Download A classic example of an innate releasing mechanism

A classic example of an innate releasing
mechanism: Gull chicks pecking parent’s beak to
get food.
Red spot
The red spot is a key stimulus for the baby chick
to peck at the bill. It “releases” pecking behavior.
Sign or key
stimulus
CNS evaluates
sensory input:
does it meet
preset criteria? YES
NO
Release
pecking
FAP*
Do
nothing
At the same time, the parent having its bill pecked
is a releaser for the behavior of regurgitating food.
* Command neuron effectively disinhibits the CPG for
pecking.
The red spot on the yellow bill is a detected by the
visual system. A CNS releasing mechanism (AKA
neural feature detector) qualifies the signal and
releases a pattern generator to start pecking
“Releaser” or releasing stimulus
≠ releasing mechanism.
The releaser is a key or sign
stimulus.
The releasing mechanism is a
neural process that receives
input from recognition circuits
and communicates with motor
control circuits to activate
(release) a behavior.
Releasing mechanisms can be very simple, requiring
just one or two key stimulus parameters.
This means they are easily tricked!
.
Why do such vulnerable neural mechanisms persist?
•  Processing a few simple key stimuli is faster,
relative to CNS processing.
•  They are good enough! Predators and parasites
that do “code break” and deceive animals based
on particular stimuli they are looking for will
indeed drive an evolutionary response for the
receiver to be more selective.
If there is no code-breaking, there is no selective
pressure to build a more elaborate recognition
mechanism.
Code breaking…
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8
Example 1
Testosterone and aggressive and reproductive behavior
Based on placental circulation and random
arrangement of embryos, some embryos get a
double dose of testosterone produced by neighbors.
“2F” males
have 1/2X
the amount
of T
14
“2M” males
have 2X the
amount of T
2M males provide less parental care… but are more
aggressive about mating.
2M less contact
with pups
As adults, compared with 2F males, 2M males…
•  received 2X the amount of T in utero.
•  mounted females more rapidly.
•  produced more offspring over time.
•  spent more time searching for females.
•  spent more energy searching for females.
•  spent less effort relative to parental care.
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Neurons in Hypothalamus (part of brain (CNS))
GnRH
pituitary
FSH, LH
testes
testosterone
Castration
gets rid of
testosterone
Reverse experiment
re: mice in utero.
Now get rid of T 
increase parental
care.
… and even better, if you can replace the T in
a castrate and restore function:
Can say that T is both necessary and sufficient
for the behavior.
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In this case, Guinea pigs
Guinea pig copulatory behavior
one
21 can only imagine…
Castrated garter
snakes
Hormones act on brain neurons as triggers, in other cases as
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maintenance
factors  very different time constants
Vasopressin and Oxytocin
Ancient hormones found in nearly all animalia
Oxytocin – many different functions.
Knockout mice (Oxt -)  behavioral
deficit of social amnesia.
Every time a male interacts with the
same female, the male sniffs as if a novel
female.
The proximal cause of social amnesia, a “behavioral”
deficit, is really a loss of olfactory memory due to nonproduction of oxytocin.
normal
mouse
26
With a defective gene, sniffing
persists as if a particular ♀ is
always novel.
The vasopressin receptor in the ventral pallium.
Prairie voles and Meadow voles differ in the
amount of V1R in their brains…
…and also differ in parental care.
Prairie voles are
monogamous.
Meadow voles are
polygamous (polygynous =
one male, multiple females)
1.  How monogamy might have evolved?
2.  How do you increase V1a receptors?
Once upon a time… Mutation in a polygamous ancestral
Prairie Vole V1aR gene  perhaps ‘a’ allele binds V more
strongly.
male vole
copulates
vasopressin
release
V1aR gene expressed in
neurons of the ventral pallium.
New V1aR in pallial neurons =
greater response from those
neurons when vasopressin binds.
monogamy
Happier male vole,
spends more time with
female.
Greater neural response =
increased activation of reward
system of brain.
So one individual vole has a mutation that leads to...
•  a variation of the V1a receptor that binds hormone
more strongly... or
•  a transcription regulator that causes more V1aR to
be present in neuron membranes...or
•  a variant of the receptor with lower turn-over... or
•  etc, etc
This vole leaves more offspring in the next generation, and
so do those offspring, etc., fixing the gene rapidly in the
population
How to get more V1R in the vole brain
The V1aR gene inserted using an adeno-associated viral vector. Vectors contained
either:
1. Prairie vole VIaR gene or modified V1aR gene from a genomic library
a. Including a neuron-specific enolase promoter
2. Prairie vole VIaR gene and Escherichia coli lacZ
a. Including a cytomegalovirus promoter
The gene is spliced at the neuron-specific enolase promoter to create a NSEpvV1aR viral vector.
Properties of Adeno-associated viruses:
1. Contain a single strand of DNA
2. Infect non-dividing cells
