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Find out the correct sequence of a simple reflex are :-
  • a)
    Brain-spinal cord - nerves - effector
  • b)
    Effector - CNS - sensory nerves - receptor
  • c)
    Muscles - spinal cord - brain - receptor
  • d)
    Receptor - sensory nerves - CNS - effector
Correct answer is option 'D'. Can you explain this answer?
Verified Answer
Find out the correct sequence of a simple reflex are :-a)Brain-spinal ...
When a receptor is stimulated, it sends a signal to the central nervous system, where the brain coordinates the response. But sometimes a very quick response is needed, one that does not need the involvement of the brain. This is called as the reflex action. In a simple reflex action:
Stimulus -> Receptor -> Sensory neuron -> Relay Neuron -> Motor neuron -> Effector (Muscle).
So, the correct answer is 'Receptors - Sensory neuron - Spinal cord - Motor neuron - Muscle'
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Most Upvoted Answer
Find out the correct sequence of a simple reflex are :-a)Brain-spinal ...
Correct Sequence of a Simple Reflex:

The correct sequence of a simple reflex is as follows:
Receptor - Sensory Nerves - Central Nervous System (CNS) - Effector.

Explanation:

The simple reflex arc is the basic pathway through which a reflex action occurs. It involves a stimulus that is detected by a receptor, which then sends a signal through sensory nerves to the central nervous system (CNS), where it is processed. The CNS then sends a signal through motor nerves to an effector, which carries out the appropriate response.

1. Receptor:
The first step in a simple reflex arc is the detection of a stimulus by a receptor. Receptors are specialized structures, such as sensory neurons, that can detect changes in the external or internal environment. They are typically located in organs, tissues, or specialized cells, and they convert the stimulus into an electrical signal.

2. Sensory Nerves:
Once the receptor detects a stimulus, it sends an electrical signal through sensory nerves. These nerves are responsible for transmitting the signal from the receptor to the CNS. They are specialized for carrying information from the periphery of the body to the CNS.

3. Central Nervous System (CNS):
The sensory nerves carry the signal to the CNS, which consists of the brain and spinal cord. The CNS is responsible for processing and integrating the incoming sensory information. In the case of a simple reflex, the CNS quickly analyzes the signal and generates a motor response.

4. Effector:
After processing the sensory information, the CNS sends a signal through motor nerves to an effector. The effector is the structure or organ that carries out the appropriate response to the stimulus. It can be a muscle, gland, or any other tissue that can produce a response. The effector receives the signal from the motor nerves and executes the required action, such as contracting a muscle or secreting a hormone.

Importance of the Correct Sequence:
The correct sequence of a simple reflex is crucial for the proper functioning of the body. If the sequence is disrupted or the signals are not transmitted correctly, the reflex action may be delayed or impaired. This can lead to difficulties in responding to stimuli, which can have serious consequences for an individual's health and well-being.

Conclusion:
In summary, the correct sequence of a simple reflex is receptor - sensory nerves - CNS - effector. This sequence ensures that the stimulus is detected, transmitted to the CNS, processed, and then elicits an appropriate response from the effector. Understanding this sequence helps in understanding the basic functioning of reflexes and their importance in maintaining homeostasis and protecting the body.
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For some time, scientists have believed that cholesterol plays a major role in heart disease because people with familial hypercholesterolemia, a genetic defect, have six to eight times the normal level of cholesterol in their blood and they invariably develop heart disease. Scientists also noticed that people with familial hypercholesterolemia appear to produce more LDL’s (low-density lipoproteins) than normal individuals. However, scientists wondered, could a genetic mutation that causes a slowdown in the removal of LDL’s from the blood also result in an increase in the synthesis of this cholesterol-carrying protein? Since scientists could not experiment on human body tissue, their knowledge of familial hypercholesterolemia was severely limited. However, a breakthrough came in the laboratories of Yoshio Watanabe of Kobe University in Japan in 1980. Watanabe noticed that a male rabbit in his colony had ten times the normal concentration of cholesterol in its blood. By appropriate breeding, Watanabe obtained a strain of rabbits that had very high cholesterol levels. These rabbits spontaneously developed heart disease. To his surprise, Watanabe further found that the rabbits, like humans with familial hypercholesterolemia, lacked LDL receptors. What scientists learned by studying the Watanabe rabbits is that the removal of the VLDL (very low-density lipoproteins) remnant requires the LDL receptor. Normally, the majority of the VLDL remnants go to the liver where they bind to LDL receptors and are degraded. In the Watanabe rabbit, due to a lack of LDL receptors on liver cells, the VLDL remnants remain in the blood and are eventually converted to LDL’s. The LDL receptors thus have a dual effect in controlling LDL levels. They are necessary to prevent over synthesis of LDL’s from VLDL remnants and they are necessary for the normal removal of LDL’s from the blood.Q. According to the passage, by studying the Watanabe rabbits’ scientists learned that

