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Neurobiology -BIOL4370 > Lecture 6-Mood Disorders > Flashcards

Lecture 6-Mood Disorders Flashcards

1
Q

What role does the hippocampus play in regulating stress?

A

The hippocampus reduces cortisol release by activating glucocorticoid receptors, which in turn inhibit CRH release from the hypothalamus and calm down the HPA axis.

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2
Q

What is the effect of chronically elevated cortisol on the hippocampus?

A
  1. Can damage hippocampal neurons
  2. Prolonged stress reduces CRH neuron sensitivity to cortisol, preventing it from stopping the stress response and keeping the body in a heightened stress state.
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3
Q

What are the key steps involved in serotonergic signaling regulation?

A
  1. Serotonergic neurons produce the enzymes tryptophan hydroxylase and Aromatic L-amino acid decarboxylase (AADC), which convert tryptophan into serotonin.
  2. VMAT2 loads serotonin into vesicles for storage and release.
  3. When a signal arrives, serotonin is released from vesicles into the synapse.
  4. SERT (5-HT transporter) facilitates the reuptake (recycling) of serotonin
    by pulling it back into the neuron.
  5. 5-HT1D autoreceptors can detect when there is too much serotonin and can reduce or stop further release.
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4
Q

What is reserpine and what effect did it have in treating depression?

A

Originally used for high blood pressure, but it caused severe depression in 20% of people by depleting catecholamines (chemicals like dopamine and norepinephrine, which affect mood)

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5
Q

What effect did the tuberculosis drug have in treating depression?

A

The tuberculosis drug unexpectedly elevated mood by inhibiting monoamine oxidase, an enzyme that breaks down catecholamines, keeping these mood-related chemicals active longer.

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6
Q

What effect do SSRIs have on 5-HT (serotonin)?

A

SSRIs prolong the effects of secreted 5-HT by preventing its reuptake into the presynaptic neuron, increasing its levels in the brain

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7
Q

How do SSRIs affect glucocorticoid receptor (GR) expression in the brain?

A

SSRIs increase GR expression in the hippocampus, which creates more receptors for cortisol to bind to. This helps the brain respond better to stress hormones, allowing it to manage stress more effectively.

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8
Q

What is the effect of SSRIs on corticotropin-releasing hormone (CRH) neurons in the hypothalamus?

A

SSRIs enhance feedback inhibition of CRH neurons in the hypothalamus (reduce the activity of CRH neurons in the hypothalamus), lowering stress hormone production and helping to lower stress overall.

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9
Q

How does Imipramine function as an antidepressant?

A

Imipramine inhibits the reuptake of serotonin and norepinephrine, allowing more of it to stay around and work longer to improve mood.

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10
Q

What is suggested by the use of Imipramine for treating depression according to the slide?

A

The use of Imipramine suggests that depression may be the result of disruptions in modulatory systems involving neurotransmitters like serotonin and norepinephrine.

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11
Q

What are the long-term effects of Imipramine on gene expression and neurogenesis according to the slide?

A

Imipramine may alter gene expression, increase glucocorticoid receptor (GR) expression, and enhance neurogenesis in the hippocampus.

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12
Q

What role do benzodiazepines play at the GABAA receptor to treat anxiety?

A

Benzodiazepines act as modulators of GABAA receptors, enhancing the inhibitory effect of GABA.

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13
Q

How do benzodiazepines reduce neuronal activity?

A

Benzodiazepines keep GABAchloride channels open longer, allowing chloride to enter neurons and make them less active, which reduces anxiety.

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14
Q

What is the mechanism of action of fluoxetine in treating affective disorders?

A

Fluoxetine treats affective disorders by inhibiting the reuptake of serotonin, thus increasing its availability and activity in the brain

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15
Q

How are SSRIs effective in treating anxiety disorders like OCD?

A

SSRIs are effective for OCD because they help reduce the recurrence of intrusive thoughts and the compulsion to perform repetitive behaviors by increasing serotonin levels in the brain.

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16
Q

How do MAO inhibitors like phenelzine work to treat affective disorders?

A

Phenelzine works by inhibiting the enzyme monoamine oxidase, which normally breaks down neurotransmitters like serotonin and norepinephrine, thereby increasing their levels and improving mood.

