Affiliative Behaviour Flashcards

(117 cards)

1
Q

Where are primal emotional systems located in the brain?

A

All primal systems are situated subcortically. They consist of large transverse networks interconnecting circuits concentrated in midbrain regions.

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2
Q

How do these primal emotional systems generate behaviour?

A

Each system has abundant descending and ascending components that work together to generate various emotional behaviours. Experientially defined neural circuits generate well-organised behaviour sequences that can be evoked by localized electrical stimulation of the brain or the alteration of key neuropeptides.

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3
Q

What are the seven emotional systems?

A

Seven emotional systems: SEEKING, RAGE (Anger), FEAR (Anxiety), LUST, CARE (Maternal Nurturance), PANIC (Separation Distress), and PLAY (Rough-and-Tumble, Physical Social-Engagement).

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4
Q

Which brain regions are considered more important for generating emotional feelings?

A

The lower regions of the brain are more important for generating emotional feelings than the higher regions.

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5
Q

Why are animal models useful for studying emotions according to the sources?

A

A diversity of brain networks for basic emotional instinctual behaviours, homologous across vertebrate species, are situated in ancient brain regions evolutionarily similar in all mammals. The basic neurochemistry for emotional feelings appears essentially the same in all mammals, hence there are many animal models to study emotions.

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6
Q

What was the primary focus of interest in Oxytocin (OT) until recently?

A

Until recently, interest in OT was largely confined to its role in female reproduction, specifically milk ejection during lactation and smooth muscle contraction during parturition.

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7
Q

What findings shifted the research focus on OT?

A

Research interest shifted with findings such as intracerebroventricular (icv) OT inducing maternal behaviour in female rats, OT association in mate attachment in prairie voles, and OT involvement in social recognition in mice.

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8
Q

Where is OT released from into the general circulation?

A

OT is released from the posterior pituitary into the general circulation, acting on target organs like the uterus and mammary glands.

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9
Q

Where is OT produced in the brain?

A

The PVN and SON (hypothalamic nuclei) produce OT.

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10
Q

How is OT transported from the hypothalamus to the posterior pituitary?

A

The PVN and SON project long axons to the posterior pituitary. OT (and vasopressin) is carried in proteins called neurophysins down the axons to the neurohypophysis (posterior pituitary). Axonal terminals, called Herring bodies, store the neurophysin-hormone complex and release hormones upon stimulation.

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11
Q

Does the anterior pituitary store OT?

A

Yes, parvocellular neurons in the PVN project via the median eminence to the anterior pituitary, which stores a ‘back-up’ supply of OT.

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12
Q

Besides neuroendocrine effects, what other role does OT have?

A

OT also behaves as a social neuropeptide affecting fear, trust, and other social behaviours.

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13
Q

How does social contact influence OT levels in the brain?

A

Social contact enhances OT levels in the brain, which sets the biological basis for the formation of social bonds.

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14
Q

What are the different modes of transmission for OT?

A

OT can mediate functions through different modes of transmission: Endocrine, Paracrine, and Synaptic.

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15
Q

Describe endocrine OT transmission.

A

OT is released into the bloodstream by the posterior pituitary, targeting various organs.

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16
Q

Describe paracrine OT transmission.

A

OT acts within the brain; OT receptors are found in the nucleus accumbens and parvocellular neurons.

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17
Q

Describe synaptic OT transmission.

A

Released from via parvocellular granules of OT, serotonin and glutamate neurons are affected.

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18
Q

How does OT interact with its receptor in the CNS?

A

OT interacts with its GPCR in the CNS, leading to intracellular activity via calcium signalling.

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19
Q

How similar are OT and Arginine Vasopressin (AVP) structurally?

A

OT and AVP are structurally similar, differing in only 2 of 9 amino acids.

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20
Q

What is the homology between OT and AVP receptors?

A

There is high homology (>85% within species) between OT and AVP receptors.

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21
Q

Where have OT receptors (OTR) been identified outside the brain?

A

OTR have also been identified in tissues including kidney, heart, thymus, pancreas, and adipocytes.

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22
Q

Does OT bind to AVP receptors?

A

Yes, OT also binds the V1a subtype receptor with good affinity, acting as a partial agonist, highlighting the similarity between OT and AVP.

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23
Q

Which receptor does AVP bind to with higher specificity?

A

When individually expressed in a cell line, AVP binding to the V1a receptor showed a 10-fold difference in Ki values compared to AVP binding to the OT receptor (low Ki = high specificity).

