Module 2 Flashcards

1
Q

What are the Biological Bases of Behaviour?

A

There are three bases; genetic factors, structural abnormalities, and chemical “imbalances.”

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2
Q

Regarding twin studies, how prevalent is genetic factors in the development of personality disorders.

A

If one twin had a disorder there is a 50% chance the other twin will also develop it

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3
Q

How may gene-environment interactions effect a disorders development?

A

A person with schizophrenia, maybe have been in the womb while the mother had a flu virus which effected the development of their brains

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4
Q

Would someone develop Schizophrenia if they only had the gendetic predisposition that did not interact with the psychochological (extreme stress or trauma) predisposition?

A

the studies suggest that he likely would not have developed schizophrenia if this genetic predisposition had not interacted with other biological (viral) or psychological (extreme stress or trauma) factors.

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5
Q

How is the Phineas Gage story related to structional abnormalities effect on behaviour?

A

physical damage, either from an accident or pathological process, such as stroke or tumour, can lead to changes in behaviour

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5
Q

How is the H.M sorry related to structional abnormatilites effect on behaviour?

A

H.M. underwent surgery in which a large section of his hippocampi (both sides) were purposely lesioned/damaged in an attempt to stop severe seizures that could not be controlled by medication.
He woke up after surgery with his personality intact.
However, he had developed what is called anterograde amnesia. In other words, he lost the ability to form new long-term memories, although his working memory and procedural memory still functioned.

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6
Q

What’s parts of the brain of a Schizophrenic person may be smaller than a person without the disorder?

A

frontal cortex would likely be smaller and less active

abnormalities have been tied to abnormally high circulating levels of the stress hormone cortisol

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7
Q

What’s parts of the brain of a Depressed person may be smaller than a person without the disorder?

A

both the hippocampus and prefrontal cortex, as suggested by both animal and human studies

abnormalities have been tied to abnormally high circulating levels of the stress hormone cortisol

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8
Q

Does cortisol levels effect cognition? If so why?

A

the hippocampus appears to be extremely resilient, yet subject to plasticity (think of plastic clay) induced by circulating stress and sex hormones. These mechanisms of plasticity, in conjunction with evidence suggesting that cortisol levels have differential effects on cognition

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9
Q

What is the HPA axis’ role in stress response?

A

well-known that the hippocampus is involved in negative feedback regulation of the HPA axis , which is a neuroendocrine (nervous system + hormonal/endocrine) system responsible for shutting down unnecessary functions during stress, and, ultimately for shutting off the stress response itself.

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10
Q

What appears to differentially regulate in the PFC hippocampus, and hypothalamus regarding stress? And what does it affect?

A

Chronic stress appears to differentially regulate GR(GR; the protein molecules that receive the stress hormones) levels in the PFC, hippocampus, and hypothalamus in an animal model (Mizogushi, 2003), suggesting that these abnormal levels might profoundly affect HPA function and subsequently cognition through the dopamine system

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11
Q

What are nuearons highly specialzed for?

A

Neurons are similar to other cells in structure; however, they are highly specialized for intercellular communication

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12
Q

What are the dendrites, axon, node of ranvier functions?

A

The dendrites are processors that receive input from other neurons; the complexity of the dendritic structure determines the number of neurons that the cell may receive messages from other neurons

The portion of the cell made for signal conduction is called the axon
number of layers of a fatty substance called myelin, which insulate the conducting fibre and speeds up transmission

The node of ranvier (the space between the myelin), is where the electrical signal is propagated. The axon terminals act as transmitters of the signal.

Overall, synaptic transmission consists of both electrical processes (within the cell) and chemical processes (between cells)

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13
Q

Where does information enter through in the cell?

A

Info comes through dendrites and soma
Then transmits down the axon outwards other neurons

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14
Q

How do concentrations of sodium and potassium ions differ between the inner and outer environments?

A

sodium(Na+) concentration being higher in the extracellular environment

potassium(K+) concentration higher in the intracellular environment.

Chloride(Cl-) ion concentration is also higher outside the cell

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15
Q

What are the steps of action potential?

A

1.resting potential
2.Threshold
3. rising phase
4. falling phase
5. recovery phase.

16
Q

Explain All or none Law.

A

The principle that once an action potential is triggered in an axon, it is propagated without growing or diminishing to the end of the fiber (terminal buttons).

17
Q

What are the steps of Neurochemical Transmission

A

1.Action potential reaches the axon terminal.
2. Voltage-gated Ca2+ channels open and trigger the release of neurotransmitter from synaptic vessicles (storage chambers within the cell).
3. Vesicles fuse with membrane and release neurotransmitter into the synaptic cleft.
4. Transmitter binds to post-synaptic receptors (in a lock-and-key fashion).
5. Transmitter is brought back into pre-synaptic cell for recycling (re-uptake) or is deactivated by enzymes in the synaptic cleft.

18
Q

Can too little or too much neurotransmitter in the gap between cells (synaptic gap or cleft) promotes vulnerability to or increases the risk for psychopathology?

A

Yes

Too few or too many receptors or receptors that are either too sensitive or not sensitive enough, may confer risk for abnormal behaviour

19
Q

What neurotransmitter/s may manifest schizophrenia, and how?

A

dopamine

excessive dopamine in the mesolimbic pathway (involved in cognition and emotion) and low dopamine levels in the prefrontal cortex

Dysfunction or deficiencies with other neurotransmitters, such

20
Q

What neurotransmitter/s may manifest depression, and how?

A

norepinephrine, serotonin, and dopamine

Studies suggest that depletion of these substances in the synaptic cleft or problems with the number or sensitivity of receptors may be involved.

21
Q

Why is the “Chemical Imbalance” reasoning for depression wrong?

A

First, the notion of an “imbalance” suggests that we know what the “balance” should be among neurotransmitters to ensure good mental health—we don’t have an answer to this; we do not actually know.

Second, in decades of research, there has never been an actual demonstration of a direct, causal connection between a neurotransmitter imbalance and the development of specific mental disorders.

Finally, there are no reliable and valid (research these terms again if they are rusty for you) tools for detecting imbalances in neurotransmitters. The chemical imbalance explanation remains unsubstantiated at this time (Deacon, 2013).

21
Q

How may psychological factors affect behaviour? Consider the case study of schizophrenia.

A

In our case of Joe, the level at which a family member is critical of and hostile toward Joe and his symptoms is likely to affect the likelihood of his return to the hospital for a psychotic episode