The Enigma Of Working Memory: Changing Views Part 1

Abstract

Working memory is of great interest because of its importance in cognitive function, its relation to consciousness, and its impairments in disease, but the cellular mechanisms remain elusive and controversial. 

Cellular mechanisms are inseparable from memory. Research shows that the formation and preservation of memory are related to the activity of neurons. Cellular mechanisms are the basic units that constitute neurons, so their function, structure, and regulation have an important impact on the formation and preservation of memory. The following will introduce the process of memory formation, preservation, and forgetting from the perspective of cellular mechanisms.

The formation of memory mainly relies on changes in synapses. Synapses are key parts of communication between neurons. Their connections not only determine the formation and function of neuronal networks but are also the main place where memory is formed. Research has found that the strength and number of synaptic connections can be enhanced through training and learning, which is called synaptic plasticity. Synaptic plasticity mainly includes long-term potentiation (LTP) and long-term depression (LTD). LTP can prolong the excitability of neurons, enhance neuronal activity, and promote memory formation. LTD, on the contrary, can weaken neuronal activity, leading to forgetfulness and extinction. Synaptic plasticity is therefore key to memory formation and preservation.

Cellular mechanisms also play an important role in the formation and preservation of memory through neurotransmitters. Neurotransmitters are chemical signals that communicate between neurons and regulate neuronal activity and synaptic plasticity. Past research has shown that dopamine is an important neurotransmitter in the formation and preservation of memory. Dopamine can promote the formation of LTP and prevent the occurrence of LTD, thereby strengthening the connections between neurons and promoting the formation and preservation of memory.

In addition, cellular mechanisms also influence the formation and preservation of memory through epigenetic regulation. Epigenetics refers to genetic phenomena that affect gene expression, including DNA methylation, histone modifications, etc. These modifications can change gene transcription levels, promoter activity, etc., thereby affecting neuronal activity and mutual connections. Research has found that memory formation and preservation are related to regulatory mechanisms such as histone modification and DNA methylation.

In summary, cellular mechanisms play a critical role in the formation and preservation of memory, not only through synaptic plasticity, neurotransmitter modulation, and epigenetic regulation but also through many other mechanisms. Therefore, we should carefully study these mechanisms and understand their functions and modes of action, to better utilize these mechanisms and promote the improvement of our memory. It can be seen that we need to improve our memory. Cistanche deserticola can significantly improve memory, because Cistanche deserticola can also regulate the balance of neurotransmitters, such as increasing the levels of acetylcholine and growth factors. These substances are very important for memory and learning. In addition, meat can also improve blood flow and promote oxygen delivery, which can ensure that the brain receives sufficient nutrients and energy, thus improving brain vitality and endurance.

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A recent article by Barbosa and colleagues overturns the conclusions of an influential study by Wolff and colleagues, which concluded that working memory can be maintained in a hidden state by the transient plasticity of synaptic connections that form dynamic ensembles of neurons encoding information temporarily. A reanalysis of the data reveals that there is a persistent electrically active signature in the EEG recordings that is sustained for the duration of the working memory. 

This reanalysis adds to a large body of evidence indicating that working memory is encoded by sustained action potential firing. 

However, several studies show that unconscious (unattended) working memories can be recalled even in the absence of measurable neural activity, suggesting that electrically silent mechanisms may be involved. Testing that hypothesis is problematic, given that it posits no neuronal firing that could be easily measured.

Keywords

Working memory, attention, hidden states, subliminal perception, synaptic plasticity, EEG, fMRI, and short-term memory.

In contrast to other forms of memory that retain past experiences for future recall, working memory sustains information in real-time while performing a task. The cellular mechanisms of working memory may also differ from other forms of memory, and this is a matter of ongoing research. 

Working memory has very limited capacity and a short duration (for review, see Linden 2007), but this capability is essential for diverse cognitive functions and behaviors. It is a major component of intelligence, and working memory is often diminished by impairments from aging, disease, or intoxication.

There are two leading theories for the mechanism of working memory; each one is supported by electrophysiological and functional brain imaging data. A recent study (Barbosa and others 2021) overturns the conclusions of a seminal study (Wolff and others 2017) which supported the theory that working memory is dependent upon activity-dependent synaptic plasticity. 