3. Non-pathogenic
4. Site specific insertion of genetic material
The Adeno-associated viral vectors were syringe-injected into specific sites: The
ventral pallium or the caudate putamen. Transduction occurs and the NSE
promoter works to restrict expression of the gene to neurons in the brain.
Reference:
Lim, M.M., Wang, Z., Olazábal, D.E., Ren, X., Terwilliger, E.F., and Young, L. J. Enhanced partner
preference in a promiscuous species by manipulating the expression of a single gene. Nature. 429, 754
-757 (2004).
If you provide more receptors to the brain of a nonmonogamous meadow vole, it will start behaving somewhat like
the monogamous prairie vole.
Meadow voles
with tweaked
brains.
Bees have pretty small brains and you might
think all their behaviors are innate,
programmed, and each bee is a behavioral
duplicate of the next.
In fact, different bees in a hive have different
behaviors, and this is under hormonal
control.
Bee brains (which control bee behavior!) vary in terms of gene
expression. So even though the genotype is the same across
individuals, gene expression is not.
Juvenile hormone and octopamine are involved
in transitioning young hive cleaner bees into
forager bees.
Surgically remove corpora allata  no JH
made  delayed transition to forager bees.
Methoprene (JH analog) injection to allatectomized
(!) bees restored timing (normal transition)
Octopamine levels in bee brain higher when bees
become foragers.
Inject octopomine  more foraging flight
behavior.
How bee behavior changes over time
sterile ♀ worker bees
less binding to transcription
regulator
initially
nurse bees:
low level of juvenile hormone
later
forager bees
high level of juvenile hormone
So an old hive: build up higher %
forager bees
more binding to transcription regulator
Another chemical regulator, ethyl oleate,
modulates the overall rate at which bees
transition to foragers.
How bee behavior changes over time
sterile ♀ worker bees
initially
nurse bees
Feed to nurse bees
later
forager bees
Synthesize ethyl oleate
Ethyl oleate slows transition of nurse bees to worker
bees.
Old hive: Higher % forager (old) bees. Old bees die off,
less EO, increase transition to foragers.
Old hive: Higher % forager (old) bees. Old bees
die off  less EO  faster transition to foragers.
sterile ♀ worker bees
initially
nurse bees
Feed to nurse bees
later
forager bees
Synthesize ethyl oleate
Experimental addition of old (forager)
bees  slows transition to make new
foragers  old bees die off  too few
foragers
Add young bees – amount of EO
per bee goes down  fast
transition to make lots of
foragers.
Bottom line:
“Nurture” (development)
can affect non-learned/
genetically programmed
behaviors.
Two different physiological and behavioral male morphs in
the midshipman fish (Porichthys notatus).
Type I males – Delayed maturity: incr growth, larger vocal
apparatus
Type II males – Put more developmental energy into
gonads. Smaller as adults, don’t advertisement call.
good dads
sneaker deadbeats
Note error in text pg 95 – “…type II males, have a very high gonad-to-body size…”
Should be “…type II males have a small gonad-to-body size…” as per this table.
Court
females
Do not
court
females
Sonic muscles larger in type I males.
Command neurons  pacemaker neurons (CPG)  sonic
motor nucleus  sonic muscles
Preoptic area (POA)
Command
neurons
Arginine vasotocin (AVT) inhibits command neurons in Type II
males.
6x more AVT-ir (immunoreactive) neurons per gram body
weight in type II males!
Preoptic area (POA)
pacemaker neurons
(CPG)
Command
neurons
Natural populations of midshipmen – more dense
and less dense.
Lab raise fish in low density or high density.
Low Density
juveniles
Fewer AVT-ir neurons
& type I morph
High Density
juveniles
More AVT-ir neurons &
type II morph
Hormones and long term oscillators
White Crowned Sparrow
experiment
Birds have seasonal sensitivity to light level.
When daytime coincides with a period of light sensitivity,
reproductive development is triggered.
An oscillator is reset every day at dawn.
Light sensitivity occurs 16 – 20 hours later. Will it be light
out 16-20 hours after dawn?
White Crowned Sparrow circannual synchronization
What the oscillator controls...
environmental synchronization
(light level & duration)
oscillator
Change in hormone levels
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Change in behavior:
Territoriality
Aggression
Mating
Parental care
Counting mechanisms
Artificial day length manipulation can change when a
mouse loses its tendency for infanticide.
Is the control…
(1)  the number of light/dark cycles post copulation,
or
(1)  the “real” amount of time that has passed?
55
Day length manipulations: make 22, 24, or 27 hour days.
Infanticide stops on day 22 for slow days and day 22 for
fast days  counting
Infanticide stops here for long days
56
Interpretation of previous slide:
Probably a stable chemical is produced, one burst
per day/night cycle.
The rate of accumulation corresponds to the # d/
n cycles, not on the absolute amount of time that
has passed (next slide).
57
The behavior match is with number of light/dark
cycles since mating, not the “real” days since mating.
Match with hours: NOT
58
Match with #cycles: YES
REPRODUCTIVE BEHAVIOR AND HORMONES IN RED-SIDED
GARTER SNAKE
 
