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Review
. 2022 Dec 7;23(24):15467.
doi: 10.3390/ijms232415467.

Vasopressin as a Possible Link between Sleep-Disturbances and Memory Problems

Bibiána Török  1   2 , János Varga  2 , Dóra Zelena  1   2
Affiliations
Review

Vasopressin as a Possible Link between Sleep-Disturbances and Memory Problems

Bibiána Török et al. Int J Mol Sci. .

Abstract

Normal biological rhythms, including sleep, are very important for a healthy life and their disturbance may induce-among other issues-memory impairment, which is a key problem of many psychiatric pathologies. The major brain center of circadian regulation is the suprachiasmatic nucleus, and vasopressin (AVP), which is one of its main neurotransmitters, also plays a key role in memory formation. In this review paper, we aimed to summarize our knowledge on the vasopressinergic connection between sleep and memory with the help of the AVP-deficient Brattleboro rat strain. These animals have EEG disturbances with reduced sleep and impaired memory-boosting theta oscillation and show memory impairment in parallel. Based upon human and animal data measuring AVP levels, haplotypes, and the administration of AVP or its agonist or antagonist via different routes (subcutaneous, intraperitoneal, intracerebroventricular, or intranasal), V1a receptors (especially of hippocampal origin) were implicated in the sleep-memory interaction. All in all, the presented data confirm the possible connective role of AVP between biological rhythms and memory formation, thus, supporting the importance of AVP in several psychopathological conditions.

Keywords: Brattleboro rat; EEG; circadian rhythm; memory; novel object recognition; sleep; vasopressin.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 3
Figure 3
Sleep stages and involvement of vasopressin (AVP). S1: first stage of sleep, S2: second stage of sleep, S3: third stage of sleep; REM: radip eye movement; NREM: non-REM stage; icv: intracerebroventricular administration.
Figure 1
Figure 1
Vasopressin-related brain areas in the rodent brain. (A) Localization of the major V1a receptor-containing areas. (B) Magnocellular vasopressinergic cells. (C) Major parvocellular vasopressinergic cells. (D) Suprachiasmatic nucleus. Abbreviations: BNST—bed nucleus of stria terminalis, LS—lateral septum, MeA—medial amygdala, PVN—paraventricular hypothalami nucleus, SCN—suprachiasmatic nucleus, and SON—supraopticus nucleus [29].
Figure 2
Figure 2
Development of the Brattleboro rat strain. (A) Brattleboro rat strain was discovered in 1961 in Brattleboro, Vermont. It evolved from the Long–Evans rat strain through a random autosomal recessive mutation. (B) The genetic mutation of Brattleboro strain is a single nucleotide deletion of a G residue in the second exon of neurophysin gene. Due to this mutation, a reading frame shift develops, which results in different C-terminus for the precursor hormone. (C) Due to the lack of stop codon, the mRNA cannot leave the ribosomes after translation, and the incomplete protein-chain might also stall in the ribosome. Therefore, a ubiquitin ligase (LTN1), which is part of the ribosome-associated quality control complex, will induce proteolysis. All in all, vasopressin (AVP) is missing; thus, there is no physiologically active central AVP, leading to central diabetes insipidus with polydipsia and polyuria [41,42,43,44,45].
Figure 4
Figure 4
Vasopressinergic influence on theta oscillation and memory formation. Similar intervention induces similar changes in both highly connected measures. AVP—arginine vasopressin; ic—intracerebroventricular; KO—knockout; V1aR—vasopressin 1a type receptor.
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