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41 Cards in this Set

  • Front
  • Back
Where are long term memories stored?
a) anterior thalamus
b) hippocampus
c. the medial temporal lobe
d. the lateral temporal lobe
e. none of the above
long-term memories are stored in the NEOCORTEX including the various sensory areas that encoded the experience initially
What part of the hippocampus is involved in our sense of direction?

3 major things
M . AT. E
the mammillary bodies, the anterior thalamic nucleus and entorhinal cortex
How does Long term potentiation affect memory?
blocking NMDA type of glutamate receptor in hippocampus impairs both LTP and learning

NMDA receptors activate intracellular signaling pathways that result in increased AMPA type glutamate receptors increasing the postsynaptic response to glutamate

when you stimulate the CA1->CA3 connection the EPSP increases with each successive stimulation resulting in bigger EPSP that last longer
How does a heart attack affect memory?
the hippocampus is very sensitive to ischemia

a myocardial infarction can cause severe anterograde and minor retrograde amnesia.
how does the hippocampus affect memories?
hippocampal damage causes anterograde memory loss (new memory loss)

retrograde memory loss does not occur

declarative memory is affected
can't remember in words anything that happened short term

also seen in bilateral medial temporal lobectomy
Why is memory affected by Alzheimer's disease?
Alzheimer's disease affects the entorhinal cortex and hippocampus

plaques and tangles form in the entorhinal cortex and hippocampus

fornix brings output of hippocampal formation to septal nuclei

septal nuclei project back to hippocampus via fornix
this cholinergic pathway ... degenerates in Alzheimer's disease
Wernicke-Korsakoff Syndrome is?
Wernicke's encephalopathy is caused by a Vit B1 deficiency which damages the mammillary bodies and mediodorsal nucleus.
(MD nucleus plays role in affective behavior and memory. Mamm body is a relay to the hippocampus)

Usually seen in alcoholics

causes mental confusion, hypotension, nausea, vomiting, vision impairment, ataxia

Korsakoff is the chronic problem
causes memory disorders
main features are impairments in acquiring new information or establishing new memories (anterograde) and retrieving previous memories
How does age and stress affect?
Glucocorticoid hormone (cortisol) control
hippocampus contains highest

concentration of glucocorticoid receptors in brain and exerts an inhibitory control over plasma corticosteroid levels

aging leads to loss of hippocampal neurons and their glucocorticoids receptors, explaining why aged animals cannot promptly terminate stress-related secretion of corticosteroids once has ended

Old rat can't remember the experience so stress levels stay high
What is the function of the Amygdala?
amygdala sends stria terminalis pathway to ventromedial nucleus of hypothalamus and also sends its own direct connection to ANS

feeding and drinking
agonistic (fighting) behavior
maternal care
responses to physical or emotional stressors

lesions of amygdala reduce endocrine, autonomic and behavioral responses during emotional stress

bilateral amygdala lesions eliminate fear emotional responses and impair the ability to recognize facial expressions of fear

inputs to limbic, solitary nucleus, etc.
Kluver-Bucy Syndrome

what are the symptoms
bilateral lesions of the temporal lobe
including the amygdala, temporal neocortex, olfactory cortex, and hippocampus

Visual agnosia
unfamiliar things are approached and examined orally

Oral tendencies

Loss of emotions of fear and anger

How do Olfactory Receptors work?
Each receptor cell expresses only one of the hundreds of different olfactory receptor molecules encoded by the large olfactory receptor gene family

signals from same type of olfactory receptor cells converge on each glomerulus

each cell expresses only one type of olfactory receptor molecule on its cilia

Olfactory system
olfactory tract projects piriform cortex, medial amygdala and entorhinal cortex

piriform cortex projects to thalamic mediodorsal nucleus, which projects to the orbitofrontal cortex

Amygdala projects to the hypothalamus

Entorhinal cortex projects to the hippocampal formation
What are the different stages of sleep?

