Breathing, Feeding, and Neuroprotection

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Imidazoline receptors are located not only in the mammalian central nervous system CNS cells but also in the peripheral nervous system [ 9 ], being involved in the mediation of various physiological processes in the body. It is currently known that there are four types of imidazoline receptors: I1, I2, I3, I4 non I1-non I2 , from which the first three have been mostly studied [ 10 ].

It has been emphasized that these receptors play an essential role in cell proliferation, regulation of adipose tissue formation, body temperature maintenance, mediation of gastrointestinal motility, neuroprotection, inflammation, nociceptive sensitivity, and some neurological or psychiatric disorders such as depression [ 11 ]. Moreover, it is known that these imidazoline receptor subtypes exert control over the activity of the hypothalamic-pituitary-adrenal and noradrenergic axis [ 12 , 13 ]. A number of different endogenous ligands have been characterized: agmatine, the best known and largely studied, harmane and harmalane derivatives of the beta-carboline group , and the newly discovered ribotide acetic acid imidazole.

It is assumed that agmatine is also an effective neurotransmitter, due to its concentration in the brain similar to classical neurotransmitters [ 17 , 18 ]. Literature data have revealed that agmatine stimulates the activity of endothelial nitric oxide synthase [ 16 ], this effect being also proved by its level in the rat brain after cerebral ischemia [ 19 , 20 ]. All these are arguments in favor of the potential of agmatine as a new pharmacological agent for the treatment of various neurological diseases and NDDs [ 24 ].

Electrophysiological studies involving various brain areas, performed on laboratory animals with experimentally induced cerebral alterations, have demonstrated the neurotropic effects of agmatine [ 25 ]. In vitro experimental researches have shown that activation of I2 receptors via the agmatine endogenous ligand exerts neuroprotective effects by increasing the expression of glial fibrillary acidic protein in astrocyte cultures and by inhibiting MAO activity [ 26 , 27 ]. Moreover, the beneficial effects of agmatine have been observed on ischemic-hypoxic lesions, on glutamate-induced neurotoxicity by activating the imidazoline receptors [ 28 , 29 ].

Other experimental investigations highlight the neuroprotective effect of intranasal administration of agmatine in elderly female rats, with a significant improvement of neurological status and increase of survival rate [ 28 , 29 ]. The neuroprotective effects of agmatine on the morphological changes determined by repeated induced stress on medial prefrontal cortex and hippocampus of the rat were also investigated [ 31 ].

It was emphasized that under constant stress conditions, morphological alterations of the brain are associated with the reduction of endogenous agmatine levels [measured by high-performance liquid chromatography HPLC ] and with an increase of arginine-decarboxylase level in the prefrontal cortex, hippocampus, striatum, and hypothalamus [ 32 ].

The exogenous administration of agmatine lowers brain morphological impairment, suggesting thus its neuroprotective effects against structural changes in the rat brain, under recurrent stress circumstances [ 32 ]. Moreover, elevated levels of agmatine have been evidenced in the blood, cortex, hippocampus, and hypothalamus, immediately after brain hypoxic ischemia. Other studies emphasize the neuroprotective influences of agmatine, highlighted by the increase of its brain levels, in rats subjected to prolonged cold-exposure stress conditions [ 33 ].

The use of agmatine attenuates the loss of cellular dopamine from the black substance and repeated treatment improves short-term memory impairment induced by MPTP in elderly mice. The behavioral benefits of agmatine are associated with the decrease in MPTP-induced glutamate capture in the hippocampal area, suggesting thus its involvement in modulation of glutamate recapture, the possible mechanisms responsible for lowering glutamate extracellular levels, thereby alleviating its neurotoxicity [ 29 ].

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Literature data report that the administration of the N-methyl-D-aspartate NMDA receptor antagonists phencyclidine, also coded MK frequently impairs the late alternation performance in a standardized behavioral model of cognitive functions alteration similar to schizophrenia in laboratory animals [ 34 ]. This substance was used to induce the experimental schizophrenia in laboratory animals [ 35 , 36 ]. Agmatine attenuates cognitive and behavioral deficiency in rats with experimental phencyclidine-induced schizophrenic manifestations [ 37 ].

