Final Exam Flashcards

1
Q

What is the Lateral interpositus nucleus?

A

The part of the brain that responds to a CONDITIONED stimulus, but not an unconditioned stimulus.

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2
Q

What is the unconditioned response pathway?

A

Unconditioned airpuff to trigeminal nucleus, to oculomotor nucleus, to the eyeblink (UR and CR.)

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3
Q

What is the conditioned response pathway?

A

Tone CS to Cochlear Nucleus, to Pontine Nuclei, to Lateral Interpositus Nucleus, to Red Nucleus, to Oculomotor nucleus, to eyeblink (UR and CR.)

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4
Q

Where does learning occur?

A

Long Term Depression of the Cerebellar Cortex Purkinje Cells occurs when they experience repeated stimulus. This is when the parallel fibers and climbing fibers activate the Purkinje Cells at the same time. EPSPs are reduced in the Purkinje Cells, aka LTD. LTD results from a lower responsiveness to glutamate (fewer receptors) by the Purkinje cells.. This reduces the inhibition of the LIP neurons leading to increased activation to the CS. Purkinje cells become LESS responsive every time tone and puff happens, so they INHIBIT the LIP LESS every time the tone and puff happens. Purkinje cells normally inhibit LIP by releasing GABA.

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5
Q

Part of brain that tells the memory storing parts to keep the information and keeps thoughts going

A

Dorsolateral prefrontal cortex

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6
Q

What is anterograde amnesia?

A

When you can’t form new memories. Short-term memory can be left intact.

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7
Q

What is the Hebb rule?

A

The hypothesis that the cellular basis of learning involves strengthening of a synapse that is repeatedly active when the postsynaptic neuron fires.

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8
Q

What is long term potentiation?

A

A long-term increase in the excitability of a neuron to a particular synaptic input caused by repeated high-frequency activity of that input. Leads to synapses that are stronger and more efficient. Develops rapidly and is long-lasting.

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9
Q

Explain the neuroscience of LTP.

A

high frequency input, floods lots of glutamate into cleft, opens NMDA receptors, bring calcium in, brings additional AMPA receptors to postsynaptic membrane. If the NMDA receptor is blocked by a NMDA antagonist, LTP will not proceed.

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10
Q

Hemisphere lateralization of emotion?

A

Positive emotions left lateralized, negative emotions right lateralized, so left hemisphere damage makes you sad. Right hemisphere of brain reads emotion.

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11
Q

What systems mediate the stress response?

A

The sympathetic nervous system increases release of Catecholamines (NE and E) and the hypothalamic-pituitary-adrenal axis (HPA) activation increases release of cortisol. Largely under the control of the hypothalamus.

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12
Q

Explain the effects of a stroke.

A

Release of massive amounts of glutamate; prolonged opening of sodium and calcium channels. Increased sodium causes cells to absorb water and swell. Inflammation activates microglia causing them to become phagocytic. Toxic levels of calcium produce direct toxicity and instigate various second-messenger pathways. Energy crisis ensues as mitochondria reduce their production of ATP. Neuronal cell death occurs immediately after a stroke, but prompt medical attention can save the neurons and glia in the penumbra

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13
Q

Explain the effects of Alzheimer’s disease.

A

Cortical degeneration. Most affected areas are the limbic cortex, inferior temporal cortex, and posterior parietal cortex. The entorhinal cortex (link between neocortex and hippocampus) shows clearest evidence for cell loss, which may explain why memory problems occur early in the disease. Size of sulci increases because the gyri neurons have been lost

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14
Q

Describe the two hypotheses of schizophrenia.

A

The Glutamate Hypothesis - PCP produces symptoms similar to schizophrenia by blocking the NMDA glutamate receptor. Therefore, schizophrenia could be linked to an underactivity of glutamate.
The Dopamine Hypothesis - Too much dopamine in the brain can cause schizophrenic symptoms even in people WITHOUT schizophrenia, and drugs that reduce dopamine can help positive schizophrenia symptoms in some patients.

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15
Q

What brain structure facilitates INVOLUNTARY facial movement?

A

Basal ganglia.

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16
Q

What brain structure facilitates VOLUNTARY facial movement?

A

Motor cortex.

17
Q

Describe the process of stress when it activates the hypothalamic-pituitary-adrenal axis (HPA).

A

Sensory information reaches amygdala.
The amygdala sends information to the hypothalamus via the stria terminalis.
The paraventricular hypothalamus releases CRH, which affects the anterior pituitary.
The hypothalamus activates the pituitary gland, which in turn releases hormones that stimulate the adrenal glands to release the stress hormones cortisol.
The anterior pituitary releases ACTH.
In response to ACTH, the adrenal glands release cortisol.
Cortisol influences many neurons in the brain, increasing the release of several neurotransmitters.
When the hippocampus senses cortisol, it acts to inhibit CRH release by the hypothalamus. CRH is a releasing hormone. It causes the release of ACTH.
With less CRH, less ACTH and cortisol will be released

18
Q

Where are the emotions of fear, disgust, and social rejection found, respectively?

A

Amygdala, Insula, Cingulate Gyrus.

19
Q

What does the activation of the nucleus accumbens do?

A

Release dopamine.

20
Q

How does damage to the Ventromedial prefrontal cortex affect somebody?

A

Shitty emotional processing and decision making. Also, no anticipatory autonomic activation.

21
Q

Explain the process of the LTP and the NMDA receptor in memory.

A

Activation of AMPA receptors causes depolarization of postsynaptic cell membrane. When depolarization reaches NMDA glutamate receptor, Mg^2+ is expelled from its channel allowing Ca^2+ to enter. Calcium activates protein kinases, and these protein kinases may then increase the sensitivity and/or increase the number of glutamate receptors. They may also activate some type of retrograde messenger. Long term potentiation then occurs: both the pre and postsynaptic neurons are affected, and the synapse is strengthened.