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17
Q

What are the effects of a single dose of ketamine on depression symptoms?

A

A single dose of ketamine can quickly alleviate symptoms of depression by reducing brain inhibition and strengthening cell connections, facilitating synaptic plasticity and increasing synaptogenesis

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18
Q

What are some unique challenges in treating human brain diseases?

A

Challenges include the
1. Brain’s inaccessibility
2. Complex gene-environment interactions
3. Co-morbidity
4. Risk of treatments worsening conditions

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19
Q

What strucutres are involved in the control of movement? (4)

A
  1. Motor cortex: Plans movements
  2. Brainstem: Controls basic movements and postural control
  3. Basal ganglia: Initiates movements
  4. Spinal circuits: Integrate sensory and motor signal
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20
Q

What is the role of local circuit neurons in the motor system?

A

Local circuit neurons are involved in lower motor neuron integration, processing and refining motor commands within the spinal cord.

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21
Q

What are the key functions of the basal ganglia in movement?

A
  1. Regulates upper motor neuron activity
  2. Modulate UMN activity in anticipation and during movement
  3. Required for voluntary movements
  4. Ensure smooth transitions between movements.
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22
Q

With which structures does the basal ganglia interact to facilitate movement?

A

The basal ganglia interact with the substantia nigra and subthalamic nucleus, forming a subcortical loop that links cortical areas with motor neurons (MNs).

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23
Q

What are the main components of the basal ganglia shown in the diagram?

A

The components include the caudate nucleus, putamen, globus pallidus, substantia nigra, and subthalamic nucleus.

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24
Q

What is the main input structure of the basal ganglia?

A

The caudate and putamen (parts of the striatum) receive movement-related signals and process them.

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25
Q

Where do cortical inputs to the basal ganglia terminate?

A

Cortical inputs terminate on medium spiny neurons (MSNs) in the basal ganglia.

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26
Q

What is the function of medium spiny neurons (MSNs) in the basal ganglia?

A

MSNs integrate multimodal information and project to the globus pallidus and substantia nigra, which are the main output structures of the basal ganglia.

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27
Q

Two main outputs from basal ganglia

A

To motor areas via the thalamus from the Globus Pallidus internus (GPi) — regulating voluntary movement.

To eye movement areas in the brainstem, including the superior colliculus, from the Substantia Nigra pars reticulata (SNr) — controlling eye and head movements.

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28
Q

What is the corticostriatal pathway?

A

The corticostriatal pathway consists of all cortical projections to the basal ganglia.

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29
Q

What type of inputs does the caudate receive in the corticostriatal pathway?

A

The caudate nucleus primarily receives inputs from multimodal association cortices and motor areas of the frontal cortex that control eye movement.

30
Q

Which cortical areas send signals to the putamen?

A

The putamen receives inputs from primary and secondary somatosensory cortices, as well as from occipital, premotor, motor cortices, and auditory association areas

31
Q

What is the main type of output from the basal ganglia?

A

The main output of the basal ganglia is inhibitory (GABAergic).

32
Q

What is the activity level of medium spiny neurons, and what type of neurotransmitter do they use?

A

Medium spiny neurons in the striatum have low levels of spontaneous activity and are GABAergic (inhibitory).

33
Q

What are the main motor symptoms of Parkinson’s Disease?

A
  1. Hypokinesia (reduced movement)
  2. Bradykinesia (slow movement)
  3. Rigidity (increased muscle tone)
  4. Tremors.
34
Q

What is the underlying cause of Parkinson’s Disease?

A

Degeneration of substantia nigra neurons, leading to a loss of dopamine in the striatum.

35
Q

What are some treatment options for Parkinson’s Disease?

A
  1. L-DOPA supplementation
  2. Neural grafts with stem cells: Stem cells are implanted to develop into dopamine-producing neurons, potentially restoring lost function.
  3. Gene therapies: Modifies genes to protect neurons or increase dopamine.
36
Q

How does dopamine loss in Parkinson’s Disease affect movement control?

A

It reduces inhibition of the globus pallidus internus, causing excessive inhibition of the thalamus and decreased excitation of upper motor neurons, impairing movement.

37
Q

What types of movement abnormalities are associated with Huntington’s Disease?

