GRT 2111 Lecture Notes - Lecture 8: Corticotropin-Releasing Hormone, Sympathetic Nervous System, Polydipsia
29 Apr 2018
School
Department
Course
Professor
GRT2111 – Inflammation
Diabetes mellitus
- caused by hyperglycemia
- there are 3 types:
o type I insulin dependent (IDDM) juvenile-onset
o type II non-insulin dependent (NIDDM) adult-onset
o type III other diseases
- 3 symptoms increased thirst, extreme hunger, unexplained weight loss
- complications
o retinopathy – damage of blood vessels of retina
o nephropathy – damage glomeruli
o neuropathy – damage kidney and autonomic nerves
- management
o diet/meal planning
o regular exercise
o monitoring blood sugar levels
o medications
o education to patients/family
Stress Mechanisms (HPA axis)
- hypothalamus releases corticotropin releasing hormone (CRH)
- CRH stimulates production of adrenocorticotropin hormone from pituitary
- ACTH stimulates cortex of adrenal glands to make cortisol to manage stress
How does inflammation organize social behavior?
- proinflammatory cytokines signal brain to alter behavior (activating afferent
vagal nerves and cross blood brain barrier)
- cytokines signal brain to invoke behaviors called sickness behaviors (loss
appetite, sleepiness)
- threats to social connection activates the sympathetic nervous system, HPA
that upregulates proinflammatory activity, activating vagus, blood brain
barrier to alter social behavior
Inflammation & Disease
- 50% cancer developed depression after treatment (increased
proinflammatory)
- depressed people have high levels of proinflammatory cytokines
- endotoxins can lead to depressed mood in healthy people
- dealing with inflammation challenge increases feelings social disconnect
Social behavior organize inflammatory activity
- inflammation regulated neutrally, shaped by features of environment that
predicts greater likelihood of wounding and infection, leads to sympathetic
nervous system and HPA activation
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