This was not accomplished by performing new experiments, but instead by reanalyzing the data from the earlier paper. Using new analytical approaches to reanalyze the original data, the authors find evidence supporting an alternative hypothesis.

Two Theories for Working Memory

Two theories for the mechanism of working memory are “activity-silent neural networks” and “sustained activity.” The first proposes that activity-dependent synaptic plasticity couples neurons functionally into transient neural ensembles that encode the experience (GoldmanRakic 1995). According to this theory, spike-timing-dependent plasticity drives transient biochemical changes at individual synapses that increase or decrease neurotransmitter signaling to form dynamic neural networks that retain the experience. 

Intracellular calcium dynamics that influence synaptic transmission could be sufficient to form transient neural assemblies that are dynamically modified by new information (Mongillo and others 2008). Quickly these rapid activity-dependent changes in synaptic strength subside; functional coupling of the neural networks dissolves, and the working memory is lost.

The temporary storage of information in working memory by brief changes in synaptic strength would enable rapid encoding of information that can be dynamically updated to maintain new information in memory in real time. Importantly, the synaptically coupled neural networks are electrically silent. That is, information encoded in the neural networks is reactivated during recall, much the way short-term and long-term memories are stored and recalled, not by maintained action potential firing in these circuits.

The alternative hypothesis is that working memory is sustained by persistent action potential firing. Continuous firing of action potentials would be an improbable and energetically inefficient way to store information for long periods, but since working memory operates in real-time and persists for only a few seconds, synaptic plasticity mechanisms of information storage and recall that are responsible for short-term and long-term memory may not be necessary. 

Instead, persistent action potential firing in neural networks that are responsible for perception and information processing could maintain information for the immediate purpose of carrying out a specific cognitive task. Indeed, if there is conscious awareness of an event while the behavior is being carried out, persistent action potential firing in cortical circuits would be expected.

There is long-standing evidence for sustained firing of action potentials during the delay period before recall in working memory. The prefrontal cortex is the hub of working memory because this is where various aspects of sensory experience are combined to form a coherent schema. Pioneering studies in nonhuman primates established the importance of the prefrontal cortex in working memory (Butters and Pandya 1969), and electrophysiological recordings in the 1970s revealed neuronal firing in the prefrontal cortex of monkeys sustained for the duration of a working memory task (Fuster and Alexander 1971). 

Similarly, increased activity sustained during the delay period in working memory tasks has also been shown by functional magnetic resonance imaging (fMRI; Courtney and others 1997) and electroencephalography (EEG; Foster and others 2016) studies on humans. Sensory cortex and other brain regions can exhibit similar behavior.

One difficulty, however, is that such persistent activity could be ancillary to the fundamental mechanism of working memory; for example, it could reflect neural activity related to attention (Lewis-Peacock and others 2012). Indeed, other studies have shown that neural activity can wax and wane during the delay period before recall. Frequently neural activity drops to baseline and rebuilds in strength near the end of a delay period in anticipation of recall needed to execute a repetitive task (Barak and others 2010). 

Together these studies suggest that although persistent action potential firing can attend working memory, other electrically silent mechanisms may retain working memory in some cases. One parsimonious explanation is that attended working memories (those retained in conscious awareness) and unattended (nonconscious) working memories may operate through different cellular mechanisms.

Attended versus Unattended Working Memory

Working memory can be maintained without conscious awareness, and then recalled after an appropriate cue, as when one forgets their train of thought in a conversation but then recalls it immediately when reminded of what was being said only seconds previously. 

In support of this, a single TMS (transcranial magnetic stimulation) pulse can restore a lost visual working memory in studies on humans, and boost levels of neural activity detected by fMRI and EEG that are indicative of recalling the memory (Rose and others 2016). This supports the hypothesis that unattended memories are stored by mechanisms other than sustained action potential firing. 

In these experiments, participants are presented simultaneously with two objects on a computer screen. After a short delay, they were told which of the two to remember. Thus, that cued image becomes the focus of attention and is maintained in an attended working memory state. 

An increased neural response, detected by fMRI and EEG in separate experiments, was identified that corresponded to when the image was recognized.

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