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Anatomical Basis of Neurochemical pathway Flashcards

1
Q

Where are the ACh releasing neuron cell body aggregates?

A

basal forebrain

pontine tegmentum

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2
Q

ACh acts via what receptor types in the brain?

A
  • Nicotinic:
    • N2R - common in the brain
  • Muscarinic:
    • M1+3,5 - excitatory
    • M2,4 - inhibit
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3
Q

What are the cholinergic nuclei?

A
  1. Basal forebrain
    1. Nucleus basalis of meynert (NBM)
    2. Medial septal nucleus & nucleus of diagonal band of Broca (MS, DBB)
  2. Pontine tegmentum
    1. Pedunculo-Pontine Tegmental Nucleus & Lateal Dorsal Tegmental Nucleus (PPT/LDT)
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4
Q

NBM sends fibers to what cortex? Is associated with what functions?

What receptors are located here?

A

neocortex: conscious perception & cognition (M1R)

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5
Q

MS, DBB sends fibers to what cortex? Is associated with what functions?

What receptors are located here?

A

hippocampus: learning (decreases in aging)

M1,3,4R

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6
Q

Degeneration of neurons in the NBM leads to what condition?

Decreased firing?

A

Alzheimer’s disease

decreased firing may result in visual hallucinations

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7
Q

PPT/LDT sends fibers to what cortex? Is associated with what functions?

What receptors are located here?

A

spinal cord & thalamus -> cortex : musle atonia & deams during REM sleep

M1,3,4R

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8
Q

Cortical activity initiated in REM sleep by what kind of waves?

A

PGO

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9
Q

Damage to PPT/LDT projections lead to what conditions?

A
  • REM sleep disorders
    • acting out dreams (loss of muscle atonia)
    • dreamles sleep or severe dream enactment behaviors
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10
Q

What is the histamine releasing nucleus?

This has what physiological significance?

A

TuberMammillary Nucleus (TMN)

calm wakefulness

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11
Q

Histamine acts via what receptors in the brain?

Which one is unique?

A
  • H1,2,3,4R
  • presynaptic H3 is auto-receptor for negative feedback mechanism
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12
Q

TMN sends fibers where? Is associated with what functions?

What receptors are located here?

A
  • highest density to hypothalamus (H1R) : metabolic regulation
  • cerebral cortex & cholinergic nuclei: H1R
  • thalamus: H1R ; H2R
  • hippocampus, amygdala, striatum, cerebellum
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13
Q

Hypoactivation of histaminergic projections can lead to what clinical situations?

A
  • increased leep
  • abnormal appetites for food
    • typically suppressess appetite -> w/ hypoactivation -> increased appetite -> obesity
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14
Q

Hyperactivation of histaminergic projections can lead to what problems? This can occur in what clinical situations?

A
  • inability to sleep
  • night terrors
  • ABNORMALLY high
    • brain tumors & psychosis
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15
Q

What are the appropriate relative histamine levels while awake, slow wave sleep & REM sleep?

A
  • awake
    • ++
  • slow wave
    • +
  • REM
    • 0
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16
Q

What substances are synthesized from tyrosine?

A

catecholamines

dopamine, NE

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17
Q

What substances are synthesized from tryptophan?

A

indolamines

serotonin, melanin

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18
Q

What are the major aggregations of domamine secreting neurons?

Physiologic actions?

A

(Midbrain)

Ventral Tegmental Area (VTA) : motication, reward mechanism

Substantia nigra: motor control

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19
Q

Dopaminergic fibers go where? They are associated with what functions?

A
  • VTA
    • mesocortical- cognition
    • mesolimbic- emotion, reward
  • Substantia nigra
    • mesotriatal- movement
  • Tuberinfundibular- prolactin
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20
Q

Damage to the dopaminergic projections can lead to what pathologies?

A
  • mesocortical
    • negative symptoms - schizophrenia
  • mesolimbic
    • positive symptoms - schizophrenia
  • mesostriatal
    • parkinosn’s disease
  • tuberinfundibular
    • hyperprolactinemia
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21
Q

Axons in the mesocoritcal projection go where?

Function?

Result of hypofunction?

A

VTA to prefrontal cortex

cognition & executive function

hypofunction - negative schitzophrenia symptoms

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22
Q

Axons in the mesolimbic projection go where?

Function?

Result of hyperfunction?

A

VTA to limbic system & nucleus accumbens

motivation & reward ; pleasure & additcion

hyperactivation - positive schizophrenia symptoms

23
Q

Axons in the mesostriatum projection go where?

Function?

Result of hypofunction/degeneration?

A

substantia nigra to striatum (caudate & putamen)

motor control / coorination of body movements

hypofunction/degeneration - Parkinson Disease

24
Q

What part of the brain secretes 80% of dopamine

A

nigro-straital pathway

25
Q

What are the components of the tuberinfundibular projection?

Function?

Damage to this area causes?

A

hypothalamus to anterior pituitary

regulate prolactic secretion

damage - hyperprolactinemia

26
Q

How can dopamine secretion regulate prolactin secretion?