It has been revealed that agmatine diminishes the activation of hippocampal caspase-3 the early indicator of neuronal apoptosis and prevents the alteration of spatial memory induced by lipopolysaccharides, in the swimming test in rat [ 39 ], suggesting its neuroprotective effects. The neurotropic activity of agmatine has been also evidenced in the structural and cognitive alterations after the administration of NMDA N-methyl-D-aspartate in rats [ 40 ]. The use of high performance liquid chromatography HPLC and electrochemical detection allowed highlighting that the treatment with NMDA is associated with low concentrations of monoamines epinephrine, norepinephrine, dopamine, and serotonin in rat PC12 cells [ 29 , 40 ].

Immunohistochemical studies and electrophysiological investigations performed on the brain have validated the neuroprotective actions of both imidazoline receptor antagonists idazoxan and efaroxan in rats with cerebral damages caused by the use of quinolinic acid [ 41 ], and also in mice with experimentally induced autoimmune encephalomyelitis, confirming the improvement of brain structural alterations and blood brain barrier lesions curtail [ 42 ].

Dexefaroxan improves the cognitive performances in the passive avoidance test, facilitates spatial memory in the Morris swimming test in rats, and increases the object recognition ability in the specific behavioral test in mice [ 43 , 44 ]. After subcutaneous administration of dexefaroxan, its pharmacodynamic effects persist for about 21—25 days, indicating that tolerance does not occur during prolonged treatment. Moreover, it was emphasized that dexefaroxan exerts protective effects on the spatial memory deficit caused by cortical devascularization in the Morris swimming test in rats [ 43 ].

Dexefaroxan has also been shown to exhibit neuroprotective effects on the de-vascularization-induced neurodegeneration, to ameliorate the structural changes in the hippocampus, and to remove the cognitive deficits induced by cerebral ischemia in rats [ 45 , 46 ]. Literature data regarding the neuroprotective action of imidazoline agonist and antagonist agents in human studies are only few, and the mechanisms involved in these effects are not completely deciphered. It was postulated that the neuromodulatory properties of agmatine are related to the protective effects on the dopaminergic neurons, to NMDA receptor blocking, and to the decrease in oxidative stress, due to the inhibition of nitric oxide synthase NOS activity [ 48 , 23 ].

Other clinical trials highlighted that the treatment with agmatine was associated with cytoprotective actions, in patients with spinal cord injury, proved by lessening the glial weal construction, decreasing the collagen scar zone, relieving the neuronal alterations, and recovering remyelination [ 49 ]. Moreover, the beneficial effects of agmatine have been demonstrated in various CNS lesions such as: cerebrovascular accident, brain trauma, neuropathic pain, lumbar degenerative disc disease, and different other types of neuropathy [ 50 , 51 , 52 ].

The administration of dexmedetomidine has also shown neuroprotective effects in humans with acute cerebral lesions [ 53 ]. In patients with dementia due to brain frontal lesions, idazoxan alleviates attentional and executive dysfunctions evoked by classical cognitive function tests [ 54 ]. Such findings indicate that clonidine improves memory alterations caused by glutamate hypofunction, but not by hippocampal injury, implying that multiple and distinct mechanisms are involved in the development of memory disorders.


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Clonidine and guanfacine improve the lack of visual attention and spatial memory induced by phencyclidine in rats [ 34 , 36 ]. At high doses, clonidine decreases the response time and induces a lack of the choice accuracy. These results indicate that clonidine treatment can alleviate phencyclidine-induced deficit of attention and of working memory, probably by preventing some of the neurochemical and anatomical effects of this psychotomimetic drug [ 34 ]. The administration of 3-NPA induces degenerative brain damage, progressive motor dysfunction, loss of grip force, emotional disturbances, weight loss, anxiety, and impairment of learning activity and memory.

