Motivation and emotion/Book/2025/Vasopressin and motivation

Scenario On a crowded platform, someone shoving toward his partner shifts Luke from watchful to protective as a surge of vasopressin narrows attention and primes action. That night, sleep-deprived, the same vasopressin circuitry sustains patient, repetitive caregiving while he settles their newborn. Same peptide, different context - biasing social motivation toward defence and motivated care.

A surge in vasopressin can push social motivation in different directions - toward swift defence in threatening contexts and toward ongoing, patient effort in caregiving. This chapter explains how vasopressin (AVP) tunes motivational strength by linking social-behaviour networks with reward and stress systems, and why its effects differ by context, sex, and task demands (see Figure 2 for AVP production in hypothalamus, posterior pituitary release, vascular and renal effects, and social behaviours). Recent research on vasopressin's role in motivation and social behaviour include:

• How the lateral septum integrates vasopressin with reward circuits to bias approach/avoidance and drug-reward sensitivity (Chen et al., 2024).
• How vasopressin and oxytocin circuits shape social motivation across contexts, with clear sex differences and translational implications (Rigney, de Vries, Petrulis, & Young, 2022).
• How suprachiasmatic nucleus vasopressin neurons set the brain’s circadian rhythm, gating arousal/effort and motivational readiness across the day (Tsuno et al., 2023).

What this chapter shows:

• How AVP’s brain patterns and internal-state signals (e.g., stress) set the daily 'tone' of arousal and effort, shaping when we are most motivated to act.
• Explain where V1a and V1b receptors sit in social and reward circuitry, and how this placement lets AVP bias approach vs avoidance, cooperation vs competition, and persistence in goal pursuit.
• Distinguish context-dependent effects - why the same peptide can amplify caregiving and bonding in safe situations yet mobilise defensive/aggressive motivation under threat.
• Connect effects to human contexts, highlighting evidence strength, key limitations (methods, variability, mixed findings), and clinical implications.

Arginine vasopressin ('vasopressin') shapes motivation because of where it is produced, which receptors it engages, and how it is released. Together these features determine whether behaviour leans toward social salience and approach, effort mobilisation under stress, or persistence over time (Young & Wang, 2004; Dumais & Veenema, 2016).

Magnocellular neurons in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) provide endocrine vasopressin and modulate nearby hypothalamic networks. Parvocellular PVN neurons project to brain targets and to the median eminence (coupling to stress control). The SCN produces vasopressin that mounts circadian timing, and steroid-sensitive vasopressin cells in the bed nucleus of the stria terminalis (BNST) and medial amygdala position vasopressin to influence social, circadian, and stress circuits that bias approach versus avoidance choices (Young & Wang, 2004; Dumais & Veenema, 2016).

Table 1 Vasopressin receptors and motivational roles

The V1a receptor (V1a) is widespread in forebrain nodes involved in social value and reward (e.g., lateral septum, amygdala, ventral pallidum) and accounts for most central approach-related effects. The V1b receptor (V1bR) sits on pituitary corticotrophs and in select limbic sites (notably CA2), linking vasopressin to stress energisation and social memory. V2 is largely peripheral. Cross-talk with the oxytocin receptor provides another route by which social value can be modulated (Young & Wang, 2004; Tanoue et al., 2004; Dumais & Veenema, 2016).

In addition to fast axonal release, PVN/SON neurons exhibit somatodendritic (volume) release that diffuses locally and can sustain shifts in arousal or task persistence for minutes to hours - a useful mechanism for maintaining motivated states after salient events (Ludwig & Leng, 2006).

SCN vasopressin helps set the brain’s daily rhythm and gates when stress and effort systems are most responsive, explaining time-of-day variation in motivational readiness (Tsuno et al., 2023).

PVN neurons co-release corticotropin-releasing hormone and vasopressin. Vasopressin acting at pituitary V1b increases adrenocorticotropic hormone (ACTH) and the glucocorticoid surge. Knockout and antagonist studies show blunted ACTH when V1b is removed or blocked, indicating that vasopressin is a co-driver of the hypothalamic-pituitary-adrenal (HPA) axis and thus of effort mobilisation (Tanoue et al., 2004).

The lateral septum (LS) is an integration hub; it receives dense BNST/MeA vasopressin input and connects to ventral tegmental area / nucleus accumbens dopamine pathways. Vasopressin arriving in LS can tilt dopaminergic computations toward approach (affiliation, caregiving) or vigilance (competition, defence) depending on context (De Vries & Buijs, 1983; Caffé, Van Leeuwen, & Luiten, 1987; Dumais & Veenema, 2016). Experiments show that increasing V1a expression in ventral forebrain induces partner preference in voles, demonstrating that vasopressin can directly tag a partner as rewarding (Lim et al., 2004; Young & Wang, 2004). Conversely, septal vasopressin reduces amphetamine conditioned place preference and lowers accumbens dopamine, indicating a shift away from non-social rewards toward adaptive social goals (Gárate-Pérez et al., 2021).

