Transcript Document

Chapter 16
Neural Integration II:
The Autonomic Nervous System and
Higher-Order Functions
Sensory
Motor
General (15)
Somatic (15)
Special (17)
Autonomic (16)
fig. 15-1
fig. 16-1
Autonomic Nervous System (ANS)
regulate homeostasis
works independent of consciousness
Autonomic Nervous System (ANS)
compared to Somatic NS
fig. 16-2
fig. 16-3
Sympathetic
prepare body for heightened levels of
somatic activity
“fight or flight” response
•increased mental alertness
•increase metabolic rate
•reduced digestive/urinary fn
•activation of energy reserves
•increase respiration rate
•increase heart rate, bp
•activation of sweat glands
fig. 16-7
parasympathetic
stimulates visceral activity
“rest and repose”
conserve energy
promote sedentary activities
•decrease metabolic rate
•decrease heart rate, bp
•increase secretion-digestion
•more blood to digestive system
•stimulate urination/defecation
sympathetic
parasympathetic
ENS
enteric nervous system
complex visceral reflexes
sympathetic nervous system
preganglionic neurons
T1 to L2 lateral horn of spinal cord
lots of divergence (1 to many)
project to ganglia (3)
sympathetic chain ganglia
collateral ganglia
adrenal medulla
fig. 16-4
fig. 16-5
sympathetic nervous system
collateral ganglia
celiac
stomach, liver, gall bladder
pancreas and spleen
superior mesenteric
small intestine
proximal 2/3’s of large intestine
inferior mesenteric
large intestine, kidneys, bladder
reproductive organs
fig. 16-4b
Adrenal medulla
receives preganglionic sympathetic input
synapse on neuroendocrine cells of medulla
cells secrete E or NE into blood
epinephrine
norepinephrine
adrenaline
noradrenaline
fig. 16-4c
CRISIS
sympathetic activation
controlled by centers in the
hypothalamus
increased alertness RAS
feelings of energy and euphoria
(disregard for danger, insensitivity to pain)
Increase heart and lung activity
(controlled by pons and medulla)
Elevation of muscle tone
Mobilization of energy reserves
sympathetic neurotransmitters
preganglionic neurons use ACh
(cholinergic)
postganglionic neurons release NE
(adrenergic)
postganglionic cells have varicosities
instead of axon terminals
fig. 16-6
sympathetic neurotransmitters
affect is longer lasting than
at a neuromuscular jn (Ach; 20 msec)
NE affects its targets until it is
reabsorbed or broken down (seconds)
NE adrenal medulla lasts even longer
(minutes)
sympathetic neurotransmitters
Most of the NE released is reabsorbed
by the neruon (50-80%)
reabsorbed NE is re-used or broken
down by MAO (monoamine oxidase)
the rest diffuses away and is broken
down by COMT in the tissues
sympathetic neurotransmitters
receptors for NE
Two classes
alpha
beta
both are G-proteins
(second messengers; 12)
neurotransmitters and
neuromodulators
How do they work?
1. direct effect on
membrane potential
2. indirect effect on
membrane potential
3. diffusion into cell
2.
fig 12-17
fig. 12-17
sympathetic neurotransmitters
alpha receptors
a-1
more common
release intracellular Ca2+
stimulates target cell
a -2
lowers cAMP levels in cell
(inhibitory on target cell)
found on parasympathetic cells
sympathetic neurotransmitters
beta receptors
in membranes of many organs
heart, lungs, liver, muscle, …
changes metabolic activity of
target cells (intracellular cAMP)
sympathetic neurotransmitters
beta receptors
b-1
increased metabolic activity
skeletal muscle
cardiac output
b -2
inhibitory
relax smooth m. in resp. tract
easier to breath (asthma)
sympathetic neurotransmitters
beta receptors
b-3
found in adipose tissue
causes lipolysis
release fatty acids for metabolism
sympathetic neurotransmitters
other transmitters
ACh
sweat glands in skin (secretion)
blood vessels to brain and muscle
(dilation of vessels)
NO (nitric oxide)
vasodilation in brain and muscle
to here
3/16/07
lec# 27
sympathetic summary
uses
sympathetic chain
collateral ganglia
adrenal medulla
short preganglionic, long postgang.
excessive divergence (2 doz +)
pregang. cells release ACh
Most postgang. cells release NE
a few use ACh, NO
Response depends on receptors (a,b)
sympathetic summary
neurotransmitters and receptors:
pre-
ACh
post-
NE
a
receptors
a
most
commonstimulatory
ACh
b
a
b
inhibitory
b
increase
inhibitory
skel. muscle (airways)
cardiac output
b
fat cells
lipolysis
NO
Parasympathetic nervous system
fig. 16-7
Parasympathetic nervous system
preganglionic cells in nuclei in:
midbrain
pons
medulla oblongata
spinal cord
travel with:
CN III, VII, IX, X
pelvic nerves S2 to S4
Parasympathetic nervous system
preganglionic cells:
less divergence than sym.
