Respiration can be controlled voluntarily as well as involuntarily. Now it's neural control is bit complex. Let's try to understand it and why such complexity is required we will solve that also. So first let's try to understand involuntary neural regulation of respiration. Well involuntary neural regulation of respiration is brought about by various neural centers which are located in medulla and pons and actually these both the pons and medulla have two- two main centers . Medulla has a dorsal respiratory group of neurons and a ventral respiratory group of neurons. Then in pons we have a pneumotaxic center and apneustic center .So let's try to see how all these centers bring about respiration. Okay first thing is initiation of respiration. So how is respiration being initiated? Well there is a pacemaker for respiration yes like that we have for heart similarly we have a pacemaker for respiration as well. This pacemaker is pre-botzinger complex which again is located in medulla and this actually sets up the rhythm or pace for respiration. So how it does that? Well this pre-botzinger complex has neurons which fire rhythmically just like the pacemaker of heart. So there is a particular rhythm for firing. Now the impulses from this pre-botzinger complex basically excite the dorsal respiratory group of neurons and this dorsal respiratory group of neurons consist of what is known as inspiratory neurons and as the name suggests these inspiratory neurons basically supply the alpha motor neurons which are present in the spinal cord so alpha motor neurons of the inspiratory muscles right ! So you see the connection pre botzinger complex in rhythm then exciting the I neurons of dorsal respiratory group which in turn is exciting the alpha motor neurons supplying the inspiratory muscles. So obviously this is going to cause the contraction of the inspiratory muscles hence the inspiration will be initiated. Now this inspiration should stop as well so how that is occurring ?Well obviously for stopping the inspiration we want the muscles to relax isn't it ? For quite inspiration what happens that the muscles contract and for quite expiration the muscle simply relax the inspiratory muscles they relax and there is a quite expiration there is no need of contraction of the expiratory muscles. So we want these inspiratory muscles to relax how is that going to happen? Well as i told you that this pre-botzinger complex neurons are firing in a rhythm isn't it so they fire and after some time they stop firing. So by the virtue of this automatic stoppage and firing of the neurons of pre botzinger complex there will be no excitation of I neurons of DRG and hence the signal will not go to the inspiratory muscles fine but you see sometimes we need to increase the depth of respiration for example when talking we take deep inspiration and also there is prolonged expiration. Also involuntarily also there are various instances in which there is a change in rate and depth of respiration for example during exercise ,fear, anxiety. Then also there are certain reflexes isn't it? So that means only the pre botzinger complex and dorsal respiratory group of neurons that is the I neurons are not sufficient for all that .So we have some other levels of control as well .So first is ventral respiratory group of neurons which is located in medulla. Now this ventral respiratory group of neurons has two types of neurons - the I neurons that is the inspiratory neurons and there is E neurons as well that is the expiratory neurons. Now these neurons of ventral respiratory group are silent during quiet inspiration and expiration because DRG is sufficient for that but in case of increased requirement that is increase in rate and depth of respiration what happens that these neurons are also activated so whenever there is increased firing of inspiratory neurons of DRG there is a spillover of that so there is some connection between the DRG neurons and VRG neurons. So there is a spilling over of this impulse to the I neurons of ventral respiratory group and they also start firing. So understanding that now both the I neurons of DRG and VRG are going to cause excitation of alpha motor neurons which are supplying the inspiratory muscle so obviously they will contract with more strength and there may be activation of some other muscles - other inspiratory muscles as well depending on the requirement but when we are having increase in rate and depth of respiration in that case we have a forceful expiration as well so in that case relaxation of inspiratory muscles is not sufficient. What we want is that expiratory muscle should also contract so that is happening because the inspiratory neurons of VRG are connected to expiratory neurons of VRG right. So I neurons inhibit the E neurons of ventral respiratory group and E-neurons in turns inhibit the I neurons of ventral respiratory group. So this is known as mutual inhibition right so they are connected by mutual inhibition fine but still you see that here till now the expiration has not started isn't it we are just telling that there is some mutual inhibition here and we have discussed that how increase in depth of inspiration is going to occur not how expiration has started because it may be that we need to increase the rate of respiration as well isn't it? So the rhythm of pre-botzinger complex is not being followed here so there should be some other connections as well. Yes there are other connections which cause the switching of inspiration to expiration depending on requirement and that is the connection from the pons. So the pneumotaxic center which we spoke about this pneumotaxic center actually inhibits DRG so if DRG is inhibited what will be its importance physiologically. Well you see that there will be no more activation of the inspiratory muscles and hence it is causing a switch to expiration. So two things we have got so that a switch can occur just because of the inbuilt rhythm of pre botzinger complex that is during a quiet inspiration and expiration but sometimes when that switch needs to be changed also so another level of control is there that is the pneumotaxic center inhibiting DRG and causing a switch to expiration but there is another center we spoke about that is the apneustic center . This apneustic center actually excites the dorsal respiratory group I neurons so pneumotaxic center inhibiting DRG and apneustic center exciting drg. See this is very important because of the fine balance between the inhibition and excitation of DRG the switch from inspiration to expiration is smooth and it's not like a abrupt switch to expiration. So in summary we can say that pneumotaxic center acts as a switch for expiration to occur. Also one thing you note here that since it limits duration of inspiration obviously it will cause increase