Parental Behaviour Flashcards
Parental behaviour is impacted by a variety of hormones (6)
oxytocin
prolactin
testo
arginine vasopressin
progest
oestrogen
Prolactin receptor signalling (2)
Tyrosine kinase receptor:
- Jak-STAT5 mediated signalling
–“long” (coupling via Jak-STAT)
–“short” forms reported
impacts cellular function via:
-Transcriptional changes
- Changes in electrical signalling
–Transient receptor potential (TRP channels; non-selective cation channels)
–BK-type K+ channels
–L-type Ca2+ channels
Prolactin receptors are found at a variety of CNS sites (6)
brain, pancreas, kidneys, intestines (duodenum)
CSF levels of PRL typically mirror circulating levels
PRL enters the brain via circumventricular sites
Potential evidence for prolactin-receptor-mediated transport into the brain.
Sexual dimorphism between male and female rodents in brain PRL-R expression (females shown in figure).
Prolactin receptors also bind placental lactogen – a peptide release from the placenta.
TIDA neurons regulate prolactin release from lactrophs (3)
TIDA = tuberoinfundibular dopamine neurons
- in ARC projecting to ME
- DA released at ME travels in portal circulation to inhibit PRL release from AP lactotrophs via D2r
- PRL acts back in brain to inhibit its own release by increasing DA:
–PRL-R mediated ion channel opening (short-loop negative feedback)
–PRL-R mediated pSTAT5 and pERK increase TH gene expression and phosphorylation respectively to increase DA
prolactin release factors (3)
increase:
-suckling (reflex)
-stress
-other PRL releasing factor?
Decrease:
-dopamine
-sex
indirect hormonal modulators:
-oestrogen
-testosterone
-TRH
-Oxytocin
-Vasopressin
Different PRL levels during reproductive process (3)
- circulating PRL = typically low
when PRL is consistently elevated:
- preovul LH surge
- before or around birth
-by suckling (acute increases)
rodents show phasic PRL in early preg
How does PRL suppress fertility through modulation of HPG axis? (4)
GnRH neurons do not express PRL-R but kisspeptin neurons do
Acute elevations in PRL transiently inhibit kisspeptin neurons = transient suppression of LH pulsatile activity
Kisspeptin release and gene expression are not impacted
Chronic elevations in PRL eg during lactation or disease = supresses fertility by supressing kisspeptin gene/protein expression leading to loss of GnRH secretion
Lactation-induced changes in TIDA neuron phenotype maintain prolactin levels (4)
Non-lactating (negative feedback loop):
-PRL stimulates dopamine (DA) release from TIDA neurons
-DA enters the portal circulation via the median eminence, inhibiting prolactin release from pituitary lactotrophs
Pregnancy/Lactation (positive feedback loop):
-Chronic exposure to PRL r agonist placental lactogen during pregnancy promotes met-enkephalin (ENK) production from a subset of TIDA neurons
-Suckling induces ENK release = inhibits DA production from TIDA neurons. ENK also acts directly on pituitary lactotrophs. Both actions promote PRL release.
Prolactin mediates physiological adaptations during pregnancy (4)
PRL receptors are expressed in a variety of peripheral tissues.
PRL is also produced in some of these tissues and can have autocrine actions.
Increased PRL during pregnancy may help the body adapt to the changing physiological demands.
Effects may also be mediated by placental lactogen (prolactin receptor agonist).
Prolactin regulation of metabolic state during pregnancy? (3)
Pregnancy and lactation change the balance between NPY/AgRP and POMC levels in the hypothalamus.
Changes in leptin and insulin sensitivity during pregnancy.
Molecular mechanisms remain to be fully determined.
Summary: Part 1 (4)
Prolactin receptors are tyrosine kinase receptors expressed in the CNS and peripheral tissues.
Prolactin secretion from anterior pituitary lactotrophs is inhibited by TIDA neurons in the ARC.
Prolactin release is regulated by reproductive state.
Prolactin is important to physiological adaptations during pregnancy in preparation for maternity
Brain regions mediating negative pup behaviour in female mice (5)
Medial preoptic area (MPOA) is critical for maternal behaviours.
Virgin females can exhibit aggression towards pups (leading to infanticide).
Reproductive state switches on maternal behaviour.
Chemogenetic stimulation of a specific population of neurons in the bed nucleus of the stria terminalis (BNST) is sufficient to induce infanticide. Inhibition of these neurons prevents infanticide.
Reciprocal connections exist between the BNST and MPOA and the balance between these can regulate the change between hostility and maternal care
correct PRL signalling is necessary in MPOA for maternal behaviour (1)
Virally-mediated deletion of prolactin-receptors from the medial preoptic area disrupts post-partum maternal behaviours.
Paternal behaviour (4)
In many mammals, females do most of the parental care (uni-parenting).
Males can exhibit infanticidal behaviour towards pups (species dependent).
In bi-parenting species, PRL is implicated in male parental behaviour.
PRL and phasic activity of TIDA neurons has been linked to parental behaviour differences between rats (non-paternal) and mice (paternal).
Prolactin treatment is sufficient to induce paternal behaviour in male rats (3)
PRL injection increases pSTAT5 in MPOA.
Injection of PRL is sufficient to induce paternal behaviours in sexually experienced male rats.
Virgin male rats would likely kill the pups
