Cognitive idea that attentional processes are based on cholinergic

 

Cognitive psychopharmacology is concerned with identifying
theories of cognition with the use of drugs as independent variables. Drugs
affect chemical neurotransmitter functions by interacting with receptors in
terms of simulation and antagonism of their effects at pre/postsynaptic
receptors as well as the synthesis, storage and release of neurotransmitters (Ochsner
& Kosslyn, 2014). Therefore, cognitive psychopharmacology use drugs to
analyse cognitive functions (Abadinsky, 2000). The purpose of this essay will
be to evaluate experimental work that use drugs to manipulate psychological
functions such as attention, memory and metacognition. This is important as
these are fundamental daily tasks so a thorough understanding of how they work
is essential.

 

Attention is a psychological function involved in extracting
information from the environment and allocating this attention selectively. Cognitive
psychopharmacology has heightened our knowledge of the role of cholingeric
transmission this function.

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The neural systems involved are the central cholinergic
pathway, which is made up of the basal nucleus, medial septum and diagonal band
of Broca. These nuclei are based in the Basal Forebrain and possess
Acetylcholine producing neurons that project to the neocortex, hippocampus and
cingulate cortex. It has been proposed that variations in attentional capacity
are related to cholinergic afferents to the neocortex (Warburton, 1981),
therefore experimental drugs that influence Acetylcholine should influence performance
in attention tasks.

To investigate this, Wesnes and Warburton (1984) gave participants a visual
attention task in which a rapid string of digits were presented. In the control
group participants were given an Acetylcholine antagonist, Scopolamine. It was
found that there was a deficit in detection of digits following Scopolamine
administration, which supports the idea that attentional processes are based on
cholinergic transmission. An advantage of this study is that it can also be
reversed with an Acetylcholine agonist such as nicotine. Wesnes and Warburton
repeated the study and found that nicotine improved detection accuracy,
supporting the idea that variations in attentional processing is related to
variations in Acetylcholine which further supports the hypothesis that this
neurotransmitter is involved in attentional processing.

 

However, the research is fairly dated and more contemporary
research suggests that administration of scopolamine has no significant effect
on attention, and in fact increases reaction time during visual attentional
tasks (Furey et al, 2008)

 

The previous task illustrated the importance of cholinergic
transmission in a focused task with sustained attention, considering attentional
resources are flexible (Kahneman, 1973) it’s important to understand if
cholinergic transmission is important for flexibility. Drachman et al (1980)
placed participants in a dichotic listening task and were required to respond
to stimuli presented to both ears, in either a Scopolamine or control
condition. The results showed that Scopolamine decreases performance when
attention needs to be divided. This is due to a result of decreasing resource
capacity, and therefore supports the idea that cholinergic transmission is
involved in attentional processes.

 

 

Selective processing is our ability to focus on something
and selectively ignore irrelevant material, which can be tested with the Stroop
interference task. In the no interference congruent tasks, participants name
colours and in the interference incongruent participants name colours, which
leads to poor performance due to failure in selective processing. Wesnes &
Warburton (1978) used this Stroop task but administered a cholinergic
antagonist and found that interference was increased. Although this supports
the idea for the role of the cholinergic system in selective attention, replications
of results do not suggest the same. Provost & Woodward (1991) found that
when administering participant’s nicotine before a Stroop test, interference
was reduced. This therefore rejects the idea that the cholinergic system is involved
in selective attention as the agonist did not improve attention.

 

Research has shown that nicotine can moreover improve performance
on tasks that require complex cognitive control processes such as error
detection, planning and active response inhibition. Active response inhibition
is the ability to stop an automatic response, underpinned by the ability to
make use of cognitive abilities in your brain. This can be seen in the
antisaccade task, where participants are told to focus their attention on a
cross even when an image appears on one side of the screen. This requires
working memory to inhibit their natural tendency to look at the object. 

 

This test has been replicated by Rycroft et al (2006) but by
administrating nicotine to participants. As expected, nicotine reduced the
number of errors and speeded reaction times to make correct responses. This
supports the idea that the acetylcholine agonist, Nicotine, is involved in
attentional processes and further supports the idea that cholinergic transmission
is involved in attentional processes. Although majority of studies have found
cognitive enhancement following nicotine administration, the effects are
certainly not universal. Jacobsen et al (2006) argued that individual
differences play a significant role, as individuals who carry the 957T gene have
a lesser effect of nicotine on performance than those who don’t carry the gene.

 

Cognitive psychopharmacology has also advanced our
understanding on memory. Memory is another cognitive function which can be
effected by the administration of drugs. Cholinergic antagonists bring about
impairments in the initial coding of information and its found that other drugs
have a more significant influence. Benzodiazepines are psychoactive drugs that
bind to an alpha subunit which increases the affinity for the receptor for
GABA.

 

Numerous studies suggest Benzodiazepines do not influence
short term memory (e.g. Roth et al, 1984; Lister & File, 1984). However,
when testing participants on an increased number of digits to be immediately
recalled Benzodiazepines impair recall which suggests they effect long term
memory (Jones et al, 1978). Roth et al (1984) claims that this is because long
term memory is composed of several subsystems, unlike short term memory which
is a unitary construct. Considering long-term memory consists of multiple
systems served by different brain structures (Cavanaugh & Blanchard-Fields,
2009), it deems important to investigate if the effects of Benzodiazepines are
specific to particular memory systems or functions.