For some time, scientists have believed that cholesterol plays a major role in heart disease because people with familial hypercholesterolemia, a genetic defect, have six to eight times the normal level of cholesterol in their blood and they invariably develop heart disease. Scientists also noticed that people with familial hypercholesterolemia appear to produce more LDL’s (low-density lipoproteins) than normal individuals. However, scientists wondered, could a genetic mutation that causes a slowdown in the removal of LDL’s from the blood also result in an increase in the synthesis of this cholesterol-carrying protein? Since scientists could not experiment on human body tissue, their knowledge of familial hypercholesterolemia was severely limited. However, a breakthrough came in the laboratories of Yoshio Watanabe of Kobe University in Japan in 1980. Watanabe noticed that a male rabbit in his colony had ten times the normal concentration of cholesterol in its blood. By appropriate breeding, Watanabe obtained a strain of rabbits that had very high cholesterol levels. These rabbits spontaneously developed heart disease. To his surprise, Watanabe further found that the rabbits, like humans with familial hypercholesterolemia, lacked LDL receptors. What scientists learned by studying the Watanabe rabbits is that the removal of the VLDL (very low-density lipoproteins) remnant requires the LDL receptor. Normally, the majority of the VLDL remnants go to the liver where they bind to LDL receptors and are degraded. In the Watanabe rabbit, due to a lack of LDL receptors on liver cells, the VLDL remnants remain in the blood and are eventually converted to LDL’s. The LDL receptors thus have a dual effect in controlling LDL levels. They are necessary to prevent over synthesis of LDL’s from VLDL remnants and they are necessary for the normal removal of LDL’s from the blood.Q. The passage implies that Watanabe rabbits differ from normal rabbits in which of the following ways?

For some time, scientists have believed that cholesterol plays a major role in heart disease because people with familial hypercholesterolemia, a genetic defect, have six to eight times the normal level of cholesterol in their blood and they invariably develop heart disease. Scientists also noticed that people with familial hypercholesterolemia appear to produce more LDL’s (low-density lipoproteins) than normal individuals. However, scientists wondered, could a genetic mutation that causes a slowdown in the removal of LDL’s from the blood also result in an increase in the synthesis of this cholesterol-carrying protein? Since scientists could not experiment on human body tissue, their knowledge of familial hypercholesterolemia was severely limited. However, a breakthrough came in the laboratories of Yoshio Watanabe of Kobe University in Japan in 1980. Watanabe noticed that a male rabbit in his colony had ten times the normal concentration of cholesterol in its blood. By appropriate breeding, Watanabe obtained a strain of rabbits that had very high cholesterol levels. These rabbits spontaneously developed heart disease. To his surprise, Watanabe further found that the rabbits, like humans with familial hypercholesterolemia, lacked LDL receptors. What scientists learned by studying the Watanabe rabbits is that the removal of the VLDL (very low-density lipoproteins) remnant requires the LDL receptor. Normally, the majority of the VLDL remnants go to the liver where they bind to LDL receptors and are degraded. In the Watanabe rabbit, due to a lack of LDL receptors on liver cells, the VLDL remnants remain in the blood and are eventually converted to LDL’s. The LDL receptors thus have a dual effect in controlling LDL levels. They are necessary to prevent over synthesis of LDL’s from VLDL remnants and they are necessary for the normal removal of LDL’s from the blood.Q. The passage supplies information to answer which of the following questions?

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Find out the correct sequence of a simple reflex are :-a)Brain-spinal cord - nerves - effectorb)Effector - CNS - sensory nerves - receptorc)Muscles - spinal cord - brain - receptord)Receptor - sensory nerves - CNS - effectorCorrect answer is option 'D'. Can you explain this answer?
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