Mechanistically, vasopressin coordinates three signals: (i) social value via V1a in LS/ventral forebrain, (i) stress-energy via V1b in the pituitary (and CA2 linked to social memory), and (iii) timing/persistence via SCN rhythms and dendritic release. The general effect is a context-based tuning of motivational strength and direction (Dumais & Veenema, 2016; Tsuno et al., 2023; Tanoue et al., 2004; Young & Wang, 2004).

Much of the evidence for vasopressin’s motivational roles comes from rodents and voles, where species‐specific septal-amygdala-hippocampal circuitry and receptor distributions may not map neatly onto humans (de Vries & Buijs, 1983; Caffé et al., 1987; Caldwell & Albers, 2016; Dumais & Veenema, 2016). Knockout and viral overexpression studies demonstrate powerful effects on social memory and partner preference (Bielsky et al., 2004; Hitti & Siegelbaum, 2014; Lim et al., 2004), but these manipulations can exaggerate pathway influence relative to typical physiology. Moreover, vasopressin’s somatodendritic release and volume transmission complicate simple links between peripheral levels and central action (Ludwig & Leng, 2006). The lateral septum itself contains heterogeneous subcircuits with distinct reward roles, so AVP effects are likely subregion and task specific (Chen et al., 2024).

Human findings are mixed and often small; intranasal AVP modulates social communication in a sex-specific, context-dependent manner (Thompson et al., 2006), and AVPR1A diversity associate with pair-bonding but with modest effects (Walum et al., 2008). Motivational changes attributed to AVP may also reflect stress-system arousal, given V1bR’s central role in HPA activation (Tanoue et al., 2004). Finally, AVP neurons in the SCN set the pace for circadian dynamics (Tsuno et al., 2023), implying time-of-day as an under controlled moderator; reward-related findings such as decreased amphetamine CPP with septal AVP may therefore vary with state and context (Gárate-Pérez et al., 2019; Chen et al., 2024; Young & Wang, 2004; Rigney et al., 2022).

In everyday social settings, central vasopressin shifts what feels significant and how much effort is worth investing. In safe, cooperative contexts, signalling at V1a receptors in the lateral septum and ventral forebrain raises the perceived value of partners and caregiving, biasing behaviour toward approach. Under threat or competition, stress-linked signalling via V1b receptors and heightened V1a activity in limbic circuits direct behaviour toward vigilance, caution, and defensive action. These effects are sex-sensitive because vasopressin pathways are regulated by steroid hormones. (Rigney et al., 2022; Dumais & Veenema, 2016; Young & Wang, 2004).

Rodent studies show that increasing V1a receptor expression in the ventral pallidum and lateral septum is sufficient to induce partner preference in a normally non-monogamous vole - direct evidence that vasopressin can make a social partner rewarding and sustain cooperative effort (Lim et al., 2004; Young & Wang, 2004). In familiar, low-threat situations, projections from the bed nucleus of the stria terminalis and medial amygdala to the lateral septum, together with V1b-rich CA2 contributions to social memory, heighten social strength and persistence in caregiving tasks (Young & Wang, 2004; Rigney et al., 2022).

When danger or rivalry is prominent, vasopressin released from the paraventricular nucleus amplifies the hypothalamic-pituitary-adrenal axis via V1b receptors, while V1a signalling in septal and amygdala-connected pathways increases vigilance and anxiety. Depending on species, sex, and situation, signalling across the lateral septum and extended-amygdala can either facilitate or inhibit aggression - evidence that effects are conditional rather than uniformly pro or anti-social. Functionally, motivational resources shift away from affiliation toward defence or competition when threat is high (Dumais & Veenema, 2016; Rigney et al., 2022; Tanoue et al., 2004).

The platform (rapid protective action) and newborn-care (patient, repetitive effort) example illustrates how the same peptide can pull motivation in different directions. Vasopressin signalling in gates when these tendencies are strongest, helping explain why similar challenges may draw different responses in the morning versus evening (Tsuno et al., 2023). In summary, safe or familiar contexts primarily engages social-value signalling, while threatening contexts engage stress-energy activation; the balance between these - shaped by sex and hormonal state - determines how vasopressin biases motivation; toward approach-oriented caregiving or toward defensive action, and how strongly that motivation is expressed (Young & Wang, 2004; Rigney et al., 2022; Dumais & Veenema, 2016).

The motivational impact of vasopressin depends on who the person is (sex, genotype), their current state (stress load, hormones, circadian phase), and how effects are measured. Understanding these moderators clarifies when vasopressin amplifies cooperative persistence versus defensive mobilisation and guides human application (Caldwell & Albers, 2016; Dumais & Veenema, 2016; Tsuno et al., 2023; Rigney, de Vries, Petrulis, & Young, 2022).