An increase in cerebral acetylcholinesterase level, enhancement of oxidative stress, and impairment of the activity of mitochondrial enzyme complexes I, II, and IV were also noted [ 28 ]. The treatment with moxonidine resulted in the alleviation of disturbances caused on animal weight, motor activity, gripping ability, anxiety, impairment of learning ability and memory, and biochemical disturbances, thus indicating that substances modifying the activity of I1 receptors may be potential pharmacological agents for the treatment of degenerative brain disorders [ 55 ].

The effects of clonidine have also been evaluated in mice with subacute brain ischemia obtained after permanent ligation of common carotid arteries. The subsequent brain damages consisted of expansion of cerebral infarction areas, assessed by computed tomography scans.

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Subacute treatment with clonidine for 7 days increases the expression of neuronal nuclei, glutamic acid-decarboxylase, and gamma-aminobutyric acid GABA B receptor GABA B 1 in hippocampal subregion cornu amonis CA 1 but does not influence the level of these elements in the hippocampal area CA 3, nor in the dentate gyrus. These data support the idea that clonidine exerts neuroprotective effects on chronic cerebral ischemic lesions, by regulating GABA B 1 receptors and the activity of glutamic acid-decarboxylase [ 25 ].

Additionally, the decrease in superoxide dismutase SOD , catalase CAT , and glutathione levels as well as the increase of both malondialdehyde MDA level and cerebral acetylcholinesterase activity were noted in animals with brain ischemic lesions [ 28 ]. Both moxonidine and clonidine have shown a decrease in histopathological changes, oxidative stress, central cholinesterase activity, as well as a reduction in memory disturbances and learning deficits in mice with vascular dementia induced by subacute ischemia after permanent bilateral cerebral artery ligation [ 28 , 40 ].

In vitro cell culture studies from the rat frontal cortex with glutamate-induced neurotoxicity revealed the partial neuroprotective effects of moxonidine, with a significant decrease in the number of dead cells [ 26 ].

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Moxonidine has shown beneficial effects on cerebral spasm in an experimental rabbit model of subarachnoid hemorrhage [ 40 , 56 ]. Different pathological conditions of the body, as well as the physiological process of aging, can cause cognitive impairment and free oxygen radicals production, being responsible for abnormal functioning and cell death.

Subsequently, a new idea has emerged claiming that nitric oxide NO , along with the free radicals, plays a key role in the aging process, due to neurotoxic effects on the brain exerted by its excessive levels [ 57 ]. Nitric oxide is generated from L-arginine under the action of nitric oxide synthase NOS.

Numerous experimental researches reveal that NOS activity is significantly elevated in the brain of elderly rats, being associated with existing cognitive alterations [ 57 , 59 ]. Mediated by the competitive inhibition of nNOS and iNOS, and correlated with the stimulation of NOS, agmatine contributes to the improvement of cognitive functions [ 19 , 60 , 61 ], while exhibiting neuroprotective effects [ 38 , 39 ].

Literature data have shown that agmatine eliminates neuroinflammation and lipopolysaccharide-induced memory impairment which is known to stimulate iNOS activity and, implicitly, the NO production in laboratory animals. It prevents cognitive alterations, probably as a result of inhibition of iNOS activity [ 39 ]. Other researchers have disproved these results by showing that agmatine can cause cognitive impairment due to the inhibition of NMDA receptors and of NO, important elements in the modulation of learning and memory processes [ 62 , 63 ].

On the other hand, it is known that the central cholinergic system plays a crucial role in the mediation of cognitive functions. Cognitive deficits have been induced in laboratory animals by using an anticholinergic agent, scopolamine, its administration producing a significant reduction in NOS activity, and an increase in arginase activity, of L-ornithine and putrescine levels in the hippocampus [ 51 ].

It has been observed that agmatine eliminates the scopolamine-induced alterations of memory and learning capacity [ 64 , 65 ]. Although glutamatergic activity is required for cognitive processes, it is assumed that the increase of glutamate levels or of NMDA activity would also be responsible for the scopolamine-induced cognitive disturbances [ 66 ]. Abnormal release and disturbances of neuromodulatory activities due to variation in cerebral agmatine levels may be correlated to different CNS diseases such as schizophrenia.

