Olf. system.

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Olf. system.
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LIMBIC SYS
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Limbic System Limbic lobe hippo., fornix,
MMBs, MTT, ant. nuc. thal., cingulate cortex,
cingulum, parahippo. gyrus then into hippo.
stria terminalis? Papez circuit?
Limbic Lobe
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NUTS IN YOUR BRAIN
K-B AND SM ? ? ? ??
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KLUVER BUCY SYNDROME
TAME-no display anger or fear VISUAL AGNOSIA oral
compulsions may provide alternate means of
object identification HYPERPHAGIC HYPERSEXUAL RECE
NT MEMORY DEFICIT Emotional Blunting
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bilateral lesionsUrbach-Wiethe diseasepatient
SM insensitivity to the intensity of fear shown
by face hyaline-like deposits skin, muc. memb.
does not show autonomic fear responses to
arousing stimuli fear learing is lost her
memory was not enhanced by emotionally arousing
pictures


cant tell negative emotions expressed by other
people. Because she often fails to recognize
criticism or aggression, S.M. has difficulty
interacting socially.
no uneasy feeling about someone who is in fact
predatorial does not recognize fear in herself
does not evince normal facial expressions in
fearful situations
Fear conditioning ? ? ? ??
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• programmed by evolution
• to detect certain input triggers
• important for survival
• genetically hardwired
• natural triggers
• rats are afraid of cats

AMYG
HPA AXIS
BEHAVIOR
pain/foot shock bear in woods- smells/sounds-how
bear looks

ANS
Fear conditioning ? ? ? ??
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FEAR CONDITINING! Keeps organism alive!!
THAL
AMYG
HPA AXIS
FEAR REACTION
sound bear makes river where seen learned
triggers
Sound bear
BEHAVIOR

ANS
big bear
Amyg. org ? ? ??
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• SENSORY inputs to LATERAL NUCLEUS then relayed
  to basal, and accessory basal to reach
• CENTRAL NUC OUTPUT
• CRH receptors on cells and
• uses CRH as transmitter to LC ? adrenal medulla
  via pregang. sym.
• severe

CRH?ventricles ? ??
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• CRH into ventriclesturn on fear response and
  hypervigilance
• CRH antagonists
• central nucreduction in the occurrence of above
  reactions
• Target CRHCRH

severe
Amyg. conn ? ? ??
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electrical stimulation?

cortisol ? ? ??
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CORTISOL CORTISOL CORTISOL CORTISOL

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1. cortisol goes up with novelty, uncertainly,
threat, conflict, unpredictability, pain,
maternal separation 2. cortisolkills
hippo bad memory and kills PFC short term
memory in depression bad decisions under stress
robs hippo of glucosetoxic effect
of glutamate-Cushings disease 3. cortisol
highest AM and lowest 12 hrs later 4.
depressionloss diurnal cortisol levels
elevated

Amyg?hypo ? ? ??
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• Amygdala projects to hypo
• descending input to T1L2
• sym.input to adrenal medullaepi and norepi
  (hormones)

Amyg.?LC? ? ??
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70 of the noradrenergic neurons in the brain
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PTSD? ? ??
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• PTSD (shell shock!)
• NE and CRH ? and cortisol ?
• (cortisol ? acutely)
• increase in cortisol receptors on
• ACTH producing cells
• exaggerated response to
• yohimbine triggers
• flashbacks
• decrease in size of hippo
• startle response (eye-blink) exaggerated
• (Xanax) lowers CRH levels in LC