A
  1. Hyperkinesia (excessive
    movements)
  2. Dyskinesia (abnormal
    movements)
  3. Chorea (spontaneous,
    uncontrollable, rapid movement)
  4. Dementia
38
Q

What protein is associated with Parkinson’s Disease? How does it contribute to Parkinson’s Disease?

A

In Parkinson’s, alpha-synuclein proteins form clumps (Lewy bodies) in brain cells, damaging dopamine-producing neurons.
- This neuron loss disrupts movement control, leading to symptoms like tremors and stiffness.

39
Q

What neurotoxin is used to induce Parkinson’s Disease in animal models, and what movement impairments does it cause?

A

MPTP is used to induce Parkinson’s Disease, causing movement impairments such as gait impairments, hunched posture, and saccadic deficits in animals.

40
Q

What brain regions show neuronal loss in Huntington’s Disease?

A

Caudate, putamen, and globus pallidus.

41
Q

Name three cognitive or emotional symptoms of Huntington’s Disease.

A

Depression, irritability, and impulsivity.

42
Q

What genetic mutation causes Huntington’s Disease?

A

Unstable triplet repeat (excessive CAG repeats) in the Huntington gene.

43
Q

What is the effect of excessive CAG repeats in Huntington’s Disease?

A

They increase the number of glutamines, alter protein folding, and trigger cell death pathways.

44
Q

What is Deep Brain Stimulation (DBS) and how does it help in treating movement disorders?

A

DBS involves activating underperforming brain pathways, such as the substantia nigra in Parkinson’s Disease to increase dopamine release, and can help manage symptoms of movement disorders.

45
Q

What effect does degeneration in the caudate and putamen have on the neural pathways in Huntington’s Disease?

A

It reduces inhibitory input to the GPe, increases tonic inhibition of the subthalamic nucleus, decreases excitation of the GPi, and leads to increased excitation of the frontal cortex.

46
Q

What changes occur in GPi neuron firing patterns in a rhesus monkey before, during, and after DBS treatment?

A

Before DBS, neuron firing is disordered; during DBS, firing becomes more coordinated; and after DBS, a more normal activity pattern is restored.

47
Q

What are the two categories of symptoms in schizophrenia?

A

Schizophrenia symptoms are categorized as positive and negative symptoms.

48
Q

What are positive symptoms in schizophrenia?

A

They are unusual experiences added to a person’s perception, such as:
1. Hallucinations: Mostly auditory, like hearing voices.
2. Delusions: Strong false beliefs, e.g., thinking “aliens are controlling my thoughts.”
3. Disorganized thoughts: Confused, jumping between unrelated ideas.
4. Loose associations: Thoughts are loosely connected, making speech hard to follow

49
Q

What structural brain changes are observed in schizophrenia?

A

Enlarged ventricles, cortical thinning, smaller hippocampus and reduced dentate gyrus output, indicating widespread brain tissue loss.

50
Q

What are risk factors for schizophrenia?

A
  1. Genetic and environmental
    components
  2. Higher rates in urban settings (exposure to toxic metals)
  3. Difficulties during pregnancy
  4. Viral infections
  5. Season of birth effects
  6. Mostly left-handed
51
Q

What are key negative symptoms in schizophrenia?

A
  1. Flat affect
  2. Catatonia: Abnormal movement or behavior, like staying still, not speaking, or repetitive actions.
  3. Social withdrawal
52
Q

What pathway do medium spiny neurons of the putamen follow in the basal ganglia output system?

A

Medium spiny neurons project to both the internal and external segments of the globus pallidus, with the GPi segment projecting further to thalamic nuclei and then to the motor cortex.

53
Q

How does the direct pathway of the Basal Ganglia facilitate voluntary movement?

A

The direct pathway decreases the inhibition of the GPi on the thalamus, allowing increased activation of the motor cortex, thus facilitating voluntary movement.

54
Q

What are the steps of the basal ganglia “Direct” pathway, including excitatory and inhibitory signals?

A
  1. The cerebral cortex excites striatum (+, transient).
  2. The striatum inhibits the GPi and Substantia Nigra Pars Reticulata (SNr) (-, transient).
    Note: The GPi is responsible for body movement, and the SNr is more involved in eye movement.
  3. GPi inhibits thalamus (-, tonic), but inhibition from the striatum reduces this, disinhibiting the thalamus.

