Biopsychology of declarative memory Flashcards

1
Q

What is the hippocampus?

A

Brain region in the medial temporal lobe. It has a very complicated shape because it is folded in one dimension and curved in another.

Is the first brain structure that has been specifically associated with long-term memory.

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2
Q

Define the term anterograde and retrograde amnesia.

A

Neuropsychological condition characterized by an impairment of retrieving memories about events happened before (retrograde) or after (anterograde) the brain lesion.

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3
Q

Define the term long-term potentiation and depression.

A

Cellular mechanisms associated with learning.

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4
Q

What are the two levels that occur from changes to the nervous system due to learning?

A

Gross Level
Cellular Level

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5
Q

What is gross level?

A

➢ Changes in brain structure occurring over time, for example, experienced London taxi drivers have larger hippocampi than controls (Maguire et al., 2000, PNAS).
➢ Changes in brain function, for instance, changes in brain activation or neural connectivity during a memory task or during consolidation.

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6
Q

What does lesions in the hippocampus induce?

A

Amnesia

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7
Q

What is amnesia?

A

Chronic impairment of memory encoding or retrieval. In neurodegenerative diseases, amnesia is slow and progressive. In other cases, the impairment follows a traumatic event. There are two types of amnesia: anterograde amnesia involves a failure to remember events after the traumatic experience (e.g., new memories). Retrograde amnesia involves a failure to remember events before the trauma.

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8
Q

What do studies on patients with amnesia provide?

A

One of the strongest evidence in favour of a multi-component view of long-term memory.
Usually patients have impairments in declarative memory, especially episodic memory, but not in other types of memory.

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9
Q

What happened to HM?

A

HM had a bilateral medial temporal lobectomy (meaning that he had most portion of his hippocampus, parahippocampus and amygdala surgically removed on both hemispheres) to treat his epilepsy. After the surgery, he did not have seizures anymore but he was left with a severe anterograde amnesia.

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10
Q

Explain HM’s memory ability.

A

His short-term memory was unimpaired.
His procedural memory was unimpaired.
His semantic memory was relatively unimpaired.
His episodic memory for events that happened before the surgery was unimpaired (= he did not suffer from retrograde amnesia).
What was impaired in HM was his ability to form new memories (= anterograde amnesia).

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11
Q

What does the case of HM tell us about memory and the hippocampus?

A

❖ The hippocampus is not involved in short-term, semantic or procedural memory. HM could learn new procedures and could remember short-term relatively well. His semantic memory was relatively intact

❖ The hippocampus is not the location of (or it is not necessary for) long-term memories in general. HM could retrieve details from his past and events that happened prior to
the surgery. This suggests that the key role of the hippocampus is to learn and form NEW episodic memories.

❖ The hippocampus is responsible for explicit memory retrieval, but not for implicit memory retrieval. Some amnesic patients can store a record of an episode in their memory, although they are not able to explicitly retrieve that record, and/or to provide details of when or where they have acquired that memory.

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12
Q

Who did research on patient HM?

A

Scoville & Milner, 1957

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13
Q

Provide further investigations on patients with brain lesions who showed different patterns of memory impairments.

A

Patients with Korsakoff’s syndrome (lack of vitamin B1 due to alcohol abuse) develop similar memory impairments as those found in HM, but their hippocampus is intact. They have neuronal loss in the thalamus and hypothalamus.
Patients with similar lesions to HM develop different memory profiles. For instance, patient KC (Tulving, 1989) with bilateral hippocampal lesions suffered from retrograde as well as anterograde amnesia with no memory for remote events.

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14
Q

What are the discrepancies of investigations on patients with brain lesions?

A

Brain lesions in humans are never limited to specific parts of the brain but extend to neighbouring regions related to other cognitive functions. It is impossible to find two patients with exactly the same lesion!

More recent neuroimaging investigations using fMRI, EEG and brain stimulation suggest that episodic memory is associated with a network of brain regions, rather than with the activity of one single region.

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15
Q

What else is involved in learning brain activations?

A

Using fMRI, scientists have shown that during learning brain activations are not limited to the hippocampus, but also involve the parietal and prefrontal cortex (e.g., Schott et al., 2013, PNAS). These brain regions are functionally connected during learning.

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16
Q

What is involved in memory formation?

A

Using non-invasive brain stimulation,
scientists have found that the lateral
prefrontal cortex is involved in memory formation for verbal material (Galli et al., 2017 Biological Psychology; Medvedeva et al., 2019, Cerebral Cortex; Medvedeva et al., 2021, Brain Stimulation).

17
Q

What is involved in episodic memory formation?

A

The prefrontal cortex, parietal
cortex and the hippocampus.

The temporal dynamics of memory formation are very complex and different brain regions may be active at different points in time during
encoding. Recent fMRI and TMS studies showed that the hippocampus and the ventrolateral prefrontal cortex are particularly active after the offset of an encoding stimulus (Cooper & Ritchey, 2021, Journal of Neuroscience; Medvedeva et al., 2021, Brain Stimulation).

18
Q

What part of the brain is followed by semantic memory deficits?

A

Semantic memory deficits follow a damage to the anterior temporal lobe. This is very evident in patients with semantic dementia. These patients show deficits in semantic memory tasks with relatively unimpaired episodic memory (Chan et al., 2001).

19
Q

Give counterevidence for the temporal lobe causing semantic memory deficits.

A

Patients with anterograde amnesia following temporal lobe damage show relatively unimpaired semantic memory (Manns, Hopkins, & Squire, 2003).

20
Q

What is cellular level?

A

Learning is related to the concept of synaptic plasticity – it induces changes in the biochemistry or structure of presynaptic or postsynaptic neurons. This includes greater release of neurotransmitters or change in the number or sensitivity of post-synaptic cells, which in turn induce an increase of the size of the postsynaptic potentials.

21
Q

What are the cellular mechanisms?

A

▪ Long-term potentiation.
▪ Long-term depression.

22
Q

What is long-term potention?

A

Is a phenomenon observed in the hippocampus, a region of the brain associated with learning and memory, where there is a long-lasting increase in the strength of synaptic connections between neurons.

23
Q

How can LTP be induced in experimental settings?

A

Long-term potentiation can be induced in the hippocampus
of the rat:
A stimulating electrode is placed in a pre-synaptic neuron in the hippocampus (A below), and a recording electrode is placed in the post-synaptic neuron (B below). This set up is used to examine how the stimulation of the pre-synaptic neuron affects post-synaptic potentials recorded in the post-synaptic neuron.

A train of high-frequency stimulation (100 pulses within a few seconds, tetanic stimulation), mimicking the activation induced by learning, is delivered through the stimulating electrode. Neurophysiologists look at the changes in the post-synaptic potentials following this stimulation.

LTP is an increase or strengthening (compared to baseline) of the postsynaptic response in the dentate gyrus following the tetanic stimulation that lasts for approximately one hour.

24
Q

What is long-term depression’s role in memory?

A

Thought to play a role in memory formation and learning, because neural circuits that contain memories are established by strengthening some synapses and weakening others.

Long-term depression is induced by delivering low-frequency stimulation (below 10 Hz), instead of tetanic stimulation.

This causes postsynaptic neurons in the dentate gyrus to decrease their synaptic strength, rather than increase.