Latent inhibition

Latent inhibition (LI) is a technical term in classical conditioning, where a familiar stimulus takes longer to
acquire meaning (as a signal or conditioned stimulus) than a new stimulus.[1] The term originated with
Lubow and Moore in 1973.[2] The LI effect is latent in that it is not exhibited in the stimulus pre-exposure
phase, but rather in the subsequent test phase. "Inhibition", here, simply connotes that the effect is expressed
in terms of relatively poor learning. The LI effect is extremely robust, appearing in both invertebrate (for
example, honey bees[3]) and mammalian species that have been tested and across many different learning
paradigms, thereby suggesting some adaptive advantages, such as protecting the organism from associating
irrelevant stimuli with other, more important, events.

Theories
The LI effect has received a number of theoretical interpretations. One class of theory holds that
inconsequential stimulus pre-exposure results in reduced associability for that stimulus. The loss of
associability has been attributed to a variety of mechanisms that reduce attention, which then must be
reacquired in order for learning to proceed normally.[4] Alternatively, it has been proposed that LI is a result
of retrieval failure rather than acquisition failure.[5] Such a position advocates that, following stimulus pre-
exposure, the acquisition of the new association to the old stimulus proceeds normally. However, in the test
stage, two associations (the stimulus-no consequence association from the pre-exposure stage and the
stimulus-consequence stimulus association of the acquisition stage) are retrieved and compete for
expression. The group not pre-exposed to the stimulus performs better than the pre-exposed group because
for the first group there is only the second association to be retrieved.

Variation
LI is affected by many factors, one of the most important of which is context. In virtually all LI studies, the
context remains the same in the stimulus pre-exposure and test phases. However, if context is changed from
the pre-exposure to the test phase, then LI is severely attenuated. The context-dependency of LI plays major
roles in all current theories of LI, and in particular to their applications to schizophrenia,[4] where it has been
proposed that relationship between the pre-exposed stimulus and the context breaks down; context no
longer sets the occasion for the expression of the stimulus-no consequence association. Consequently,
working-memory is inundated with experimentally familiar but phenomenally novel stimuli, each
competing for the limited resources required for efficient information processing. This description fits well
with the positive symptoms of schizophrenia, particularly high distractibility, and with research findings.

Physiology
The assumption that the attentional process that produces LI in normal subjects is dysfunctional in people
with schizophrenia has stimulated considerable research, with humans, as well as with rats and mice. There
is much data that indicate that dopamine agonists and antagonists modulate LI in rats and in normal humans.
Dopamine agonists, such as amphetamines, abolish LI whereas dopamine antagonists, such as haloperidol
and other anti-psychotic drugs, produce a super-LI effect.[6] In addition, manipulations of putative
dopamine pathways in the brain also have the expected effects on LI. Thus, hippocampal and septal lesions
interfere with the development of LI, as do lesions in selective portions of the nucleus accumbens.[7] With
human subjects, there is evidence that acute, non-medicated people with schizophrenia show reduced LI
compared to chronic, medicated schizophrenics and to healthy subjects, while there is no difference in the
amount of LI in the latter two groups. Finally, symptomatically normal subjects who score high on self-
report questionnaires that measure psychotic-proneness or schizotypality also exhibit reduced LI compared
to those who score low on the scales.[8]

In addition to LI illustrating a fundamental strategy for information processing and providing a useful tool
for examining attentional dysfunctions in pathological groups, the LI procedure has been used to screen for
drugs that can ameliorate schizophrenia symptoms of LI. LI has also been used to explain why certain
therapies, such as alcohol aversion treatments, are not as effective as might be expected. However, LI
procedures may be useful in counteracting some of the undesirable side-effects that frequently accompany
radiation and chemo-therapies for cancer, for example food aversion. LI research also has suggested
techniques that may be efficacious in the prophylactic treatment of certain fears and phobias. Of popular
interest, several studies have attempted to relate LI to creativity.[9]

In summary, the basic LI phenomenon represents some output of a selective attention process that results in
learning to ignore irrelevant stimuli. It has become an important tool for understanding information
processing in general, as well as attentional dysfunctions in schizophrenia, and it has implications for a
variety of practical problems.