(6-8)
postganglionic cells:
in terminal ganglia (near organ)
or
intramural (in organ)
effects more localized and specific
CN III
VII
IX
X
pelvic
fig. 16-8
Parasympathetic nervous system
CN III, VII, IX
control visceral structures in the head
CN X
neck, thoracic and abdominal cavities
(75% of parasympathetics)
Parasympathetic activation
constrict pupils
close vision
stimulate digestion secretions
secretion of hormones-cellular nutrient use
sexual arousal changes
increase smooth m. activity - digestive sys.
stimulate/coordinate defecation
contract urinary bladder for urination
constrict airways
reduce heart activity
Parasympathetic neurotransmitters
ACh
fast acting
inactivated quickly by AChE
localized effects
Parasympathetic neurotransmitters
Receptors
two types:
nicotinic
on ganglion cells
most muscles (SNS)
lead to epsp
muscarinic
parasym. muscle, glands
G proteins
epsp or ipsp
longer lasting
Parasympathetic neurotransmitters
Receptors
nicotinic
nicotine poisoning (50 mg):
vomiting, diarrhea, high bp
rapid heart rate, sweating,…
muscarinic
nausea, vomitting, diarrhea,
constriction of airways, low bp
low heart rate
100 keys (pg. 530)
“The preganglionic neurons of the autonomic
nervous system release acetylcholine (ACh) as
a neurotransmitter. The ganglionic neurons of
the sympathetic division primarily release
norepinephrine as a neurotransmitter (and both
NE and E as hormones at the adrenal
medulla). The ganglionic neurons of the
parasympathetic division release ACh as a
neurotransmitter.
Table 16-2
fig. 16-9
summary and interactions
sympathetic
widespread distribution
parasympathetic
visceral structures served by CN
or in abdominopelvic cavity
most organs receive input from both
(dual innervation)
actions are usually opposite
anatomy of dual innervation
head
parasympathetics with CN
sympathetic via superior cevical ganglion
thorax and abdomen
sympathetics and parasympathetics mix
autonomic plexuses
cardiac
pulmonary
esophageal
celiac
hypogastric
fig. 16-10
autonomic tone
background stimulation
allows for more control
two examples:
autonomic tone
1. heart receives dual innervation
review:
cardiac muscle has pacemaker
ACh from parasym. slows rate
NE from sympath.
accelerates rate
both are released all the time but,
normally parasym is in control
can modulate heart rate up or down
autonomic tone
2. blood vessel diameter
review:
only get sympathetic
background NE from sympathetic
partial constriction of vessels
need more blood
stop NE release
increase ACh release
blood vessels dilate
autonomic tone
2. blood vessel diameter
review:
only get sympathetic
background NE from sympathetic
partial constriction of vessels
need less blood
increase NE release
blood vessels constrict
autonomic integration and control
centers are found all over the CNS
primary motor cortex (UMN) …
…LMN of cranial and spinal reflexes
also
visceral reflexes
example
visceral reflexes
shine a light in one eye…
…both pupils will constrict
(consensual light reflex)
parasympathetic
in the dark…
…pupils dilate
(pupillary reflex)
sympathetic
visceral reflexes
motor muclei controlling the pupils are
controlled by hypothalamic centers
responding to emotions too
nauseated/queasy
sexually aroused
pupils constrict
pupils dilate
autonomic integration and control
visceral reflex arc
receptor (sensory neuron)
processing center (interneurons)
two visceral motor neurons
long or short reflexes
autonomic integration and control
long reflexes
equivalent to the spinal reflex (13)
processing (interneurons) in CNS
fig. 16-11
autonomic integration and control
short reflexes
bypass the CNS
processing (interneurons) in ganglion
fig. 16-11
autonomic integration and control
short reflexes
bypass the CNS
processing (interneurons) in ganglion
used extensively in digestive system
ENS
autonomic integration and control
other autonomous reflexes
respiration,
cardiovascular,
…
table 16-4
autonomic integration and control
other autonomous reflexes
respiration,
cardiovascular,
…
parasympathetic
sympathetic
divergance
organ or
organ system
activated as
a whole
higher levels of control
centers for:
cardiovascular
respiratory
swallowing
salivation
digestive secretions
peristalsis
urinary functions
nuclei in
medulla
oblongata
hypothalamus
integration of ANS and SNS
see fig. 16-12
Higher order functions
•need cerebral cortex
•involve conscious and unconscious
•not part of “hardwiring”
subject to modification and adjustment
memory / learning
consciousness
sleep / arousal
brain chemistry / behavior
aging
Higher order functions
memory / learning
fact memories bit of info
skill memories learned actions
short term (primary)
memory consolidation
long term
secondary
may fade with time
tertiary
lifetime
fig. 16-13
Higher order functions
memory / learning
memory consolidation
involves
amygdoloid body
hippocampus
damage hippocampus
cannot convert short-term to long-term
existing long term remains intact
Higher order functions
memory / learning
memory consolidation
involves
amygdoloid body
hippocampus
nucleus basalis ?
