Warning: foreach() argument must be of type array|object, bool given in /var/www/html/web/app/themes/studypress-core-theme/template-parts/header/mobile-offcanvas.php on line 20

Signals carried by hormones must eventually be terminated. Describe several mechanisms for signal termination.

Short Answer

Expert verified
Hormonal signals terminate via degradation, receptor desensitization, internalization, feedback inhibition, and diffusion.

Step by step solution

01

Hormone Degradation

Hormones can be quickly degraded by enzymes in the bloodstream or in target tissues. This enzymatic breakdown reduces the level of active hormones, effectively terminating the signal and allowing for temporary regulation of hormone activity.
02

Receptor Desensitization

Another mechanism for signal termination is the desensitization of receptors, often through phosphorylation. When receptors on the target cell surface are repeatedly exposed to a hormone, they can become less responsive or inactivated, which diminishes the signal.
03

Receptor Internalization

Receptors bound to hormones can also be internalized, or pulled into the cell from the surface, which removes them from the cell surface where they can interact with more hormones. This reduces the cell’s responsiveness to the hormone, effectively terminating the signal.
04

Feedback Inhibition

Hormones often regulate their own production through feedback mechanisms. When enough hormones are present, they can signal upstream components to decrease hormone synthesis or secretion, thus terminating further signaling.
05

Diffusion and Dilution

Hormones can diffuse away from the target cell or be diluted in the bloodstream. This physical removal from the site of action reduces their ability to stimulate receptors continually, thus contributing to signal termination.

Unlock Step-by-Step Solutions & Ace Your Exams!

  • Full Textbook Solutions

    Get detailed explanations and key concepts

  • Unlimited Al creation

    Al flashcards, explanations, exams and more...

  • Ads-free access

    To over 500 millions flashcards

  • Money-back guarantee

    We refund you if you fail your exam.

Over 30 million students worldwide already upgrade their learning with Vaia!

Key Concepts

These are the key concepts you need to understand to accurately answer the question.

Hormone Degradation
Hormone signaling relies on the precise regulation of hormone levels within the body. One critical way to end these signals is through hormone degradation. This process involves enzymes in the bloodstream or target tissues that break down hormones.

Think of it like this: enzymes act like tiny scissors that cut hormones into smaller pieces, disabling their active form. By doing so, they quickly lower hormone levels and stop the signal from affecting the body further.
  • This enzymatic breakdown ensures that hormones don't linger longer than necessary.
  • The fast degradation allows tissues to reset and respond to subsequent signals effectively.

Without this process, the body could become overwhelmed by overactive hormonal signals, leading to unbalanced physiological conditions.
Receptor Desensitization
The cells in our body have receptors that bind hormones to initiate a response. Over time, if a receptor sees the same hormone repeatedly, it can become desensitized. This is a protective mechanism to prevent overstimulation.

Receptor desensitization often involves phosphorylation, where phosphate groups are added to the receptor. This modification reduces the receptor's activity:
  • Desensitized receptors respond less vigorously to the hormone, gradually diminishing the signal.
  • This ensures cells are not perpetually activated by high hormone concentrations.

Overall, desensitization helps cells maintain balance and prevent damage from excessive hormone exposure.
Feedback Inhibition
Feedback inhibition represents a sophisticated method of controlling hormone levels and their effects within the body. Hormones, after reaching a high enough concentration, can send signals back to limit their own production.

This feedback loop ensures a balance, where hormone levels increase and decrease as needed:
  • If there's too much hormone, the feedback decreases synthesis or secretion, stabilizing levels.
  • This mechanism prevents unnecessary production, preserving energy and resources.

Feedback inhibition is like a smart thermostat that adjusts the air conditioning when the room gets too hot, keeping conditions comfortable and controlled.
Receptor Internalization
Sometimes, the body needs to ensure that receptors stop signaling. A more complete shutdown can be achieved through receptor internalization. Here, receptors bound to hormones are pulled into the cell, away from the cell surface.

Once internalized:
  • Receptors cannot interact with hormones on the cell surface, effectively halting any further signaling.
  • This allows the cell to temporarily remove part of its sensitivity to the hormone.