Pathology

Low latent inhibition

Most people are able to ignore the constant stream of incoming stimuli, but this capability is reduced in
those with low latent inhibition. Low latent inhibition seems to often correlate with distracted behaviors, and
may resemble hyper-activity, hypomania, or attention deficit hyperactivity disorder (ADHD) in early
decades of life.[10] This distractedness can manifest itself as general inattentiveness, a tendency to switch
subjects without warning in conversation, and other absentminded habits. Not all distractedness can be
explained by low latent inhibition, and not all people with low LI lack attentiveness. It does mean, however,
that the higher quantity of incoming information requires a mind capable of handling it. Most people with
autism are thought to have especially low levels of latent inhibition. Depending on their intelligence and
social skills, it can often lead to sensory overload.

More generally: those of above average intelligence are thought to be capable of processing this stream
effectively, enabling their creativity and increasing their awareness of their surroundings.[11] Those with
average and less than average intelligence are less able to cope, and as a result are more likely to suffer from
mental illness and sensory overload.[12] Correspondingly, it is hypothesized that a low level of latent
inhibition can cause psychosis, a high level of creative achievement,[13] or both, as a function of the
respective individual's intelligence.[14]
High levels of the neurotransmitter dopamine (or its agonists) in the ventral tegmental area of the brain have
been shown to decrease latent inhibition.[15] Certain dysfunctions of the neurotransmitters glutamate,
serotonin, and acetylcholine have also been implicated.[16]

See also
Genius
Highly sensitive person
Salience (neuroscience)

References
1. Bouton, M. E. (2007) Learning and Behavior Sunderland, MA: Sinauer
2. Lubow, R. E. (1973). Latent inhibition. Psychological bulletin, 79(6), 398.
3. Fernández V.M, Giurfa M., Devaud J.-M., Farina W.M. (2012) "Latent inhibition in an insect:
the role of aminergic signaling." Learn Mem, 19(12), 593–597.
4. Lubow & Weiner, 2010
5. "Data" (https://lowlatentinhibition.org/). www.lowlatentinhibition.org. Retrieved 2019-12-24.
6. Weiner & Arad, 2010
7. Weiner, 2010
8. Kumari & Ettinger, 2010; Lubow, 2005
9. Carson, 2010
10. Lehrer, Jonah (14 September 2010). "Are Distractible People More Creative?" (https://www.
wired.com/wiredscience/2010/09/are-distractible-people-more-creative/). Wired.
11. Chirila, CR; Feldman, AN (2011). "Study of latent inhibition at high-level creative personality
The link between creativity and psychopathology" (https://doi.org/10.1016%2Fj.sbspro.2012.
01.142). Procedia - Social and Behavioral Sciences. 33 (1): 353–357.
doi:10.1016/j.sbspro.2012.01.142 (https://doi.org/10.1016%2Fj.sbspro.2012.01.142).
12. Lubow RE, Gewirtz JC (1995). "Latent inhibition in humans: data, theory, and implications for
schizophrenia". Psychological Bulletin. 117 (1): 87–103. doi:10.1037/0033-2909.117.1.87 (ht
tps://doi.org/10.1037%2F0033-2909.117.1.87). PMID 7870865 (https://pubmed.ncbi.nlm.nih.
gov/7870865).
13. Decreased Latent Inhibition Is Associated With Increased Creative Achievement in High-
Functioning Individuals (http://www.nidsci.org/pdf/carson-peterson-higgins.pdf);Archive link
(https://web.archive.org/web/20071129121745/http://www.nidsci.org/pdf/carson-peterson-hig
gins.pdf)
14. "Creative people more open to stimuli from environment" (https://web.archive.org/web/20120
601115849/http://talentdevelop.com/articles/CPMOTSFE.html). Talentdevelop.com. Archived
from the original (http://talentdevelop.com/articles/CPMOTSFE.html) on 2012-06-01.
Retrieved 2013-07-07.
15. Swerdlow NR, Stephany N, Wasserman LC, Talledo J, Sharp R, Auerbach PP (2003).
"Dopamine agonists disrupt visual latent inhibition in normal males using a within-subject
paradigm". Psychopharmacology. 169 (3–4): 314–20. doi:10.1007/s00213-002-1325-6 (http
s://doi.org/10.1007%2Fs00213-002-1325-6). PMID 12610717 (https://pubmed.ncbi.nlm.nih.g
ov/12610717). S2CID 18485036 (https://api.semanticscholar.org/CorpusID:18485036).
16. Bills C, Schachtman T, Serfozo P, Spooren W, Gasparini F, Simonyi A (2005). "Effects of
metabotropic glutamate receptor 5 on latent inhibition in conditioned taste aversion".
Behavioural Brain Research. 157 (1): 71–8. doi:10.1016/j.bbr.2004.06.011 (https://doi.org/10.
1016%2Fj.bbr.2004.06.011). PMID 15617773 (https://pubmed.ncbi.nlm.nih.gov/15617773).
S2CID 30377004 (https://api.semanticscholar.org/CorpusID:30377004).

