Regulatory Systems

By the end of this chapter, you should understand:

The general organization, structure, and function of the autonomic nervous system.
The role of hormones in brain-body signaling and homeostasis, exemplified by leptin.
General principles for the neural control of motivation, such as hunger and thirst.
The molecular and anatomical components of the circadian clock.
The role of neuromodulatory systems in sleep.

Both the sympathetic nervous system (SNS) and parasympathetic nervous system (PNS) are critical components of the autonomic nervous system.
They transmit signals from preganglionic neurons to postganglionic neurons, ultimately affecting effector cells.
Acetylcholine is used as a neurotransmitter within these systems; however, for the SNS, it is only used at the preganglionic synapse.
Figure 9-1 illustrates the signaling pathways involved in the SNS and PNS interactions.
Most, but not all, visceral organs and tissues receive input from both SNS and PNS, highlighting their complementary nature.
Figure 9-2 shows that these systems interact and support each other in regulating bodily functions efficiently.
Regions of the CNS that control both the SNS and PNS are highly interconnected, providing a level of redundancy and efficiency in bodily responses.
Figure 9-3 depicts the CNS connections involved in the regulation of the autonomic nervous systems.

The interoceptive system is responsible for relaying feedback about the physiological state of internal organs to the central nervous system.
Figure 9-4a, 9-4b, 9-4c provide insight into the feedback mechanisms employed by this system.
Hering-Breuer Reflex: A physiological response where stretching in the lungs results in a decrease in respiratory rate. This reflex necessitates the expression of the stretch receptor, Piezo2, located in the nodose ganglion (a type of vagal sensory ganglion).
Figure 9-4d discusses how hypoxia (low oxygen levels) prompts a shift in cellular metabolism from aerobic respiration (mitochondrial) to anaerobic glycolysis. This shift activates petrosal ganglion neurons, mediated by the Or78 receptor.
Different populations of vagal sensory neurons encode various types of visceral information, providing a nuanced understanding of internal organ states.
Figures 9-5a and 9-5b show the role of specific receptors such as Gpr65 and Glp1r expressed by different nodose neurons: Gpr65+ neurons sense nutrients in the gut while Glp1r+ neurons detect stretch in the stomach.

The hypothalamus consists of multiple subregions (or nuclei) that are both anatomically and functionally interconnected.
Figure 9-6a illustrates these different hypothalamic subregions, emphasizing their roles in homeostatic regulations.
The hypothalamus employs both feedforward and feedback mechanisms to maintain homeostasis, influencing various physiological and behavioral changes.
Figure 9-6b explains that such mechanisms are essential for the organism's adaptability to internal and external changes.

Neuroendocrine neurons play a crucial role in signaling pituitary neurons, particularly through the pituitary portal system in the anterior pituitary.
Hormones can also be released directly into the bloodstream from the posterior pituitary, illustrating a direct hormonal regulation mechanism.
Figure 9-7 provides a visual representation of these processes.
Table 9-1 lists hormones released by neuroendocrine neurons or signals they send to influence pituitary cell functioning.

Parabiosis refers to the surgical joining of two organisms to share circulatory systems. These experiments have shown significant insights into feedback mechanisms regulating eating behaviors.
Figure 9-8a depicts the experimental setup used.
Notable studies, such as by Anand and Brobeck in 1951, have highlighted how feedback signals influence feeding behavior, suggesting complex regulatory patterns.
Figure 9-8b relates these historical findings to current understandings of appetite regulation.

Research on mutant mice, specifically Ob/Ob mice, revealed key information about leptin, a hormone involved in regulating energy balance.
Ob/Ob mice exhibit a natural mutation in the leptin gene, resulting in the absence of the hormone.
Figure 9-9a demonstrates the underlying genetic findings.
Figure 9-9b shows that Db/Db mice lack leptin receptors, illustrating a different mutation that similarly affects the feedback signaling related to energy regulation.
Leptin treatment has been shown to effectively decrease food intake and body mass significantly in Ob/Ob mice.
Figure 9-10a and Figure 9-10b illustrate the impact of leptin treatment on these mice.
Leptin's effects extend to human physiology, where treatment has been documented to decrease body mass in leptin-deficient individuals. Figure 9-11 outlines these clinical implications.

The arcuate nucleus of the hypothalamus contains populations of neurons critical in managing eating behaviors.
Figures 9-12a, 9-12b, 9-12c provide comprehensive details about these key neuronal populations, specifically POMC (Pro-opiomelanocortin) neurons and AgRP (Agouti-Related Peptide) neurons, highlighting their roles as regulators of hunger and satiety.