in rate of respiration. See increased depth is taken care by simultaneous activation of I neurons of ventral respiratory group right so early switch will not that much matter so that's how that increase in rate and depth of respiration is brought about when required. But who will activate pneumotaxic center .Well there is a negative feedback mechanism also operating. See there are stretch receptors which are present in tracheobronchial tree so when there is lung inflation there is a stretch and these stretch receptors are stimulated which sends afferents via vagus nerve from a stretch receptor to this pneumotaxic center causing its activation. So this vagus nerve is actually inhibiting the I neurons via the pneumotaxic center that means more inflation will cause a stopping of inspiration and switch to expiration. This is also the mechanism of Hering Breuer reflex that is the lung inflation when it goes above 1 liters then it initiates lung expiration. So i hope you have understood that how it is happening lung inflation causing the stimulation of the stretch receptors, activation of the vagus and then inhibition of the I neurons so there is a kind of negative feedback operating here. So we have developed our flow flowchart for the neural control of respiration ah just before going further just if you see here that we have spoken about the switch and here we spoke about that how I neurons are mutually inhibiting the E neurons in VRG isn't it ? So this is because that when I neurons are active we don't want E neurons to be active and with the inhibition of the I neurons of DRG what is going to happen that these I neurons of VRG will also stop firing and hence the inhibition from the E neurons will be removed and E neurons will become active then they are going to stimulate the alpha motor neurons which are supplying the expiratory muscle so that is going to cause the deep expiration as well. Fine so this is a flow chart for involuntary neural control of respiration what about voluntary control? Well it will be from the cerebral cortex so from the corticospinal tract there is information going to the alpha motor neurons of the inspiratory muscles and expiratory muscles which is going to control this voluntarily. Now apart from the control by these neural centers you might be aware that there are certain protective reflexes as well. There is cough reflex, sneeze reflex and J reflex .The cough and sneeze reflex occur because of the presence of irritant receptors in larynx, trachea and bronchi and whenever there is some irritant there is a stimulation of these irritant receptors and there is again the vagal afferents which go from these to the neural centers and this results in bronchoconstriction, hyper apnea and cough so that is the cough reflex and sneeze reflex obviously you know that because of these irritant receptors just to throw out the irritant from the body there is a sneeze. Then what about J reflex? Well J receptors are present in interstitium in between the alveoli and the blood vessels so here J receptors are present and what happens that if there is a stretch in interstitium then these J receptors are stimulated. So when there will be stretch in the interstitium- see when there is increase in pulmonary hydrostatic pressure what happens that with the hydrostatic pressure rise there might be leakage of some fluid into the this pulmonary interstitium and this is going to increase the stretch in the interstitium. Now this rise in pulmonary hydrostatic pressure can occur in case of when we go to very high altitudes or in case of severe exercise because the cardiac output is increasing so more blood is flowing through the pulmonary vessels which causes increase in pulmonary hydrostatic pressure right ! So high altitude and exercise ,these J reflexe is stimulated so what happens because of the increase in the stretch these J receptors are stimulated and the end result is apnea, bradycardia, hypotension and inhibition of stretch reflex. So obviously you might have understood the physiological significance. If a person is exercising too much right so inhibition of stretch reflex, bradycardia, hypotension will not allow him to continue the exercise any further. So yes this is also a protective reflex. With this now let's try to solve the very famous question of lesions at various levels in brain stem that how it is going to affect the respiration. When you see if a lesion is above pons say here what will be the effect? See basically voluntary control will be lost because it is coming from the motor cortex but involuntary control will be normal since none of the centers of respiration are affected. So let's draw it say suppose this represents a normal inspiration and expiration and let us see two ways one that if vagus is intact and another one in which vagus is cut. so if vagus is intact we will get a normal inspiration and expiration and in case if the vagus is cut what is going to happen the feedback control is going to be lost isn't it ? So switching to expiration is being delayed- basically rate of respiration is going to decrease and depth of respiration is going to increase because the switch to inspiration is not happening. Okay next level - suppose the lesion is between pneumotaxic center and apneustic center what will happen? Well now obviously the pneumotaxic centre will not be able to inhibit DRG but apneustic center is still active so what is going to happen the depth of respiration will increase too much right and this is known as apneusis so it's like a gasping too much depth of respiration while rate of respiration is much less and what will happen if vagus is cut . Well it will be too much aggravated isn't it because switching to expiration is being prevented so further there will be increase in depth and decrease in rate of respiration. Now third if the lesion is between pons and medulla then what is going to happen? We will see some pattern of respiration that coming from the pre botzinger complex but it is not fine-tuned so the fine-tuned respiration which we get because of the action of so many centers that will be missing and what about if vagus is cut ? Well some pattern will be there but the depth of respiration will be more and finally the fourth region that is below the medulla what is going to happen obviously all the centers are cut off so no information is going to the alpha motor neurons of inspiratory muscles or expiratory muscles and hence there will be complete stoppage of respiration that is apnea so that's all for the neural regulation of respiration. I hope you understood that what is the physiological significance of so many centers and how it helps us in changing the respiration according to the needs of the body involuntarily as well as voluntarily. 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