Sources
Carson, S. (2010). Latent inhibition and creativity. In R.E. Lubow & I. Weiner (Eds.). Latent
inhibition: Data, theories, and applications to schizophrenia. New York: Cambridge
University Press.
Carson SH, Peterson JB, Higgins DM. Decreased latent inhibition is associated with
increased creative achievement in high-functioning individuals. J Pers Soc Psychol. 2003
Sep;85(3):499-506.
Escobar, M., Oberling, P., & Miller, R.R. (2002). Associative deficit accounts of disrupted
latent inhibition and blocking in schizophrenia. Neuroscience and Biobehavioral Reviews,
26, 203-216.
Kumari, V., & Ettinger, U. (2010). Latent inhibition in schizophrenia and schizotypy: A review
of the empirical literature. In R.E. Lubow & I. Weiner (Eds.) Latent inhibition: Data, theories,
and applications to schizophrenia. New York: Cambridge University Press.
Lubow R.E. (2005). "Construct validity of the animal latent inhibition model of selective
attention deficits in schizophrenia" (https://doi.org/10.1093%2Fschbul%2Fsbi005).
Schizophrenia Bulletin. 31 (1): 139–153. doi:10.1093/schbul/sbi005 (https://doi.org/10.109
3%2Fschbul%2Fsbi005). PMID 15888432 (https://pubmed.ncbi.nlm.nih.gov/15888432).
Lubow, R.E., & Moore, A.U. (1959). Latent inhibition: The effect of non-reinforced
preexposure to the conditioned stimulus. Journal of Comparative and Physiological
Psychology, 52, 415-419.
Lubow, R.E., & Weiner, I. (Eds.) (2010). Latent inhibition: Data, theories, and applications to
schizophrenia. New York: Cambridge University Press.
Weiner, I. (2010). What the brain teaches us about latent inhibition (LI): The neural substrates
of the expression and prevention of LI. In R.E. Lubow & I. Weiner (Eds.) Latent inhibition:
Data, theories, and applications to schizophrenia. New York: Cambridge University Press.
Weiner, I., & Arad (2010). The pharmacology of latent inhibition and its relationship to
schizophrenia. . In R.E. Lubow & I. Weiner (Eds.) Latent inhibition: Data, theories, and
applications to schizophrenia. New York: Cambridge University Press.
WHO - World Health Organization.

External links
Creativity (http://www.news.harvard.edu/gazette/2003/10.23/01-creativity.html)

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