State Dependence of Memory. Fig. 5. The shaping of mood states in ontogenesis. Though multiple states can exist, it is sufficient to assume here that memory operates in one of just two cyclically recurrent states (A or B) that are induced by some biological rhythm and are mutually exclusive. Throughout ontogeny (horizontal dotted line), the individual experiences and memorizes life events that have an affective valence that is positive (+) or negative (—). There is no a priori relationship between a state on the one hand and the (valence of) the events that are encountered in a state on the other. In this manner is most likely established in both states A and B, a cumulative memory that retains both positive and negative items (panel I); the overall affective valence of memory is rather neutral in either state and does not greatly differ, or swing, between A and B. This outcome being most probable, panel I represents what because of this greatest likelihood is perceived as a normal individual. However, chance may have it that the events experienced in A or B happen to predominantly be negative or positive (panels II and III, respectively); thus is established in one state a memory that retains items of polarized valence and that differs from the alternative, normal-affect state. These outcomes are less likely and result in recurring episodes of monopolar, depressed or manic, mood. An even smaller chance may result in large-amplitude bipolar mood swings (panel IV) (Colpaert et al. 2000).

whether such failure to remember results from a time-dependent dissipation of the engram or from the non-restoration of the state that prevailed in ontogeny at the time that the memory was established. State dependence definitely does not require forgetting to account for profound retrieval deficits, and state changes constitute a mechanism whereby an engram can be erased; when in an initial state the subject has learned and remembers and when then an alternative state is instituted shortly after retrieval (i.e., at the time of re-encoding), it may be the case that the engram in question is no longer available in the initial state. Further, such a state change may establish, in the alternative state, a memory that is then false (► false memory).

A weakness of state-dependence research resides with a certain vagueness as to what defines a state. Awareness of state dependence historically arose from observations of humans who were "under the influence'' of exogenous agents, and the use of drugs in studying state dependence has allowed that in this case states can at least operationally be defined in a highly precise, accurate, and reproducible manner. However, states also arise en-dogenously and current neurobiology and medicine invoke the existence of a varied array of states that operate at levels of integration ranging from the whole organism to cell assemblies, single cells, or molecular signal transduc-tion (Lydic and Baghdoyan 1999). Fascinating examples include hormone-controlled phases, pacemaker assemblies and circadian and seasonal rhythms, as well as the rise and fall of entire neurotransmitter and other signaling systems in the course of ontogeny. Such states are usually investigated with regard to the particular stimulus-response relationships that they demonstrate, but a wide realm of knowledge remains to be gained in terms of whether and how those states regulate memory.

Learning and memory are also investigated from such perspectives as context-dependence and coincidence detection; how these perspectives shed light on and interlock with state dependence remains to be explored.


I thank Drs. V. Curran, I. Kiss, A. Newman-Tancredi, and A. Young for comments and discussions. This essay is dedicated to the memory of Dr. Liesbeth Bruins Slot.


► Addictive Disorder: Animal Models

► Analgesics

► Animal Models of Psychiatric States

► Antidepressants

► Behavioral Tolerance

► Benzodiazepine Agonists

► Benzodiazepines

► Bipolar Disorder

► Declarative and Non-Declarative Memory

► Dementias and Other Amnestic Disorders

► Dissociative Anesthetics

► Drug Discrimination

► Dysthymic Mood Disorder

► Emotion and Mood

► Generalized Anxiety Disorder

► Inhibition of Memory

► Mood Stabilizers

► Opioid Dependence and Its Treatment

► Reference Memory and Consolidation


Blaney PH (1986) Affect and memory: a review. Psychol Bull 99: 229-246 Bower GH (1981) Mood and memory. Am Psychol 36:129-148 Bruins Slot LA, Colpaert FC (1999) Opiate states of memory: receptor mechanisms. J Neurosci 19:10520-10529 Colpaert FC (1990) A mnesic trace locked into the benzodiazepine state of memory. Psychopharmacology 102:28-36 Colpaert FC, Bruins Slot LA, Koek W, Dupuis DS (2000) Memory of an operant response and of depressed mood retained in activation states of 5-HT1A receptors: evidence from rodent models. Behav Brain Res 117:41-51 Colpaert FC, Koek W, Bruins Slot LA (2001) Evidence that mnesic states govern normal and disordered memory. Behav Pharmacol 12:575-589 Colpaert FC, Deseure K, Stinus L, Adriaensen H (2006) High-efficacy 5-HT1A receptor activation counteracts opioid hyperallodynia and affective conditioning. J Pharmacol Exp Ther 316:892-899 Eich E (2007) Mood and memory at 26. In: Lesgold A (ed) Memory and mind. CRC Press, London, pp 1-7 Girden E, Culler EA (1937) Conditioned responses in curarized striate muscle in dogs. J Comp Psychol 23:261-274 Lydic R, Baghdoyan HA (1999) Handbook of behavioral state control.

CRC Press, Boca Raton, p 700 Overton D (1983) State dependent learning and drug discrimination. In: Iversen LL, Iversen SD, Snyder SH (eds) Handbook of psychophar-macolgy, vol 18. Plenum Press, New York, pp 59-127 Siegel S (1985) Psychopharmacology and the Mystery of the Moonstone. Am Psychol 40:580-581

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