D’YOUVILLE COLLEGE
PMD 604 - ANATOMY, PHYSIOLOGY, PATHOLOGY II
Lecture 13: Basic organization & synaptic function in nervous system
G & H chapter 45
1.
Body's Control Systems: nervous & endocrine systems; collaborate in
numerous functions; nervous system is most often rapid, short-term responses, while
endocrine is most often slower, more enduring responses
2.
Nervous System:
• anatomical organization of nervous system:
- central nervous system – CNS (brain & spinal cord) (ppt. 1) contains
billions of neurons
- brain includes cerebrum, diencephalon, midbrain, pons, medulla &
cerebellum (ppt. 2)
- produces 12 pairs of cranial nerves (nn.)
- spinal cord extends from skull through cervical, thoracic, lumbar & sacral
regions & produces 31 pairs of spinal nn.
- organized into grey matter (site of neuron cell bodies & synapses) and
white matter (nerve tracts) (ppts. 3 & 4)
- peripheral nervous system – PNS (spinal & cranial nerves & ganglia);
includes sensory (afferent) fibers & motor (efferent) fibers (ppts. 5 - 7)
• neurons: (fig. 45 - 1 & ppts. 8 & 9)
- cell body (soma) - metabolic center; many fibrous processes arise from
soma
- numerous dendrites (receptors of synaptic connections – from hundreds to
hundreds of thousands of other neurons)
- single axon (transmitting process that may have few to many branches,
leading to separate destinations
- because of the property of synaptic connections, transmission is normally oneway, from axon of input cell to dendrites (&/or soma) of output cell
• functional patterns:
- somatosensory axis (fig. 45 - 2 & ppt. 10) - sensory receptors respond to
stimuli, pass signals to spinal cord (spinal nn.) or brain (cranial nn.)
- input delivered to various destinations in CNS: cord, reticular
substance of medulla, pons & midbrain, cerebellum, thalamus & cerebral cortex
- nerve tracts in cord are ascending (ppt. 11)
- motor axis (fig. 45 - 3 & ppt. 10) - skeletal muscle responds to output from
- motor neurons of anterior horn of cord gray matter
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- output signals originate from various sources in CNS: cord, reticular
substance of medulla, pons & midbrain, basal ganglia, cerebellum, & cerebral cortex
- nerve tracts in cord are descending (ppt. 12)
- integrative component involves screening out majority of sensory signals
(largely in thalamus)
- synapses play major role in controlling input signals – screening many &
amplifying others through mechanisms of facilitation & inhibition
- stored sensory inputs (memory) reside mainly in the cerebral cortex
- function of synapses in memory: repeated sensory inputs may facilitate a
certain sequence of synapses to such a level of sensitivity that other signals in the brain
may excite the same sequence of synapses, independent of any sensory input
• levels of control in CNS:
- spinal level – many neuron circuits that control actions such as walking,
withdrawal movements, postural muscle contractions + smooth muscle of blood
vessels, urinary & gastrointestinal tracts
- higher brain regions issue ‘commands’ that activate programs of output that
reside in circuitry of cord
- brainstem and subcortical level – many functions including control of
respiration, cardiovascular regulation, maintenance of posture & equilibrium
- also, patterns of emotional and sexual responses may be activated,
independently of the cerebral cortex, by such regions as medulla, pons, midbrain,
cerebellum, thalamus, basal ganglia & hypothalamus
- cerebral cortex – repository of vast amount of stored information (memory)
that exerts more precise control of responses delivered by lower levels & by cord
- never operates alone; interacts with other levels, deciding to activate or
suppress circuitry patterns present in the lower levels
- computer analogy: nervous system may be compared to organization of a
computer (fig. 45 - 4 & ppt. 13)
3.
Neurotransmission:
• synaptic functions: modification of neural inputs: inhibition of input signal,
amplification of signal, or integration with inputs from other neurons
- electrical synapses: cell-to-cell current flow via gap junctions, e.g. smooth
muscle, cardiac muscle
• chemical synapses (fig. 45 – 6 & ppts. 14 & 15): one-way conduction
(presynaptic to postsynaptic neuron) through release of a neurotransmitter
- presynaptic terminal contains neurotransmitter vesicles and mitochondria
(provide energy for synthesis); is separated from postsynaptic membrane (of
dendrites, soma or axon) by a gap (synaptic cleft)
- arrival of AP at presynaptic terminal activates voltage-gated Ca2+ channels;
calcium influx triggers neurotransmitter release
- postsynaptic membrane features receptors (excitatory or inhibitory) for
neurotransmitter
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- receptors may operate chemically gated channel or protein complex that leads
to second messenger formation and modification of metabolism of postsynaptic cell;
second messenger systems cause prolonged response (fig. 45 – 7 & ppt. 16)
- excitatory receptors: open chemically gated sodium channels or close
chemically gated potassium or chloride channels; or they may stimulate second messenger
pathway to increase excitatory receptors or decrease inhibitory receptors
- postsynaptic membrane is depolarized
- inhibitory receptors: open chemically gated potassium or chloride channels;
or stimulate second messenger pathway to decrease excitatory receptors or increase inhibitory
receptors
- postsynaptic membrane is hyperpolarized
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- number of presynaptic terminals connecting with postsynaptic cell
(excitatory or inhibitory synapses) may vary from a few thousand up to 200,000 (fig. 45
- 5 & ppt. 17)
- terminals may be from a few to a very large number of input neurons
5.