damage to nucleus leads changes
with Alzheimers (later)
Higher order functions
memory / learning
memory consolidation
long term memories
stored the cerebral cortex
association areas
some memories are dependent on the
activity of a single neuron
to here 3/19
Lec #28
Higher order functions
memory / learning
memory consolidation
anatomical/physiological D
neurons and synapses
Higher order functions
memory / learning
memory consolidation
increased nt release
facilitation at synapses
additional synaptic connections
create anatomical changes in circuits
1 circuit/1 memory = memory engram
Higher order functions
memory / learning
memory consolidation
take time
nature
intensity
frequency
influenced by:
of stimulus
strength, extremeness,
frequency, drugs
Higher order functions
memory / learning
memory consolidation
hippocampus
NMDA-receptors
chemically gated Ca2+ channels
blocking NMDA receptors prevents
formation of long-term memory
Higher order functions
memory / learning
amnesia
loss of memory because of
disease or trauma
Higher order functions
memory / learning
amnesia
retrograde
lose memory of past events
e.g., head injury-forget accident
anterograde
inability to store new memories
common sign of senility
living in “new” surroundings
Higher order functions
memory / learning
amnesia
can occur suddenly or progresively
recovery can be:
complete
partial
non-existent
depending
on problem
Higher order functions
memory / learning
amnesia
diazepam (valium)
Halcion
can cause brief periods of
anterograde amnesia
100 Keys (pg. 539)
“Memory storage involves anatomical as
well as physiological changes in neurons.
The hippocampus is involved in the
conversion of temporary, short-term
memories into durable long-term
memories.”
Higher order functions
States of consciousness
conscious
unconscious
awake
coma
really asleep
asleep…
Higher order functions
sleep
deep sleep
aka., slow wave sleep
non-REM sleep
REM sleep
rapid eye movement sleep
Higher order functions
sleep
deep sleep
body relaxes
cerebral activity is minimal
heart, resp, bp, energy
utilization all decrease (30%)
Higher order functions
sleep
REM sleep
active dreaming
D resp. rate, bp
EEG looks similar to awake, but
less response to outside stimuli
decrease in muscle tone
(intense SNS inhibition)
eye muscles escape inhibition
Higher order functions
sleep
REM sleep
cycles of REM, non-REM
fig. 16-14a
fig. 16-14b
Higher order functions
sleep
sleep disorders
25% of Americans
abnormal REM
sleepwalking
…
Higher order functions
arousal
awakening
controlled by the reticular formation
extensive interconnections with:
sensory
motor
integrative nuclei
Higher order functions
arousal
RAS
reticular activating system
from medulla to midbrain
projects to thalamus
cortex
activity of cortex
is proportional
activity of RAS
fig. 16-15
Higher order functions
arousal
RAS
sleep is ended by activation
effects last short time (min)
positive feedback keeps us awake
Higher order functions
arousal
nuclei
maintains
alertness
NE
+
RAS
serotonin
promotes
sleep
nuclei
100 keys (pg. 541)
“An individual’s state of consciousness is variable
and complex, rangeing from energized and “hyper” to
unconscious and comatose. During deep sleep, all
metabolic functions are significantly reduced; during
TEM sleep, muscular activities ar inhibited while
cerebral activity is similar to that seen in awake
individuals. Sleep disorders result in abnormal
reaction times, mood swings and behaviors.
Awakening occurs when the reticular activating
system becomes active; the greater the level of
activity, the more alert the individual.”
Brain chemistry and behavior
changes in the balance of nt’s can affect
brain function.
sleep-wake cycles
Huntington’s disease
Brain chemistry and behavior
Huntington’s disease
destruction of ACh and GABA secreting
neurons in the basal nuclei
loss of basal nuclei, frontal lobes
loss of muscle control and
intellectual abilities
Brain chemistry and behavior
serotonin
LSD activates serotonin receptors
hallucinations
enhance serotonin activity
Brain chemistry and behavior
serotonin
block serotonin
depression and anxiety
slow serotonin removal
increase serotonin
(SSRI’s)
Prozac, Paxil, Zoloft
Brain chemistry and behavior
serotonin
variety of pathways delivering
serotonin to nuclei and higher
centers
affect sensory interpretation and
emotional states
Brain chemistry and behavior
dopamine
needed to reduce muscle tone
stimulated by “speed”
causes “schizophrenia”
disturbances in
mood
thought and
behavior
Aging
affects all body systems (including brain)
changes begin around 30
reduction in brain size and weight (cortex)
reduction in # of neurons (cortex)
decreased blood flow to brain (arteriosclerosis)
changes in synaptic organization (fewer)
cellular changes
accumulations inside the cells (tangles)
accumulations outside the cells (plaques)
Aging
Alzheimer’s
progressive disorder characterized by
loss of higher order cerebral functions
15% of people over 65
50% of people over 85
100,000 deaths/year
Aging
Alzheimer’s
areas develop “plaques” and “tangles”
??
genetics
late onset chromosome 19
early onset
chromosomes 21 and 14
no cure, but may slow progression
Integration of Nervous System with
other body systems
monitors all systems
adjusts their activity
level of impact is variable
skeletal muscle
cardiac muscle
fig. 16-16