 

Episodic memory is a subsystem of long term memory which
refers to memories of autobiographical events. To test episodic memory a
laboratory memory experiment is conducted which consists of two phases: an
encoding phase where information is studied and a retrieval stage, where memory
is tested. Drugs can then be administered at different points so we can see the
effects it has on either encoding or retrieval.

 

Hinrichs et al (1984) administered Benzodiazepines either
prior to encoding or retrieval to investigate this claim and found that
episodic memory was only impaired if the drug was given prior to encoding,
suggesting benzodiazepines do not influence retrieval processes.

However, it could be that participants simply did not encode
the information. Evidence suggests memory impairments may be due to sedative
and attentional deficits, instead of a deficit in memory. For example, Coul et
al (1995) found that Benzodiazepines impaired performance on a computer
attention task, suggesting the drug impairs focused attentional processing not
just encoding of information.

 

Against this point is the fact that covarying out sedation
produced by benzodiazepines still leaves behind memory impairments, if the only
factor influencing performance was sedation then removing it should eradicate the
deficit found.  This claim is backed up
by research from Reinsel et al (1997) who compared a benzodiazepine with a
sedative, fentanyl. Both drugs produced the same degree of sedation but only
the benzodiazepine reduced episodic memory. Thus suggesting central memory deficits
are influenced by benzodiazepines due to either impairments in the
consolidation process or other aspects of episodic memory formation.

 

Context memory, another subsystem, is memory for where
something was studied. Memory for context forms the foundation of episodic
memory, so without memory for the context of a situation an episodic memory
cannot be possessed. To investigate the claim that deficits in contextual
memory impairs episodic memory Brown & Brown (1990) found that participants
confused words presented in a recognition tests with words presented in earlier
word lists. These findings therefore support the contextual memory deficit
hypothesis that episodic memories cannot be possessed without the memory for
the context something took place.

Furthermore, Gorissen et al (1998) found that memory for words
presented in the context of another (apple-fire) showed significant reduction
after benzodiazepine intake. This supports the claim that benzodiazepines are
involved in contextual memory processes.

 

Semantic memory refers to the capacity for recollecting
general knowledge about the world (Manns et al, 2003). Research suggests
semantic memory isn’t affected by benzodiazepines (Curran et al, 1991;Weingarten,
1992) however the time to retrieve semantic information may be impaired. We
cannot entirely assume this as general response slowing may be due to the
sedative of benzodiazepines instead of impairment to semantic memory processes.

 

Semantic memory retrieval can be influenced by
benzodiazepines by creating semantic illusions. Participants can retrieve
information based on partial matches and when this occurs errors are likely. Izaute
et al (2004) administered Lorazepam to participants and asked misleading
questions. It was found that benzodiazepines increased the number of semantic
errors and made participants less likely to spot the misleading questions. Cognitive
psychopharmacology has enhanced our understanding that benzodiazepines can
impair semantic processing under certain conditions.

 

Procedural memory is “knowing how” and refers to unconscious
memory (Finn et al, 2016). To explore the effect of benzodiazepines on this
type of memory system Martin et al (2002) gave participants either Lorazepam or
Oxazepam and then observed participants’ accuracy on a computer task. It was
found that there was no effect for either of the drugs. Therefore,
benzodiazepines do not have any effect on this type of memory.

 

 

Implicit memory is an unintentional memory that refers to
unconscious retrieval of experience (Mulligan, 2011). However, only certain
types of benzodiazepine impair this type of memory. Curran & Gorenstein (1993)
found that Oxazepam only impaired performance on an explicit memory task whereas
Lorazepam impaired both explicit. Results from other studies have suggested
similar, with Lorazepam but not Diazapem to effect both explicit and implicit memory
(Vidailhet et al, 1995)

 

There is no singular explanation for this, however one
possible one is that the differences relate to the time course of the drugs.

For example, benzodiazepines have been found to impair implicit memory only
when tested at peak plasma levels (Buffet-Jerrott et al, 1998). However, as the
answer remains elusive we cannot assume benzodiazepines influence the implicit
memory system.  

 

One major issue of cognitive psychopharmacology is that is
relies on the long term memory systems being distinct from each other. The
brain is a complex structure in which all systems interact, making it difficult
to measure a single system entirely.

 

Cognitive psychopharmacology uses drugs to advance our
understanding of metacognition. This term refers to ones knowledge about their
cognitive processes and how one monitors their own thought (Kuhn and Dean,
2004). Roy-Byrne et al, (1987) found that participants sensed impairment in a
recall task after taking benzodiazepines, suggesting some aspects of metacognition
are unimpaired.

 

However, it seems certain aspects of metacognition are
impaired and some still intact. Bacon et al (1998) asked benzodiazepine treated
participants to estimate if they thought they knew the answer to a question
when unable to recall it. It was found benzodiazepine participants were
significantly impaired at this metacognitive task. Therefore, suggesting drugs
can impact accurate judgement. These differing findings flag the need for
further research in the area.

 

More contemporary research by Kirkpatrick et al (2008) found
that when administering methamphetamine (which increases dopamine levels in the
brain), small amounts of the drug improved judgments of their sense of control.

To further support this Joensson et al (2015) found that when dopamine was
administered orally, metacognition and self-awareness was improved. These
results suggest cognitive psychopharmacology has improved our understanding of
metacognition.

 

In summary, across a broad range of attentional processes we
can see that the cholinergic pathways are involved in attentional processing
with Acetylcholine underpinning our ability to focus, divide and select our
attention. Furthermore, experimental studies on benzodiazepines illustrate the
validity of the idea that memory has distinct separate memory systems and that
metacognition is a neuropsychological function influenced by drugs.

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