Neurotransmitters:
• small molecular, rapidly acting: (table 45 - 1 & ppt. 18)
- acetylcholine (neurons of cerebral cortex, basal ganglia, presynaptic &
postsynaptic parasympathetic neurons, presynaptic sympathetic neurons &  motor
neurons to skeletal muscle); usually excitatory, but occasionally inhibitory
- norepinephrine (neurons of brainstem [locus ceruleus], hypothalamus &
postsynaptic sympathetic neurons); excitatory or inhibitory
- dopamine (neurons of substantia nigra of basal ganglia); inhibitory
- serotonin
- GABA ( amino butyric acid) (neurons of spinal cord & several areas of
brain); inhibitory
- glycine (neurons of spinal cord, cerebellum & basal ganglia); inhibitory
- glutamate (neurons of sensory pathways); excitatory
- nitric oxide (certain brain areas involved in behavior & memory); longer
acting -- enters postsynaptic cell and modifies excitability
- also aspartate, epinephrine & histamine
• large molecular, slowly acting: (table 45 - 2 & ppt. 18)
- neuropeptides: endorphins, enkephalins (involved in CNS analgesic system);
& substance P (involved in neurons transmitting slow pain signals)
6.
Summation of Postsynaptic Potentials:
• responses of postsynaptic cell (fig. 45 - 9 & ppt. 19):
- individual synapses produce graded potentials (insufficient strength to
reach threshold)
- EPSPs: rise in membrane potential toward threshold (depolarization) with
duration of 1 – 2 msec. (neuron is facilitated) (ppt. 20)
- IPSPs: drop in membrane potential toward more negative state
(hyperpolarization); postsynaptic neuron is more difficult to excite (neuron is
inhibited)
• summation: duration of each EPSP is long enough for several APs to trigger
neurotransmission before an EPSP expires
- summation occurs; usually a minimum of 16 synapses may be necessary
to elicit AP in postsynaptic cell (fig. 45 – 10 & ppt. 21)
- spatial summation: APs from several input neurons arrive at postsynaptic
neuron simultaneously; resulting EPSPs summate producing ‘excitatory state’ (ppt. 22)
- temporal summation: APs from single input neuron arrive with sufficient
signal strength to summate & produce excitatory state (ppt. 22)
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- neurons with EPSP maintained above threshold, will fire multiple APs
with a frequency related to magnitude of excitatory state
- rate of AP firing = signal strength; different neurons have different
sensitivity to stimulation & respond with different signal strengths (fig. 45 – 12 & ppt. 23)
- EPSPs arriving at soma of postsynaptic cell produce currents in cytoplasm
(highly conductive) that summate at initial segment of axon (fig. 45 - 11 & ppt. 24)
7.
Effects of Activity, pH, PO2 & Drugs:
• synaptic activity: fatigue of synaptic transmission is a gradual decline of
signal strength (from initially high firing rate) that occurs with repetitive rapid rate
of stimulation
- likely due to depletion of neurotransmitter in presynaptic terminal, but also
possibly due to loss of post synaptic receptor sensitivity and/or abnormal ionic
conditions in post synaptic cell
- synaptic fatigue is protective against excessive excitability in the nervous
system (e. g. epileptic seizure)
- synaptic delay results from time taken to complete steps of
neurotransmission process (= approx. 0.5 msec/synapse); information can be used to
estimate # of neurons (synapses) in a circuit
• acidosis & alkalosis: depressed pH (e.g., ketoacidosis) depresses neural
activity, whereas elevated pH (alkalosis) increases neural activity (e.g.,
hyperventilation may induce seizures in epileptic individuals); pH effects may be caused
by facilitation or inhibition of neurons
• hypoxia: oxygen deprivation quickly causes complete loss of excitability in
some neurons; loss of consciousness ensues within a few seconds
• drugs: stimulants such as caffeine increase neuron excitability probably
through lowering their thresholds
- strychnine inhibits inhibitory synapses resulting in uncontrolled excitation
- most anesthetics inhibit neuronal activity, likely by raising thresholds for
excitation