A

secreted dopamine stimulates lactotrope D2 receptors, which leads to inhibition of prolactin release

27
Q

How do you treat hyperprolactinemia caused by damage to the TIDA nurons?

A

D2 agonist drugs

bromocriptine, cabergoline

28
Q

What is the term for concentrations of noradrenergic projections in the brain?

What is their unique appearance in a unstained brain?

A

Locus coeruleus

blue spot in unstained brain - neuromelanin with NE

29
Q

Neurepinephrine targets what receptors in the brain?

A
  • Excitatory
    • a1
    • B1
  • Inhibitory
    • a2
30
Q

Noradrenergic projections to the cortex & thalamus utilize what receptors? Function?

What is there is damage to this system?

A

a1

attention, focus, alertness

damage (hypoarousal) - ADHD

(hyperarousal) - anxiety disorders

31
Q

Noradrenergic projections to the limbic system utilize what receptors? Function?

What is there is damage to this system?

A

to amygdala

a1R

fear, anxiety

hyperarousal- mania, stress, PTSD

32
Q

Noradrenergic projections to the hypothalamus utilize what receptors? Function?

What is there is damage to this system?

A

a2

inhibition of hypothalamus

damage - (hyperarousal) sleeplessness, sleep disturbance

(hypoarousal) clinical depression

33
Q

What is the function of noradrenergic projections to the cerebellum?

They utilize what receptor?

A

motor learning

a1

34
Q

How can we have hyperarousal of cortex & thalamus by NE?

Leads to?

A

neocrotex NE neuron firing

anxiety disorder

35
Q

What are the appropriate relative NE levels while awake, slow wave sleep & REM sleep?

A
  • awake
    • ++
  • slow wave sleep
    • +
  • REM sleep
    • 0
36
Q

Clnical depression is caued by hypoarousal of projections of what neurotransmitters?

A

NE

serotonin

dopamine

37
Q

Where are the Serotonin releasing neuron cell body aggregates? Function?

A

Raphe nuclei - brainstem

Rostral RN (to corticla areas) : mood, sleep, satiety

38
Q

The dorsal raphe nuclei sends projections where? Function?

Result of damage?

A

cortex, amygdala, basal ganglia: wake sleep cycle

damage - mood disorders

39
Q

The ventral raphe nuclei sends projections where? Function?

Result of damage?

A

hypothalamus, pituitary, limbic

damgage - suicidal tendency

40
Q

Impact of normal levels serotonin (5-HT)?

Hyperactivation?

Hypoactivation?

A
  • normal: overall well being
    • satisfaction
    • self-esteem
    • inner strength
  • hyperactivation
    • decreased libido
    • sleep disturbances
  • hypoactivation
    • amygdala - sadness
    • hypothalamus - appetite changes
      • anorexia
      • hyperphagia
    • pituitary - hormonal imbalance
      • menstrual irregularities
      • sleep disturbance
    • overall - MAJOR role depression
41
Q

Serotonin acts on what receptors in the brains?

42
Q

What are the appropriate relative serotonin levels while awake, slow wave sleep & REM sleep?

A
  • awake
    • ++
  • slow wave sleep
    • +
  • REM sleep
    • 0
43
Q

Where do orexinergic projections go to in the brain?

Function?

A

throughout brain - EXCEPT in cerebellum

maintain proper viligance

44
Q

Major orexinergic projections go to?

A
  • hypothalamus
    • TMN
    • VLPO
    • SCN
  • cerebral cortex
  • LC, RN (prevent atonia)
45
Q

Where are the orexinergic nuclei located?

Orexin utilizes what receptors in the brain?

What is its function?

A

LH

OX1R, OX2R

neuropeptide that stabilizes the wake-sleep cycle

46
Q

A lesion in the LH can cause what problem?

A
  • narcolepsy (loss of orexin neurons)
  • narcolepsy + cataplexy: (additional loss of atonia neurons)
    • sudden loss of muscle tone while still awake
    • dream like hallucinations
  • primary hypersomnia
47
Q

How does caffeine affect GABA & glutamate?

A

suppress GABA

stimulate glutamate

48
Q

How does alcohol affect GABA & glutamate?

A

stimulate GABA

suppress glutamate

49
Q

Where is the GABAerigic nuclei?

Function?

Result of lesion?

A

VLPO : “sleep switch” of brain (to sleep)

VLPO fire most vigourously during sleep

lesion - insomina

50
Q

Axons from VLPO project where?

function?

A
  • primary arousal centers - inhibit
    • ​TMN
    • LH
    • PPT/LDT
    • RN
    • LC
51
Q

What substance stimulates the release of GABA from VLPO? Via what receptors?

A
  • adenosine
    • A1 / A2 receptors
53
Q

Alchohol has what impact on neurosignaling pathways of the brain?

NOT TESTED

A
  • GABAenergic (enhance)
    • sedative effect
  • noradrenergic projections (release NE)
    • excitement, pleaseure, addiction
  • dopamine pathway (indirect)
    • increases DA only at reward pathway
    • inhibits GABA & endorphin sysem
  • glutamate (inhibits)
    • disorientation, slurrd speech, memory disruption

Neuro II (30 decks)

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