR
DISORDERS-TARDIVE DYSKINESIA
Drugs ‘of abuse’ have effects by acting on receptors in the brain
Nicotine
Attaches to nicotinic receptors
Increases dopamine release in the nucleus accumbens
Opiates
Derived from opium poppy
Attach to opioid receptors in the brain
Result in increased dopamine release
PCP
Inhibits some glutamate receptors
Results in reinforcement in the nucleus accumbens
Marijuana/Cannabinoids
Bind to specific receptors in the brain
Leads to euphoria
Other drugs of recreation
Hallucinogenic and stimulant Drugs (amphetamine, cocaine,etc.)
Distort Perception
Many resemble activities of neurotransmitters
Caffeine
Constricts blood vessels in the brain
Interferes with the effects of the neurotransmitter adenosine
(ANTAG)
Alcohol-multiple effects on brain NTs
Inhibits flow of sodium across the membrane
Expands the surface of membranes
Decreases serotonin activity (ANTAG)
Facilitates GABA responses (AGO)
Blocks glutamate receptors (ANTAG)
Increases dopamine activity (AGO)
Video
HORMONES AND BEHAVIOR
Hormones are chemicals secreted by endocrine organs
in the body into the circulatory system
Hormones act at a distance from where they are released
NTs act close to release point
Hormones act on receptors in other organs and in the brain
Hormones act on general metabolism, arousal, and growth
Hormones act in the brain to regulate behavior
WHAT ARE THE ENDOCRINE (HORMONE-PRODUCING) ORGANS ?
WHAT ARE THE ENDOCRINE (HORMONE-PRODUCING) ORGANS ?
1
2
3
WHAT ARE THE ENDOCRINE (HORMONE-PRODUCING) ORGANS ?
pituitary
adrenals
ovaries
Hormonal Changes Associated with
the Menstrual Cycle in Women
LH and FSH from pituitary
Estrogen
Progesterone
Ovarian changes
follicular ovulation luteal
Age of onset of menarche in
different cultures- Effect of diet?
1840
1970
HORMONES also affect
BEHAVIOR
Behaviors activated by hormones include
Sexual behavior
Maternal behavior
Aggression
Arousal
Eating
Drinking
Learning
Etc.
RAT SEXUAL BEHAVIOR-differences
between males and females
Female
Male
Hop-darts
Ear-wiggles
Lordosis reflex
Mounts
Intromits
ejaculates
Rat SEX
Male sexual behavior activated by androgens
Method: baseline-castration-test-testosterone-test
Result: behavior intact-reduced-reinstated
Female sexual behavior activated by
estrogen & progesterone
Method: baseline-ovariectomy-test-E&P-retest
Result:behavior intact-eliminated-reinstated
IN HUMANS, ANDROGENS
INFLUENCE MALE SEXUAL DESIRE
IN BOTH MALES AND FEMALES
WOMEN TREATED
WITH ANDROGENS
INTACT
YOUNGER
WOMEN,
UNTREATED
WOMEN TREATED
WITH ESTROGENS
WOMEN
GIVEN
PLACEBO
SEX DIFFERENCES IN ADULT BEHAVIOR ARE DUE TO
1.
2.
3.
4.
Differences in genes (XX,XY)
Differences in prenatal hormone exposure
Differences in upbringing
Differences in cultural norms
All of which produce
1. Differences in brains
2. Differences in hormones
3. Differences in gender identity
HENCE-differences in feelings,attitudes, and behavior