At the beginning of the mating season, Red-Sided Garter Snakes have a low level of hormones as well
as the smallest size of gonads. The cue for the beginning of the mating season is the increase in
temperature when they come out of their dens. Also, female garter snakes have small ovaries at the
beginning of the mating season. The gametogenesis in garter snakes begins at the end of the mating
season. In males the testicles grow during six weeks after mating season when they reach their
largest size. The sperm is stored in the vas deferens for mating during the following spring. When
they enter their dens in the fall their testicles have regressed. Their testicles do not grow until the
end of the next mating season. If the male garter snake does not use the stored sperm for the next
mating season then the stored sperm will disintegrate. In the female garter snake mating induces the
follicles to grow and to fill with yolk. Females store sperm in the oviduct while the follicles mature
during a six to eight week period. At the beginning of the next mating season the female garter
snake will expulse the stored sperm in her oviduct that is not used. Other studies have described the
relationship of hormones and hibernation in the Red-Sided Garter Snakes. Still other studies have
tried to explain the relationship of the gonads, adrenal gland, pituitary gland, and other hormones
that may be involved with mating behavior when the snakes emerge from their dens in the spring.
Postmating gametogenesis is an advantage for Red-Sided garter snakes. Also, in Mexico garter snakes
do not hibernate and they have several mating seasons, unlike Canada garter snakes.
P
M
M
V
M
P
P
There is genetic control
over monogamy – a
complex behavioral
trait!
Yellow circle: mostly
monogamous, (except 2
Microtus species
recently polygynous).
P
M
Likely ancient split: Monogamy behavior arises
Is the new monogamy behavior adaptive?
Would it win?
We can imagine a scenario in which the new behavior
becomes established…. (next slide) Evolutionary or adaptive reason keeping genes in population
Guarding females = guarding pups from other
males*.
Males fight back [new gene arises ??!!] by
guarding females, so parentage is certain. Females become promiscuous so males can
never be sure which pups carry their genes.
Kill pups you believe are not your own;
potentially allows mating with female who
enters estrous sooner.
*You have less chance to mate with many females, but higher chance that all of your
offspring survive. Fitness must be higher for parental care than promiscuity!
So the gene we are looking for causes males to hang
with females more, compared with the ancestral type
behavior
Insertion of the V1aR Gene in the Prairie Vole
 The V1aR gene is inserted using an adeno-associated viral vector.
 A modified V1aR gene is used from a genomic library.
 The gene is spliced at the neuron-specific enolase promoter
to create a NSE-pvV1aR viral vector.
 The viral vector is inserted into the ventral pallidum of anesthetized prairie voles.
 Transduction occurs and the NSE promoter works to restrict
expression of the gene to neurons in the brain.
 
 
 
 
 
Adeno-associated viral vectors contained either:
1. Prairie vole VIaR gene
a. Including a neuron-specific enolase promoter
2. Prairie vole VIaR gene and Escherichia coli lacZ
a. Including a cytomegalovirus promoter
 
 
 
 
 
Properties of Adeno-associated viruses:
1. Contain a single strand of DNA
2. Infect non-dividing cells
3. Non-pathogenic
4. Site specific insertion of genetic material
 
The Adeno-associated viral vectors were injected into specific sites; the ventral pallium
or the caudate putamen, of the Prairie vole’s brains using a syringe.
 
 
 
Reference:
Lim, M.M., Wang, Z., Olazábal, D.E., Ren, X., Terwilliger, E.F., and Young, L. J. Enhanced partner
preference in a promiscuous species by manipulating the expression of a single gene. Nature. 429, 754
-757 (2004).
A cross-section of a vole brain
cross and sagittal
sections
Mechanistic reasons for behavior can be tested
Experimental manipulation: add hormone receptors to
the vole brain.
How do you do that?
→  Use adeno-associated viral vector with prairie vole V1aR
gene.
→  Use micro-syringe to inject solution of the single-strand DNA
vectors into a particular region of the brain (pallium or caudate
putamen).
→  Genes insert in host neuron DNA, and so that neuron overexpresses the gene product: the hormone receptor.
→  Presence of hormone in vole causes more than normal activity
from the neuron, which over-activates other neural circuits.
The ventral pallium in particular is concerned not just with reward, but
reward in the context of a familiar partner. Why is not known.
Result with monogamous vole
Induction of
more hormone
receptors leads to
more cuddling
with a familiar
vole.