Hindbrain / Brainstem Study Notes
Hindbrain / Brainstem Overview
The hindbrain includes critical areas that manage a variety of physiological and behavioral functions, particularly those related to satiation and feeding behaviors.
C-Fos as a Window into Brain Structure and Function Relationships
Immediate Early Genes: Genes activated rapidly in response to relevant stimuli or events.
C-Fos: An indirect marker of recent neural activity; expressed soon after neurons fire action potentials.
Timing: C-Fos expression occurs approximately 90 minutes after an event.
Visualization: Can be visualized in postmortem brain sections using antibody-based immunohistochemistry.
Visualization of Neurons
Procedures to visualize neurons include:
Coronal Sections: Rat brain coronal sections processed with antibodies to target specific proteins (like c-Fos).
Fluorescent Markers: Antibodies tagged with fluorescent markers (secondary antibodies) for visualization.
Methods: Brains are frozen and sectioned using a microtome or cryostat and then viewed under a fluorescent microscope with a camera.
Cell Visualization Examples
Types of Neurons:
Can observe various neuron types including pyramidal neurons.
Co-localization:
Different markers can be visualized simultaneously; for example:
CTB: Green mark
Orexin: Red mark
Merged visualization shows co-localization of these proteins.
RNA Interference (RNAi) Overview
Discoverers: Andrew Fire and Craig Mello awarded the 2006 Nobel Prize in Physiology for discovering RNAi in C. elegans (1998).
Function: Small RNA molecules (miRNA, siRNA, shRNA) bind to endogenous mRNA molecules to modulate their activity (increase or decrease).
Role in Protection: Serves as an endogenous cellular process to protect against viral infections.
Applications in Neuroscience:
Used to knock down gene expression of specific targets (like receptors) to understand feeding behavior
Achieved via the stereotaxic delivery of viral vectors (Adeno-associated virus (AAV), Lentivirus).
Satiation and Meal Size Control
Hindbrain Functions:
Satiation signals processed in the hindbrain include:
Cholecystokinin (CCK)
Serotonin (5-HT)
Gastric distension
Glutamate
Bombesin
Peptide YY
Enterostatin
Glucagon-like Peptide 1 (GLP-1)
Controversy: Some argue social and habitual factors control meal frequency while meal size determines total food intake.
Energy Intake Trends
Statistics:
Increase in total energy intake from 1977 to 2006 of 570 kcal/day.
Breakdown of portion size contribution to energy intake:
1977-1991: Portion size contributed to a rise of 15 kcal/day/year; 4 kcal/day/year from Eating Occasion.
1994-2006: Portion size's contribution decreased to 1 kcal/day/year, while Eating Occasion increased by 39 kcal/day/year.
Decerebrate Rat Studies
Definition: A decerebrate rat has a complete transection between the midbrain and the forebrain (essentially a forebrain lesion).
Hindbrain Satiation Responses:
While the hindbrain adequately controls satiation, it does not manage conditioned flavor avoidance, thirst due to dehydration, or caloric intake moderation.
Decerebrate rats still exhibit normal rejection of nutrients when full.
Experimental Findings on Caloric Intake
Study on chronic decerebrate rats indicated:
Rats were challenged to maintain three daily intraorally delivered meals, but decerebrate rats did not increase meal size when meals were reduced.
Suggests the hindbrain alone is insufficient for daily caloric intake regulation and points to the need for forebrain-hindbrain interaction for short- and long-term intake control processes.
Nucleus of the Solitary Tract (NTS)
Function: First CNS site to receive taste information and visceral information from the GI tract, relaying signals to the rest of the brain.
Medial NTS (mNTS): A critical site for meal size control, being the first to receive gut-derived sensory signals via the vagus nerve.
Involves a vago-vagal reflex pathway: afferent vagus → NTS → dorsal motor nucleus (DMX) → efferent vagus.
Gastric Distension and c-Fos Expression
Gastric distension activates c-Fos in the medial NTS, which can be observed through specific paradigms (e.g., balloon inflation studies):
Three conditions illustrated varying activation through different volumes of distension.
Activation of catecholaminergic neurons indicated by specific markers and post-mortem assessments.
Leptin and mNTS Interaction
Leptin's Role: Interacts with the mNTS to control food intake particularly affecting meal size:
Mechanism 1: POMC neurons project to mNTS, releasing alpha MSH to reduce meal size.
Mechanism 2: Leptin acts directly on mNTS receptors to reduce food intake.
Neuropharmacology Outcomes:
Knockdown of leptin receptor signaling in mNTS increases food intake and body weight gain in rat models.
Conclusion and Significance of Loss vs. Gain of Function
Overview of Findings:
Immunohistochemistry and RNA interference studies support the notion that the hindbrain can process satiation signals independent of the forebrain.
Medial NTS remains paramount for meal size control, receiving vagal sensory input and responding to satiation signals via c-Fos expression.
The role of leptin in feeding behavior is mediated through both direct and indirect pathways involving the mNTS and hypothalamus.
Questions to Ponder: Evaluate the significance of loss of function approaches compared to gain of function strategies in neuropharmacological settings (e.g., agonists vs. antagonists).