PTSD? ? ??
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• PTSD (shell shock!)
• horror of a battle is US
• sights, sounds smells are conditioned by amygdala
• CS can then turn on amygdala
• unconsciously and turn on long term memories
  about original event or recent episodes when
  trauma was relived
• patient listens to tape of traumatic experience ?
  MRI activity in amygdala and limbic cortex
  (especially on right side)

low frequency rTMS (repetitive transcranial
magnetic stimulation) leads to a decrease in
regional cerebral blood flow
shocking data ? ? ??
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About 16 of American women (about 40 million)
are sexually abused (including rape, attempted
rape, or other form of molestation) before they
reach their 18th birthday. Childhood abuse may
be the most common cause of PTSD in American
women, 10 of whom suffer from PTSD.
learned help.. ? ? ??
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LEARNED HELPLESSNESS beagles with control over
the shock normal cortisol and NE dog with no
controlincreased levels of cortisol and
DECREASED levels of NE learning that one's
behavior is ineffective in changing the
environment model for depression
dizzi-ing array of connections? ? ??
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panic attacks? ? ??
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Most commonly diagnose anxiety disorder!
Panic attacks sensitive LC-NE system CO2 turns
on solitatrius which turns on LC-NE Cant avoid
stim like PTSD-internal Yohimbine?
LOCUS COERULEUS blue spot 19,999
cells?-CCK-agoraphobia?
pharmacy? ? ??
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• THE PHARMACY
• A. monoamine oxidase inhibitors-prevent breakdown
  of monoamines (catecholamines epinephrine,
  norepinephrine, dopamine and serotonin after
  release into synaptic cleft
• B. tricyclicsprevent REUPTAKE of monoamines
  back into nerve terminalsimipramineless side
  effects
• C. SSRIs-selective serotonin reuptake
  inhibitorseven fewer side effects
• D. Roboxetine-selective norepi reuptake inhibitor
  (SNRI increases energy)
• E. drugs that block ability of CRH to lead to ?
  cortisol.
• F. circuitry reorganization CA3 and dentate gyrus
  

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THE PHARMACY ANXIETY25 of all adults
schizophrenia1 depression15 antianxiety
drugs work immediately benzodiazepinesLibrium,
Xanax, Valium mothers little
helper mechanism of actionFACILITATES GABA and
makes it harder for glutamate to excite
postsynaptic receptors (alcohol and barbituates
use this too!)
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DEPRESSION Reduction in NE and
Serotonin Suicides5HIAA and MHPG in CSFReduced

• murderers in Finland low 5-HT
• some researchers now believe that suicide may
• be the ultimate act of inwardly directed
  impulsive aggression
• depressed had a history of committing impulsive
  acts including
• overeating and aggressive behaviors such as
  lighting fires or
• fighting-5HT low in prefrontal cortex-predict
  problems

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THE WAY YOU DO THE THINGS YOU DO Working
memory?
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R.B.?
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HIPPOCAMPUS

• cells have receptors for cortisol that may be
  important in death of such cells-in moderation it
  increases memory
• participates in explicit or declarative memory
• lesion results in anterograde amnesia loss of
  memories from time of damage on -patient H.M.
• patient RB showed other closely associated
  brain areas involved in explicit memory-smaller
  lesion
• loss of synapses and lots of neurofibrillary
  tangles and senile plaques in Alzheimers which
  leads to problems in explicit memory
• cholinergic input to hippocampus is important and
  one source is nucleus basalis of Meynert loss
  of these cells seen in Alzheimers (cortical NE
  low too in Alzheimers)
• Hippo cells very sensitive to hypoxia

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AGING AND THE BRAIN
reduction in weight via loss of neurons few
hypothalamic cells lost in comparison with DA
cells (sub. nigra., VTA) and NE (LC) lots of cell
loss in hippo (20), cortex, basal forebrain
(nucleus basalis cholinergic neurofibrillary
tangles in hippo and amyg-cytoskeleton senile
plaques in hippo amyg and cortex-extracellular
space-betal amyloid protein
in young MED I, faces encoded in left PFC and
right hippo recognize faces via right PFC in
older (Nsci Profs) no encoding in left PFC and
right hippo, but recog. in right PFC. Thus,
memory impairment in elderlyno encoding leading
to errors in recog.