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24
Q

Which receptor does OT bind to with higher affinity?

A

The Ki values for OT binding to the OT receptor are 10-100 times smaller than those for OT binding to the V1a receptor. OT binds to the OT receptor with significantly higher affinity than to AVP receptors.

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25
Which receptor does AVP bind to with higher affinity?
AVP binds to the **V1a receptor** with higher affinity than to the OT receptor.
26
What triggers both central and peripheral OT release?
**Physiological stimuli** (birth, suckling, sex, stress) and **behavioural stimuli** (maternal, sexual, anxiety, social, recognition) trigger both central (from brain) and peripheral (from pituitary) OT release.
27
Can plasma OT levels indicate central OT activity?
No, various stressors can trigger OT release within hypothalamic and limbic regions, whereas neuropeptide secretion into blood may remain constant. Therefore, **plasma OT is not a marker of central OT activity**.
28
How does the effectiveness of peripherally administered OT compare to central administration for anxiolytic effects?
Substantially **larger doses** of OT were required for peripheral administration compared to central administration to achieve comparable behavioural effects. This suggests OT exerts its anxiolytic effects primarily through action on the CNS.
29
Can peripheral OT reach the brain?
Yes, studies suggest that **peripheral OT can penetrate the brain** and exert its behavioural effects centrally.
30
What are some essential physiological functions of AVP?
AVP is essential for a wide range of physiological functions, including **water reabsorption** (via aquaporins), **cardiovascular homeostasis, hormone secretion, and social behaviour**.
31
What are the receptor subtypes that mediate AVP actions?
AVP actions are mediated by receptor subtypes: **V1a, V1b, and V2**.
32
Where are V1a and V1b receptors found?
V1a receptors (V1aR) are found in **vascular smooth muscle**, and V1bR in the **anterior pituitary**.
33
How can AVP be administered to elevate CSF levels quickly?
**Intranasal AVP** elevates CSF AVP within 30 minutes. This route is routinely used for diabetes insipidus.
34
What are the proposed routes for direct passage of peptides from the nose to the brain?
Two routes are proposed: **intra-neuronal** (internalization into olfactory neurons, axonal transport) and **extra-neuronal** (diffusion through inter-cellular clefts in the olfactory epithelium). The extra-neuronal route is considered more plausible for direct passage.
35
What did studies using Brattleboro rats (AVP deficient) suggest about social recognition?
Brattleboro rats display a **deficiency in social recognition** that improved with AVP administration into the lateral septum/midbrain (LS).
36
Where is there a high density of V1aR in rats?
The **LS (lateral septum)** has a high density of V1aR.
37
What happened when the prairie vole V1aR gene was introduced into the LS of normal rats?
Introducing the prairie vole V1aR gene into the LS of normal rats **improved social recognition**, which was blocked by a selective V1aR antagonist.
38
What effect did a V1aR antagonist injection into the LS have on social recognition in normal mice?
Injection of a selective V1aR antagonist into the LS of normal mice **impaired social recognition**.
39
What effect did overexpression of V1aR in the LS have on social recognition in wild-type mice?
Overexpression of the V1aR in the LS of wild-type mice resulted in a **potentiation of social recognition behaviour**.
40
What social behaviour deficit was observed in V1aR-KO mice?
V1aR-KO mice display profound **impairment in social recognition**.
41
Could social recognition be restored in V1aR-KO mice?
Yes, re-expressing the V1aR in the LS of V1aR-KO mice using a viral vector resulted in a **complete restoration of social recognition capability**.
42
Was social recognition also affected in V1bR-KO mice?
Yes, V1bR-KO mice also showed a **mild deficit in social recognition**.
43
What behaviours do OT and AVP regulate?
OT and AVP regulate **anxiety, coping, and social behaviours**.
44
How are central and neurohypophysial release of OT and AVP related?
They can be released within the brain independently of, or coordinated with, neurohypophysial terminal secretion.
45
What are the typical effects of central OT on emotional behaviour?
Central OT typically has **anxiolytic (anxiety-reducing) and anti-depressive effects**.
46
What are the typical effects of central AVP on emotional behaviour?
Central AVP typically has **anxiogenic (anxiety-inducing) and depressive actions**.
47
What is required for balanced activity of OT and AVP?
With opposing effects on emotional behaviours, a **balanced activity** of both neuropeptides is required.
48
How might shifting the balance between OT and AVP activity impact emotional behaviours?
Shifting the balance towards OT's positive social stimuli may **improve emotional behaviours and reinstate mental health**.
49
What finding in the OTRKO mouse highlights the overlap between OT and AVP systems?
