 वल्ँचान षुछ भचोद ट्राईः ऐसकिल सरक्झाना मैंने कर वोर्चिके वोर्च्च्सें प्र經तेरने बाव्य कितें वालोग खुच्च्चरोद क्रदानेः जन्नेगस्तिर कि मेरे काईलिन्ईनाही � chance is required to resolve that also. तोछ to understand the In- valentry Neural Regulation of Respiration. तोछ कर समेज कर ब ज़ाद़्ी मेडला आग़का. आब पात समेज मेडला मेडला आप सब जो दुच जिद आप रादुज। थोड़ुचा हुभादना के जिनक। लगे नऔरस्ओद़ा. थोड़ूच कर मेडला आप नोग।. ќाख ूट्तिः ॑ट्चिय । औक ृपर । । । । । । । । । । । । ।  disregarding centre as well. surface människor is the preboard c没 complex which again is located in medulla and this actually sets up they're rhythm or base or respiration. So, how it does not, well, this preboarding car minced lake fire ridicule, just lying the pacemaker parking, so there's a particular. Changing now the impulses from fr McD reboard SNK complex basically excisés साईत the dorsal respiratory group of neurons and uh these dorsal respiratory group of neurons consist of what is known as inspiratory neurons and as the name suggests this 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-body single complex वहड़ Sanskrit anyono वहड़ iOS वहड़ स्वहद ती Form양 ती لكن nowliest णौं वूज कमब छ़ार्थ básिसabor ज़ार्थprés elmas वेरें हैं ऴृआश्ददर था fehlt ऐस मे crystals description घर उस protesters च compensation ऍिछिे वूिि Profession अख्�атि चान ऑर्द आप दाही हैं झोडब idea tap becoming the inspiration,인데 he is playing.we won the muscles to relax. isnít it? For quite,inspiration. ... So you want these inspiratory muscles to relax? How is ​​that going to happen? well as i told you that this pre-ward zinger 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 in firing of the neurons of pre-ward zinger 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 feel anxiety then also there are certain reflexes isn't it so that means only the pre-ward zinger 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 increased 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 drgi neurons and drgi 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 drg are going to cause excitation of alpha motor neurons which are supplying the inspiratory muscles 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 muscles should also contract so that is happening because the inspiratory neurons of drg are connected to expiratory neurons of drg 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 preversing the 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 nemotaxic center which we spoke about this nemotaxic center actually inhibits drg so if drg is inhibited what will be its importance physiologically when you see that there will be no more activation of the inspiratory muscle and hence it is causing a switch to expiration so two things we have got that a switch can occur just because of the inbuilt rhythm of preversing the 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 nemotaxic center inhibiting drg and causing a switch to expiration but there is another center we spoke about that is the apnoistic center this apnoistic center actually excites docile respiratory group eye neurons so nemotaxic center inhibiting drg and apnoistic 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 nemotaxic 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 eye neurons or 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 nemotaxic center well there is a negative feedback mechanism also operating see there are stretch receptors which are present in tracheobrong kill tree so when there is lung inflation there is a stretch and these stretch receptors are stimulated which sends afference via vegas nerve from a stretch receptor to this nemotaxic center causing its activation so this vegas nerve is actually inhibiting the eye neurons via the nemotaxic center that means more inflation will cause a stopping of inspiration and switch to expiration this is also the mechanism of herring brewer 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 vegas and then inhibition of the eye neurons so there's a kind of negative feedback operating here so we have developed our flow chart for the neural control of respiration just before going further just if you see here that we have spoken about the switch and here we spoke about that how eye neurons are mutually inhibiting the e neurons in vrg isn't it so this is because that when eye neurons are active we don't want e neurons to be active and with the inhibition of the eye neurons of drg what is going to happen that these eye neurons of drg 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 the 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 voluntary now apart from the control via these neural centers you might be aware that there are certain protective reflexes as well there is cuff reflex sneeze reflex and j reflex the cuff 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 afference which go from these to the neural centers and this results in bronchoponstriction hyperethnia and cuff so that is the cuff reflex and the sneeze reflex obviously you know that because of these irritant receptors just to throw out the irritant from the body there is 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 reflexes 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 of 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 brainstem that how it is going to affect the respiration well you see if a lesion is above pawn 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 vegas is intact and another one in which vegas is cut so if vegas is intact we will get a normal inspiration and expiration and in case if the vegas 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 nemotaxic center and apneustic center what will happen well now obviously the nemotaxic center 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 apneuses so it's like a gasping too much depth of respiration while rate of respiration is much less and what will happen if vegas 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-botsinger 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 vegas is cut well some pattern will be there but the depth of respiration will be more and finally the fourth lesion 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 well thanks for watching the video if you liked it do press the like button share the video with others and don't forget to subscribe to the channel physiology open thank you