ANAT 322 Lecture Notes - Lecture 11: Mitosis, Neuropeptide Y, Proopiomelanocortin
7 Jun 2018
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ANAT 322 Lecture 11
Dr. Kokoeva February 10th, 2017
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ANAT 322
Lecture 11– Neural Plasticity in the Adult Hypothalamus
Dr. Kokoeva – February 10th, 2017
NOTE: This NTC is meant to be used as a study aid to supplement your own class notes. Hence,
not all of the text contained in the lecture slides will be reproduced here.
Please send comments or questions about NTCs to us through email: [email protected].
Today
• Continue with the lectures on central control of energy homeostasis
• Today we will be speaking about neural plasticity in the adult hypothalamus
• She will just remind you that there are two systems which are complimentary to each
other: hedonic system and homeostatic system
o Homeostatic system is motivating us to eat when our energy stores are low
o Hedonic system motivates us to eat because of pleasure sensation
Review from last class – A theoretical relationship between serum leptin levels and
leptin action
• Last time she described this theoretical relationship between leptin levels and leptin action and
she got a couple of questions so she will briefly stop at this slide once again
• This slide is very theoretical
• The idea was to highlight that during millions of years of evolution organisms were living in the
green zone (see figure 1)
• When energy stores were going
down leptin levels were going down
which is signaling to increase
appetite and it is also decreasing
thermogenesis as an adaptation
o Adaptation because energy
stores go down so we are
supposed to store energy
o That is why we decrease
thermogenesis because
appetite is increased
• The organism starts to eat and from
B we get into A and we continue to
eat and leptin levels go slowly up and
we reach C
• Once we are in C, leptin is efficiently
blocking appetite and food intake is
stopped and then leptin levels go down and if there is no food around it goes further down and
at this point leptin is getting maximum action
• So lowering leptin levels is positively increasing appetite and food seeking behavior and the
organism’s hunger signals are so high that animals will risk their lives to get some food
Figure 1. A theoretical relationship between
serum leptin levels and leptin action
ANAT 322 Lecture 11
Dr. Kokoeva February 10th, 2017
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• When there is a lot of food around we don’t stop at C and we continue eating because of our
hedonic system (pleasure sensation)
• Because adipose tissue is increasing (and increasing leptin levels) we reach a situation E which
is correlated with leptin resistance
o Levels of leptin go up but they stop working
o The system is breaking down
o Researchers don’t understand why but we know that leptin stops working and although
there is a lot of leptin in this case it acts as in case of A (in terms of leptin action)
§ Leptin does not block appetite
§ That is the meaning of E and D. D is an analogue of situation A but in the case
when there is plenty of food around. E does not “go into” D. Instead, D is a point
showing that the serum leptin level at point E corresponds with the leptin action
of point A in our current situation
• In other words, we diverge off of this green line because of leptin
resistance, which causes leptin action to be lower than it should be for
the respective serum leptin level
• This slide is highlighting the difference between the situation that occurred during the many
millions of years of evolution and the situation that we are currently in (situation E)
• This is not critical, but is just to give you an idea why we are leptin resistant and how it
correlates to evolutionary situation
Neural plasticity in the adult hypothalamus
• It is poorly understood why some humans can maintain their body weights during their entire
life and some people cannot
• During specific times of their life someone may have been lean (for example, while they were
young) then some situation arises (pregnancy, quitting smoking, stress) and body weight goes
up
• Although this person wants to go back to their previous body weight it is very hard
• There are some hypotheses that these situations are due to plastic changes that occur in the brain
• Four plastic changes that can occur in the brain:
o Synaptic strengthening
o Synaptic elimination/weakening
o Synaptogenesis (formation of new synapses) and synapse remodeling
o Neurogenesis (formation of new neurons)
• For many years, people thought that these changes occur only during development and once an
organism is adult there is not much going on with regards to plasticity
o Researchers discovered that this is not true and that there are a lot of plastic changes
occurring in the adult brain
Document Summary
Lecture 11 neural plasticity in the adult hypothalamus. Note: this ntc is meant to be used as a study aid to supplement your own class notes. Hence, not all of the text contained in the lecture slides will be reproduced here. Please send comments or questions about ntcs to us through email: macss. academic@gmail. com. B we get into a and we continue to eat and leptin levels go slowly up and we reach c: once we are in c, leptin is efficiently. That is the meaning of e and d. d is an analogue of situation a but in the case when there is plenty of food around. E does not go into d. instead, d is a point showing that the serum leptin level at point e corresponds with the leptin action of point a in our current situation. Barrel cortex plasticity experiment: using genetic manipulations, they expressed gfp (green-fluorescent protein) in these neurons.