Studies showed that central injections of **either OT or AVP rescued the impaired social phenotypes in OTRKO mice**, questioning the role of strict OT/OTR interactions.
50
What receptor is implicated in the rescue effect observed in OTRKO mice with OT injection?
Co-administration of a **V1aR antagonist** along with OT in the OTRKO model prevents the rescue effects, implicating signalling via **V1aRs**.
51
Why is understanding the overlap between OT and AVP systems important for developing therapies?
The complicated pharmacology, especially **crosstalk between OT and AVP**, needs further exploration for developing specific pharmacological interventions for social impairments. Further exploration into the crosstalk that may occur in disease is necessary.
52
What prosocial behaviours has pharmacological manipulation of the OT system indicated OT promotes?
Pharmacological manipulation of the OT system has indicated that OT promotes several elements of **prosocial behaviour**, including parental behaviour and complex social interactions between adults.
53
What types of mice with genetically altered OT systems have been used to study the role of OT in social behaviour?
Three lines of mice have been evaluated: **OT KO mice, OT receptor KO mice (OTRKO), and CD38 KO mice** (CD38 regulates Ca2+-dependent OT secretion and is associated with autism).
54
Are OT KO mice viable and fertile? What is a major deficit?
OT KO mice are viable and fertile, but their pups die shortly after birth due to the dam's **inability to provide milk**. Postpartum injection of OT restores milk ejection and rescues offspring.
55
Are OTR KO mice viable and fertile? What are their deficits?
OTR KO mice are viable with no obvious defects in fertility or sexual behaviour. Dams show normal parturition but have **defects in lactation and maternal nurturing**.
56
Are CD38 KO mice viable and fertile? Do they have lactation deficits?
CD38 KO mice are viable, fertile, grow well, and gain weight from milk and solid food. CD38 is **not critically involved** in milk ejection.
57
What is essential for milk ejection in the OT/CD38/OTR signalling pathway?
**OT and OTR** are essential for milk ejection.
58
Are CD38 KO mice viable and fertile? Do they have lactation deficits?
CD38 KO mice are viable, fertile, grow well, and gain weight from milk and solid food. CD38 is not critically involved in milk ejection.
59
What is essential for milk ejection in the OT/CD38/OTR signalling pathway?
OT and OTR are essential for milk ejection.
60
What type of social cognition impairment has been identified in mice with altered OT signalling?
Impairments in social cognition, specifically social recognition, have been identified in all three models (OT KO, OTR KO, CD38 KO).
61
How do rodents primarily convey social information and recognize individuals?
Social information in rodents is primarily conveyed through olfactory cues. Rodents can differentiate between individuals based on smell and maintain that memory for up to 2 hours.
62
How is social recognition typically measured in rodents using olfactory cues?
Social recognition can be measured by a decrease in olfactory investigation of a familiar animal compared to a novel animal.
63
Which brain regions, when injected with OT, enhance social recognition in rats?
Injection of OT into the lateral septum, medial preoptic areas, and olfactory bulb of rats enhances social recognition.
64
Can the social recognition deficits in the KO mouse lines be rescued?
Yes, deficits in social recognition in all three KO lines (OT KO, OTR KO, CD38 KO) can be rescued by a single icv injection of OT given before initial social exposure.
65
Why was the efficacy of OT in restoring social recognition in the OTRKO line unexpected?
It was unexpected because they lack the primary receptor (OTR).
66
What finding in OTRKO mice further questions the role of strict OT/OTR interactions?
Central injections of either OT or AVP rescued the impaired social phenotypes in the OTRKO mice.
67
What happens when a V1aR antagonist is co-administered with OT in the OTRKO model?
Co-administration of a V1aR antagonist prevents the rescue effects, implicating signalling via V1aR’s.
68
Why is the prairie vole a notable animal model for studying social bonding?
The prairie vole is a notable model because partners form lifelong pair bonds and show high affiliative behaviour. Montane voles look similar but are asocial and polygynous.
69
Which neuropeptides are involved in pair bonding in the prairie vole?
OT and AVP are involved in pair bonding.
70
How do the brains of monogamous and non-monogamous vole species differ in terms of OT/AVP?
There are striking species differences in the distribution of OT and V1aR in the brains of monogamous versus non-monogamous vole species.
71
What effect did inserting the prairie vole V1aR gene into mice have on their behaviour when injected with vasopressin?
Mice transgenic for the prairie vole V1aR gene responded similarly to prairie voles by exhibiting increased affiliative behaviour when injected with vasopressin. Vasopressin injections did not alter social behaviour in non-transgenic mice.