Receptor internalization is crucial for regulating receptor activity and ensuring that cells are responsive only when necessary.
Diffusion and Dilution
Hormones are distributed through the bloodstream to reach target cells. However, not all hormones hit their target. Many hormones diffuse away from target cells or are diluted in the bloodstream.

This process naturally reduces the concentration of hormones at the site of action:
  • As hormones move away or dilute, their ability to continuously stimulate receptors diminishes.
  • This leads to the natural fading of signals and prevents excessive stimulation of target cells.

Diffusion and dilution help the body maintain hormone levels within a range that supports health and stability.

One App. One Place for Learning.

All the tools & learning materials you need for study success - in one app.

Get started for free

Most popular questions from this chapter

For each of the situations listed, provide a plausible explanation for how it could lead to unrestricted cell division. a. Colon cancer cells often contain mutations in the gene encoding the prostaglandin \(\mathrm{E}_{2}\) receptor. \(\mathrm{PGE}_{2}\) is a growth factor required for the division of cells in the gastrointestinal tract. b. Kaposi sarcoma, a common tumor in people with untreated AIDS, is caused by a virus carrying a gene for a protein similar to the chemokine receptors CXCR1 and CXCR2. Chemokines are cell-specific growth factors. c. Adenovirus, a tumor virus, carries a gene for the protein E1A, which binds to the retinoblastoma protein, pRb. (Hint: See Fig, 12-40.) d. An important feature of many oncogenes and tumor suppressor genes is their cell-type specificity. For example, mutations in the \(\mathrm{PGE}_{2}\) receptor are not typically found in lung tumors. Explain this observation. (Note that \(\mathrm{PGE}_{2}\) acts through a GPCR in the plasma membrane.)

Many enzymes can hydrolyze GTP between the \(\beta\) and \(\gamma\) phosphates. The GTP analog \(\beta, \gamma\)-imidoguanosine \(5^{\prime}\)-triphosphate \((\mathrm{Gpp}(\mathrm{NH}) \mathrm{p})\), shown here, cannot be hydrolyzed between the \(\beta\) and \(\gamma\) phosphates.

In principle, the physiological effects of epinephrine should be mimicked by addition of cAMP to the target cells. In practice, addition of cAMP to intact target cells elicits only a minimal physiological response. Why? When the structurally related derivative dibutyryl cAMP (shown) is added to intact cells, the expected physiological response is readily apparent. Explain the basis for the difference in cellular response to these two substances. Dibutyryl cAMP is widely used in studies of cAMP function.

An analog of cGMP, 8-Br-cGMP, will permeate cellular membranes, is only slowly degraded by a rod cell's PDE activity, and is as effective as cGMP in opening the gated channel in the cell's outer segment. If you suspended rod cells in a buffer containing a relatively high [8-Br-cGMP], then illuminated the cells while measuring their membrane potential, what would you expect to see?

The sensations of heat and cold are transduced by a group of temperature-gated cation channels. For example, TRPV1, TRPV3, and TRPM8 are usually closed, but they open at different temperatures. TRPV1 opens at \(\geq 43{ }^{\circ} \mathrm{C}\), TRPV 3 opens at \(\geq 33{ }^{\circ} \mathrm{C}\), and TRPM8 opens at \(<25^{\circ} \mathrm{C}\). These channel proteins are expressed in sensory neurons known to be responsible for temperature sensation. a. Propose a reasonable model to explain how exposing a sensory neuron containing TRPV1 to high temperature leads to a sensation of heat. b. Capsaicin, one of the active ingredients in "hot" peppers, is an agonist of TRPV1. Capsaicin shows \(50 \%\) activation of the TRPV1 response at a concentration of \(32 \mathrm{~nm}-\) a property known as \(\mathrm{EC}_{50}\). Explain why even a very few drops of hot pepper sauce can taste very "hot" without actually burning you. c. Menthol, one of the active ingredients in mint, is an agonist of TRPM8 \(\left(\mathrm{EC}_{50}=30 \mu \mathrm{M}\right)\) and TRPV3 \(\left(\mathrm{EC}_{50}=20 \mathrm{mM}\right)\). What sensation would you expect from contact with low levels of menthol? With high levels?

See all solutions

Recommended explanations on Chemistry Textbooks

View all explanations

What do you think about this solution?

We value your feedback to improve our textbook solutions.

Study anywhere. Anytime. Across all devices.

Sign-up for free