Interactions of agmatine with other central neurotransmitter systems such as glutamatergic and nitrergic appear to be particularly important in the pathophysiological mechanisms of CNS disorders associated with brain damage and cognitive functions deficit. Neurodegeneration can be caused by chronic disease progression or by acute injury cerebral ischemia—stroke or trauma [ 67 ].

Ischemic stroke represents a vascular ailment with neurological consequences produced by the obstruction of the arteries in a part of the brain, therefore by blood supply privation [ 68 ]. One mother even told me it was her fault. This highlights the complexity of oral feeding for preterm infants and the vulnerability of their parents. Through this structured learning, parents gain the feeding competence they must demonstrate and the confidence to finally take their tiny new family member home. Long before their preemie is discharged from the NICU, parents begin judging their parental competence by their ability to feed their infant.

This is an undue burden to take on, given the enormous stresses and challenges posed by preterm birth. Anxiety, depression and feelings of lost autonomy are common. Many parents experience dissonance between what they expected for their first days of parenthood and the reality of caring for a medically fragile infant. These new parents may also feel less confident when comparing themselves with highly trained and experienced NICU staff.

Breathing, Feeding, and Neuroprotection - PDF Free Download

And the fact is, their infants are at high risk for the onset of problems during feeding attempts: We often see irregular respirations and prolonged apneic pauses, which increase aspiration risk during sucking bursts. Their infant may experience unstable oxygen saturations or heart rate, disengagement, and fatigue with the challenges of feeding by mouth. The more stressful the feeding experience, the more likely it is the infant will struggle with coordination of swallowing with breathing, which can pose a threat to the airway.

Parents need guided learning to proactively structure feedings to prevent distress and anticipate what support their infant may need from moment to moment. This can then minimize infant stress and support safe, successful feeding see sources below. NICU parents begin judging their parental competence by their ability to feed their infant. This feeding approach, as described in my research see sources includes:. Observing the infant from moment to moment during feeding for cues of stress versus stability specific to swallowing, breathing, physiologic stability, postural control and state regulation.

Learning this dance is far from straightforward for new parents of preemies. The learning curve for mothers can be steep, as they report this is novel territory. Interpreting the meaning of infant communication, adaptive feeding behaviors and stress responses. Making modifications for postural support and optimal suck-swallow-breathe coordination. Providing opportunities for rest and deep breathing to promote respiratory reserves. Through structured learning, parents gain the feeding competence they must demonstrate to finally take their tiny new family member home.

In my experience, two methods of structured participatory learning are essential: anticipatory guidance and guided participation. Anticipatory guidance. Depending on their professional expertise, SLPs may also be certified lactation consultants. The SLP helps parents explore reasons for the behavior and potential interventions. Using this anticipatory guidance, the SLP models interactive problem-solving while the parent learns along with the SLP. During co-regulated feeding, the SLP:.

Provides supportive, swaddled side-lying to optimize tidal volume, alignment and midline. Provides co-regulated pacing by imposing pauses in sucking that avoid uncoupling of swallowing and breathing. Responds to loss of flow at the lips with rest periods that allow for reorganization of infant swallowing function. Decreases feeding demands at the earliest signs of disengagement, responding to infant communication. Here are three examples of SLPs using anticipatory guidance to help parents problem-solve while the SLP is feeding their infant.

Guidance is individualized based on the developing skills of the parents and their infant.

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She might be telling us she needs more time for breathing, or maybe she has a burp. Maybe that is why she is choosing not to open her mouth. I think she liked that. What do you think, Dad? Sometimes preterm infants may, despite interventions, get into trouble. As SLPs model this type of expert problem-solving, it is appropriate for parents to see the SLP struggle in the face of real difficulty. This teaches that even experts stumble. I bet he was trying to tell me he needed a break to breathe. I think if I watch his eyes more, that will help me understand.


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  6. Guided participation. In this next teaching phase, the parent feeds the infant while the SLP thoughtfully acts as a guide.