72
What biological changes at the end of pregnancy prepare for maternal behaviour?
Massive hormonal changes (declining progesterone, increasing oestrogen, prolactin, and oxytocin) at the end of pregnancy set the stage for the activation of maternal urges like nesting.
73
What neurochemicals are crucial for mother-infant bonding?
Similar neurochemicals, especially OT and endogenous opioids, promote infant bonding to the mother. Hormonal and neurochemical changes facilitate maternal moods and promote social bonding with offspring.
74
Is parental behaviour innate in mammals? Why is it important?
Parental behaviour is innate in mammals and important for offspring survival.
75
What brain region is critically involved in parental behaviour in rodents?
In rodents, the medial preoptic area (MPOA) is critically involved in parental behaviour.
76
How does destruction or inactivation of the MPOA affect parental behaviour?
Destruction or inactivation of the MPOA disrupts the onset and establishment of parental behaviour.
77
How does pup exposure affect maternal behaviour and OT levels according to the Okabe et al. experiment?
Repeated pup exposure drives maternal behaviour and its reinforcement. Pup exposure induced a higher concentration of OT in the PVN, SON, and POA.
78
What happened when an OT antagonist (OTA) was injected before the initial pup exposure in the experiment?
Injecting OTA before the paradigm meant no maternal behaviour was instigated. Retrieval latencies increased significantly in the re-exposure session compared to initial exposure. Blocking OT was enough to prevent learning maternal behaviour and increasing that behaviour.
79
What happened when an OTA was injected after high pup exposure (training) but before re-exposure?
If mice were already trained (had established maternal behaviour), blocking OT action did not prevent that behaviour from playing out upon re-exposure. There was little to no effect between the saline and OTA groups.
80
What is required for forming social bonds?
Forming social bonds requires individuals to be in close proximity.
81
What two models have focused on studying social bonds?
Models have focused on the mother-infant bond and social monogamy.
82
How can the strength of a social relationship be tested?
The strength of the relationship can be tested through separation.
83
What is a key difference in the balance of behavioural repertoires between mother-infant bonds and reproductive partner selection?
In the mother-infant bond, there's an imbalance as the infant has limited ability to move. In reproductive partner selection, there is a balance between the behavioural repertoires of the two adults.
84
What human conditions and behaviours have human studies examined in relation to OT?
Human studies have examined OT in relation to: Trust, Autism, Postnatal depression, Post traumatic stress disorder/Stress/Anxiety. Fewer studies have examined OT and social affiliation in humans.
85
What was the design and key finding of the Kosfeld et al. (2005) trust game study?
Male volunteers received intranasal OT or placebo and played a 'trust game' where they invested money. Intranasal OT significantly increased trust among participants compared to placebo.
86
What was the design and key finding of the Mikolajczak M et al. (2010) non-monetary trust study?
Participants received OT or placebo and had the option to seal a survey on sexual habits. The study indicated OT increased trust, as 60% of the OT group left the envelope open compared to only 3% of controls.
87
What happened in later replication studies of OT and trust?
Later studies by Lane A. et al (2015) failed to reproduce their earlier findings. The non-significant results clearly exclude a large effect of OT on trust.
88
What behaviours associated with autism is OT involved in?
OT is involved in grooming and stereotyped behaviours associated with autism.
89
How is CD38 related to OT and autism?
CD38 KO decreases OT. Low OT has been found in autistic children.
90
How are OT levels affected in carriers of the R140W mutation?
OT levels in carriers of the R140W mutation were lower than in relatives of non-carriers.
91
What effect did administering OT to adults with autism spectrum disorders have?
Administration of OT resulted in a significant reduction in repetitive behaviours.
92
What triggered the potential for neuropeptide therapy for disorders of social functioning?
The marked effects of intranasal OT on improving social and emotional functioning in healthy individuals and some key features in high-risk populations triggered this potential.
93
For what conditions has OT therapy been suggested and studied?
OT therapy has been suggested and studied for conditions like autism spectrum disorders (ASD), depression, schizophrenia, and social anxiety.
94
How are OT and attachment-related social behaviours related throughout life?
Reciprocal relations between OT and attachment-related social behaviours begin in the neonatal period with parents and continue through life stages.
95
How does parental touch influence OT levels?