Compare their EEG patters
➲ Awake 8-25 Hz, low amplitude waves in a state of alertness

➲ Stage 1 low freequency low amplitude waves; drowsy, easily aroused

➲ Stage 2- low frequency, medium amplitude waves

➲ Stage 3 very low frequency, high amplitude waves

➲ Stage 4- very low frequency, high amplitude waves

stage 3 and 4 are slow wave sleep; very difficult to wake from external stimuli; deepest stage of non-REM sleep

➲ REM --> EEG waves look like awake
this is because in REM our cortex is intensely active; recallable dreams occurs here, deep sleep, easy to awaken from internal not external stimuli
AKA Paradoxical sleep
How do the stages of sleep change during the night?
as the night progresses SWS phase decreases and REM sleep increases

slow wave sleep is deep sleep that is hard to interrupt by external stimuli

REM sleep is deep sleep that is very cortically active and is easily interrupted by internal stimuli

so as the night goes one once you attain a long phase of deep sleep when your body replenishes itself you spend more time in the cortically active REM sleep until your internal environment is such that you wake up
What is the function or chararacteristics of slow wave sleep?
SWS (Non-REM sleep)
<2 Hz in frequency with a very high amplitude when measured on EEG

➲ restoration, growth, immunity

➲blood to muscles is increased
➲body temperature is lower to conserved energy
➲metabolic activity is decreased: tissue growth and repair
➲growth hormone secretions at its highest
➲immunes system regulators elevated

Iteration of information
What are the characteristics of REM sleep?

aka paradoxical sleep, why?
➲ deep sleep with recallable dreams
➲ frequency of > than 10Hz and low amplitude EEG waves
➲ cortex is intensely active
➲ high O2 consumption
➲ all voluntary muscle activity stops
➲ability to thermoregulate decreases

key function is to INTEGRATE information
How does SWS and REM sleep compare to wakefulness

when we are awake we acquire information
we get it from the external environment
thru vivid sensation and perception
we think logically and can perform continuous voluntary movement

in NREM sleep
we iterate the information
we have dull sensation and perception
however we have logical thoughts and perspectives with involuntary, episodic movements (like the time I jumped out of my sleep because I felt like I was falling

during REM sleep we integrate information
we have very vivid internally generated perception and sensation however thoughts are illogical and bizarre
at this stage you want to wake up you command your eyelids and arms to move but they are inhibited
How does sleep change with age?
Sleep declines with age
- babies require ~ 16 hrs/day and senios require 6 hrs/day
For babies 50% of sleep time is spent in REM sleep
-- makes sense since they are growing and integrating new information...their cortex is more active

by 10 years old only 1/4 total sleep time is REM
What 3 hypothalamic nuclei are involved with the origin and expression of circadian rhythm?
SCN- Suprachiasmatic Nuclei
Dorsomedial- entrained by feeding
What nuclei control REM-NREM cycle?
Pontine control of the REM-NREM cycle

Mesopontine nuclei
➲ Laterodorsal tegmental- cholinergic
➲ Pedunculopontine- cholinergic
➲ Dorsal raphe- serotonin
➲ Locus Ceruleus- adrenaline
What nuclei are involved in sleep onset? arousing and waking?
basal forebrain
ventrolateral preoptic

basal forebrain and lateral are involved in arousing and waking
what are the part of the ascending arousal system?

how is it regulated?
Locus Ceruleus
Dorsal Raphe
histamine tuberomammillary nucleus
cholinergic lateral dorsal tegmental n. and pedunculopontine n

VLPO- ventrolateral preoptic area inhibits the ascending arousal system via GABA-ergic connection

orexin or hypocretin from lateral hypothalamus activates the Ascending Arousal System
How does adenosine affect sleep?

What drug blocks A2a receptors?
Adenosine decreases the activity of the cholinergic arousal network in the basal forebrain and brainstem

activates sleepiness

A2a is blocked by caffeine
What are the causes and consequences of insomnia?
Acute 1 night/wk for <3 wk
emotional or physical discomfort, stress
acute illness environmental disturbances and changes to circadian rhythm

Chronic 3 nights/wk for several wks
in conjuctionwith other health problems

daytime sleepiness
negative mood
impairment of performance
Sleep apnea
Obstructive- most common, effort to breathe
Central - rare, poorly understood
Who is at risk?
people w/ upper body obesity
large neck girth
systemic hypertension
nasopharyngeal narrowing
CV symptoms:
systemic hypertension