5.Thalamus excites frontal cortex (+, transient), initiating movement.

55
Q

What is the functional effect of the Direct pathway on eye movement?

A

It inhibits the substantia nigra pars reticulata, which releases the superior colliculus from inhibition, allowing eye movement to occur.

56
Q

What effect does dopamine have on D1 and D2 receptors?

A

D1 receptors increase cAMP and cell excitability, while D2 receptors decrease cAMP and cell excitability.

57
Q

Where are the reciprocal connections of dopamine in the basal ganglia? How do these connections affect movement?

A

Between the substantia nigra and medium spiny neurons (MSNs) in the striatum.
- These connections modulate movement by balancing excitation and inhibition.

58
Q

How does dopamine facilitate movement in the Direct pathway?

A

Dopamine excites the striatum via D1 receptors, leading to disinhibition of the thalamus and activation of the frontal cortex, initiating movement.

59
Q

Where is gray matter loss most prominent in schizophrenia and what is its impact?

A

Gray matter loss is most prominent in the dorsolateral prefrontal and parietal cortices, correlating with significant cognitive impairments.

60
Q

What cellular and structural abnormalities are associated with schizophrenia?

A

Schizophrenia is associated with reduced glutamate receptor density (impaired communication) or function, reduced spine density (fewer synaptic connections between neurons) in the prefrontal cortex, and decreased spine volume (weakened synaptic strength).

61
Q

How can positive symptoms and cognitive impairments in schizophrenia be modeled, and what substances are used?

A

Positive symptoms and cognitive impairments can be modeled using PCP and ketamine, which are NMDA receptor antagonists that increase these symptoms.

62
Q

What changes occur in the frontal lobe and default mode network in individuals with schizophrenia?

A

Individuals with schizophrenia show hypofunctionality in the frontal lobe, associated with negative symptoms, and changes in the default mode network, which correlate with positive symptoms.

63
Q

What is the main conclusion about auditory cortex responses in schizophrenia?

A

Auditory hallucinations in schizophrenia activate the auditory cortex similarly to how it responds to real speech in non-schizophrenic individuals.

64
Q

What hypothesis is proposed regarding dopamine’s role in schizophrenia?

A

The dopamine hypothesis suggests that overproduction of dopamine, particularly in the mesocortical pathway, contributes to schizophrenia symptoms, especially positive symptoms like hallucinations and delusions.

65
Q

How does the dopamine hypothesis relate to drug use?

A

Drugs like amphetamines and cocaine, which raise dopamine, can cause similar symptoms like hallucinations and delusions.

66
Q

How do antipsychotic medications work in the context of the dopamine hypothesis?

A

Atypical antipsychotics block dopamine D2 receptors to reduce dopamine’s effects, helping control symptoms like hallucinations and delusions.

67
Q

What is the potential presynaptic effect of dopamine (DA) in schizophrenia related to glutamate release?

A

Dopamine may cause extra glutamate release in response to unimportant things, making the brain treat small details as if they’re important. This can lead to confusion and symptoms like hallucinations or delusions.

68
Q

How does the Indirect Pathway work in opposition to the Direct Pathway?

A

The Indirect Pathway suppresses movement by increasing inhibition of the thalamus, while the Direct Pathway facilitates movement by reducing inhibition of the thalamus.

69
Q

What effect does dopamine have on the striatum in the Indirect Pathway?

A

Dopamine from the Substantia Nigra Pars Compacta inhibits the striatum by acting on D2 receptors, reducing the activity of the Indirect Pathway and thus allowing for more movement.

70
Q

Explain the Steps of the Indirect Pathway

A
  1. The cerebral cortex excites the striatum (+, transient).
  2. The striatum inhibits the GPe (-, transient).
  3. The GPe normally inhibits the Subthalamic Nucleus (-, tonic).
    - Inhibition from the striatum reduces this tonic inhibition, disinhibiting the Subthalamic Nucleus.
  4. The Subthalamic Nucleus excites the GPi (+, transient).
  5. The GPi inhibits the thalamus (-, tonic).
  6. The thalamus’s ability to excite the frontal cortex is reduced, suppressing movement

Neurobiology -BIOL4370 (5 decks)

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