OT levels increase with high levels of parental touch.
96
How is minimal affectionate touch related to postpartum depression and premature birth?
Postpartum depression (~18%) is associated with mothers showing minimal affectionate touch. Following premature birth (~12%), maternal touch is similarly reduced. This suggests diminished maternal contact may mediate the low levels of OT in their children.
97
What interventions might help trigger the OT system in depressed mothers or after premature birth?
Interventions educating mothers on the importance of tactile contact and teaching optimal touch techniques may help.
98
Why might fathers' touch be important?
Due to the mutual effects of maternal and paternal OT on each other and on the child, fathers' touch may also be important, especially in cases of maternal postpartum depression and premature birth.
99
How might OT therapy be used in conjunction with behavioural interventions for relationship distress?
The dramatic increase in OT during the initial stages of romantic attachment may suggest that OT therapy can be used with behavioural-relational intervention for distress.
100
Can OT administration to a parent affect the infant?
Yes, OT administration to a parent (father in the study) can lead to alterations in the physiology and behaviour of the infant that induce greater readiness for social contact. Infant salivary OT showed a dramatic rise.
101
How might OT potentially treat young children at high risk for social difficulties?
OT could potentially treat young children at high risk for social difficulties via a parental/caregiver route.
102
What types of experiences constitute Early Life Adversity (ELA)?
ELA includes experiences such as physical or sexual abuse, neglect, or poor socioeconomic conditions.
103
What long-lasting consequences are associated with ELA?
ELA is associated with increased risk for anxiety and depression later in life. Early experiences can lead to lasting consequences on autonomic, neuroendocrine, and neural function.
104
How are plasma and CSF OT levels related to depression, anxiety, and ELA history?
In humans, depression and anxiety are associated with dysregulated plasma OT. Individuals with a history of ELA had lower CSF OT levels and exhibited altered responses to intranasal OT.
105
How did children raised in an orphanage compare to children raised by biological parents in terms of OT production?
Children raised in an orphanage had lower OT production during mother-infant interactions compared to children raised by biological parents.
106
What molecular mechanism is proposed to link ELA to increased risk for mental disorders?
DNA methylation of key neuroregulatory genes is proposed as an underlying molecular mechanism.
107
Why are promoter regions common targets for DNA methylation?
Promoter regions are targets for methylation because they are enriched in both CpG dinucleotides and binding sites for transcriptional activators and repressors.
108
How can methylation in promoter regions affect gene expression?
Methylation in promoter regions can reduce interactions between DNA and transcription factors and inhibit downstream gene expression.
109
Is there an association between OTR methylation and childhood anxiousness?
Yes, there are associations between OTR methylation and childhood anxiousness. Higher childhood anxiousness is associated with greater methylation of promoter CpG 7.
110
What did in vitro experiments confirm regarding OTR promoter methylation and gene expression?
In vitro experiments confirmed that greater methylation within the promoter region resulted in lower gene expression at the OXTR promoter.
111
Was the association between OXTR DNA methylation and ELA different between sexes?
Yes, the association between OXTR DNA methylation and ELA was stronger among females than among males.
112
What might the sex difference in OXTR methylation sensitivity suggest?
This suggests that women's greater sensitivity to ELA's impact on OXTR methylation may underlie some sex differences in anxiety and depression later in life.
113
Have differences in DNA methylation been observed in patients with autism?
Yes, higher DNA methylation of CpG islands has been observed in patients with autism compared to healthy controls, in both blood DNA and brain tissue DNA.
114
What other conditions or traits have been associated with methylation at other CpG sites within OXTR?
Studies investigating other CpG sites within OXTR have found significant associations with social anxiety, depressive disorders, pessimism, and interpersonal distrust.
115
How was poorer maternal care associated with OXTR methylation?
Poorer maternal care in childhood was associated with greater OXTR methylation within exon 3 in peripheral blood cells.
116
What new opportunities are offered by advances in understanding and manipulating social cues and OT?
Advances now offer ways to supplement ‘learning to love’ when normal social cues are lost, missing, or reduced.
117
How should advances in translational OT research be integrated?
Advances in translational OT research need to be integrated with parental advice.