Males typically show greater vasopressin expression in nucleus and medial-amygdala pathways and larger behavioural effects of the V1a and V1b receptors; (reducing septal V1a is anxiolytic mainly in males in rodent work. In humans, vasopressin alters social communication in a sex-specific manner - often stronger in men - consistent with steroid-sensitivity (Dumais & Veenema, 2016; Rigney et al., 2022; Thompson, George, Walton, Orr, & Benson, 2006). Individual differences also matter: V1a variants are associated with pair-bonding and relationship quality in men, suggesting natural variation in V1a signalling maps onto differences in social motivational style (Walum et al., 2008). High stress engages V1b-mediated HPA strengthening, biasing behaviour toward vigilance/defence; in low stress/safe contexts, V1a-rich circuits favour cooperation and persistence. Vasopressin signalling in the SCN sets time-of-day responsiveness, so the same task can evoke different motivation in the morning versus evening. Since vasopressin in blood doesn’t reflect brain release well - and lab tests plus small samples add noise - stronger conclusions come from tasks matched to each receptor pathway: V1a for cooperation/recognition in the lateral septum/ventral forebrain, and V1b for stress-effort in the pituitary/CA2 (Caldwell & Albers, 2016; Dumais & Veenema, 2016; Tsuno et al., 2023; Rigney et al., 2022; Tanoue et al., 2004).

Three variables currently show the most reliable signals: (1) sex-specific behavioural effects of intranasal vasopressin in controlled social tasks; (ii) genetic associations between V1a variants and pair-bonding in men; and (iii) review evidence that V1b antagonists can reduce stress-related negative affect and alcohol use, though clinical effects remain mixed/modest (Caldwell & Albers, 2016; Thompson et al., 2006; Walum et al., 2008). In practice, expect larger effects in males and when context matches circuit (V1a to affiliation/recognition and V1b to stress-effort). To boost cooperativity, design safe, collaborative settings and reduce threat cues that would recruit V1b/HPA. V1b antagonists are a plausible option for stress-strengthened motivation problems, but they should be studied or used with designs split by sex and state and paired with behavioural strategies (Caldwell & Albers, 2016; Tsuno et al., 2023; Rigney et al., 2022; Tanoue et al., 2004).

Vasopressin influences motivation by coordinating three interacting routes: (i) social-value signalling through V1a receptors in lateral septum/ventral-forebrain circuits, which raises the reward value of partners and caregiving; (ii) stress - energy mobilisation via V1b receptors and the hypothalamic-pituitary-adrenal axis, which prepares rapid defensive action; (iii) timing and persistence set by suprachiasmatic-nucleus output and somatodendritic peptide release, which sustain motivated states.

Which route dominates depends on context (safety vs. threat), biological sex and hormones, current stress and circadian phase, and individual differences. In practice, vasopressin pulls motivation toward approach and bonding in safe settings but toward vigilance and defence when threat is salient. Human findings mirror this pattern - showing sex-specific effects of intranasal vasopressin and genetic links to pair-bonding - and point to cautious, circuit-matched applications.

• Engage prosocial (V1a) routes: Structure tasks to feel safe, familiar, and cooperative (clear goals, shared rewards, supportive tone). This raises the perceived value of partners/caregiving and biases approach behaviour. (Lim et al., 2004; Young & Wang, 2004; Rigney et al., 2022)
• Buffer acute stress before social work: Use brief de-stressers (predictable routines, breaks, slow breathing) and de-escalate conflict first. This limits V1b-HPA drive that otherwise pushes vigilance/defence. (Tanoue et al., 2004; Dumais & Veenema, 2016)
• Time it right: Schedule bonding/care or effortful tasks during the person’s alert circadian window and avoid sleep-deprived late hours when possible. (Tsuno et al., 2023)
• Tailor to person and state: Expect larger effects in males; consider hormonal status and current stress; note that V1a the variation can map onto differences in social motivational style. (Dumais & Veenema, 2016; Walum et al., 2008)
• Match measures to mechanisms: For evaluation or research, use affiliation/recognition tasks when testing V1a effects and stress-effort paradigms for V1b; avoid inferring brain AVP from blood; use adequate samples and preregistration. (Caldwell & Albers, 2016; Dumais & Veenema, 2016)
• Pharmacology: V1b antagonists may help stress-amplified problems or alcohol use, but effects are modest; combine with behavioural strategies and stratify by sex/state. (Caldwell & Albers, 2016; Rigney et al., 2022)

• Vasopressin (Wikipedia)
• Vasopressin and motivation (Book chapter, 2024)

• Offspring: Human Fertility Behavior in Biodemographic Perspective (National Library of Medicine)
• Hormones affect our physiology and behavior (BrainFacts - Society for Neuroscience)
• Oxytocin and vasopressin: Secrets of love and fear (Adam Lane Smith - blog)
• How can you tell if you're in love? (Medical News Today)