Treat with continuous positive airway pressure or surgery
What is RLS?
irresistable urge to move limbs
dorsiflexion of the ankles and flexion of the knees or hips
sleepiness and muscle weakness triggered by excitement
sudden, inappropiate emergence of REM sleep and atonia
could be caused by destruction of hypocretin/orexin neurons in lateral hypothalamus
mutation of hypocretin/orexin genes
Orexin A and B multiple receptors
Regions of the brain responsible for sleep
Ventrolateral preoptic area (a part of the diencephalic control of sleep onset)
Adenosine inhibits cholinergic activity leading to sleepiness
Pontine REM center activate REM sleep
Regions of the brain responsible for arousal/waking
Lateral Hypothalamus releases orexin/hypocretin --> wake up to feed
Tuberomammillary - release histamine
VTA - releases dopamine which controls alertness and motor function
PPT-LDT - acetylcholine
Locus Ceruleus- NE
basal forebrain cholinergic region
Describe bradykinetic syndrome
net increased inhibitory output of the GPm to the VL thalamic motor nuclei impairs stimulation of the motor cortex leading to
slow or absent movements -- hypokinesia or akinesia

In PD, loss of dopaminergic nigral neurons causes less "direct pathway" inhibition
more indirect pathway stimulation of the GPm

increasing net inhibition of the VL thalamic motor nuclei
Describe hyperkinetic syndrome
net decreased inhibitory output of the GPm to the VL thalamic motor nuclei enhances stimulation of the motor cortex leading to

hemiballismus, destruction of the STN lessens stimulation of the GPm, causing less inhibition of the VL thalamic motor nuclei

In HD, the loss of indirect pathway putaminal neurons to the GP lateral increases inhibition of the STN, lessening the GPm inhibition of VL thalamic motor nuclei thereby causing chore o athetosis
Name the 3 causes of BG disorders
ischemia infarcation, hemorrhage, or tumor in the striatum or STN


Dopamine agonists lead to hyperkinesia
Dopamine antagonists lead to hypokinesia
What are the 4 primary clinical signs of parkinsonism?
1. resting pill rolling tremor
2. rigidity
3. bradykinesia
4. loss of postural reflexes
What are the 5 secondary clinical signs of parkinsonism?
a. masked faces
b. hypophonic speech
c. stooped posture with shuffling propulsive gait
d. micrographic
e. autonomic dysfunction ie. constipation, orthostatic hypertension
Causes of clinical parkinsonism
most common cause is Parkinson's disease
some rarer neurodegenerative disorders eg. progressive supranuclear palsy, striatonigral degeneration, Shy-Drager syndrome
Dopamine antagonist medication eg. haloperidol an antipsychotic
manganese or CO poisoning
Parkinson's drug treatment
anticholinergic drugs

amantadine-- ↑ dopamine release

L-dopa -- greatest benefit
given with carbidopa a decarboxylase inhibitor so that it lasts longer and makes it to the brain

dopamine agonists

MAO type B inhibitor -- prevents break-down of Dopamine

COMT inhibitor -- inhibits catabolism L-Dopa
Parkinson's disease treatment
Surgical therapy for PD....
inhibition of STN which excites the GPm
destruction of the GPm
to counteract the increased inhibition of VL thalamic motor nuclei occuring in PD

by Pallidotomy, a stereotactic sugical lesion in the GPm
by STN stimulator inhibits the STN through repetitive programmable electrical stimulation from a special electrode
3 symptoms of Huntington's Disease
Chore o athetosis
behavioraal changes--moodiness, depression, suicide
how is HD diagnosised
blood test to detect multiple trinucleotide repeats in the huntingtin gene coded on chromosome 4
Describe the pathology of HD
atrophy is greater in the caudate nuclei than the cerebral cotex

loss of medium-sized GABA-ergic neurons with preservation of cholinergic neurons

early loss of GABA-ergic neurons projecting to the GPL leads to greater inhbition of the STN this decreases inhibition of the of VL which causes choreoathetosis
How is HD treated?
Dopamine antagonist drugs
Haloperidol --- blocks D2 receptors in the striatum, lessening inhibition of putaminal indirect pathway neurons
What are the side effects of L-Dopa?
dose-limiting side effects of hallucinations, psychosis, chorea or dystonia