EQUIPOTENCIALIDAD CEREBRAL PDF

Equipotentiality refers to a psychological theory in both neuropsychology and behaviorism. Karl Spencer Lashley defined equipotentiality as "The apparent capacity of any intact part of a functional brain to carry out… the [memory] functions which are lost by the destruction of [other parts]". The law of mass action says that the efficiency of any complex function of the brain is reduced proportionately to how much damage the brain as a whole has sustained, but not to the damage of any particular area of the brain. In this context when we use brain we are referring to the cortex.

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The hypothalamic paraventricular nucleus PVN coordinates autonomic and neuroendocrine systems to maintain homeostasis and to respond to stress. Neuroanatomic and neurophysiologic experiments have provided insight into the mechanisms by which the PVN acts.

The PVN projects directly to the spinal cord and brainstem and, specifically, to sites that control cardiorespiratory function: the intermediolateral cell columns and phrenic motor nuclei in the spinal cord and rostral ventrolateral medulla RVLM and the rostral nuclei in the ventral respiratory column rVRC in the brainstem.

Activation of the PVN increases ventilation both tidal volume and frequency and blood pressure both heart rate and sympathetic nerve activity. PVN activity alters blood pressure and ventilation during various stresses, such as maternal separation, chronic intermittent hypoxia CIH , dehydration and hemorrhage. Among the several PVN neurotransmitters and neurohormones, vasopressin and oxytocin modulate ventilation and blood pressure. That blockade of V 1A receptors in the medulla normalizes baseline blood pressure as well as blunts PVN-evoked blood pressure and ventilatory responses in CIH-conditioned animals indicate the role of vasopressin in cardiorespiratory control.

In summary, morphological and functional studies have found that the PVN integrates sensory input and projects to the sympathetic and respiratory control systems with descending projections to the medulla and spinal cord. The paraventricular nucleus PVN of the hypothalamus is a major integrative site for autonomic function in maintaining homeostasis. Neuroanatomic and electrophysiologic data indicate that the PVN is reciprocally connected to areas of the central nervous system CNS involved in cardiorespiratory function Kc et al.

The PVN contributes to the maintenance of homeostasis via bidirectional interactions between inhibitory and excitatory connectivity. Imbalance in this counterbalanced system may be pathologic; increasing sympathetic nerve activity SNA and ventilation. In this review, we discuss the interaction between excitatory and inhibitory neurotransmission within the PVN as well as the neuronal pathways between PVN and the CNS sites that are involved in regulating sympathetic nerve discharge, vasomotor tone, and the control of breathing.

A better understanding of the PVN neuronal connections, neurotransmitters and receptors will provide valuable information regarding the role of the PVN in the exaggerated sympathetic outflow associated with congestive heart failure, hypertension as well as genetic disorders including Prader-Willi syndrome. The PVN, a hypothalamic structure, is located bilaterally bordering the third ventricle and is composed of magno- and parvo- cellular divisions.

The magnocellular division is subdivided into the anterior, medial and posterior regions, all of which are composed predominantly of either oxytocinergic or vasopressinergic cells. The parvocellular division is subdivided into the periventricular, anterior, medial, dorsal and lateral regions.

The PVN integrates higher-order sensory and central inputs related to autonomic function. The magnocellular neurons project to the posterior pituitary and secrete vasopressin and oxytocin into the blood stream.

Parvocellular neurons project to sites within the CNS, including regions that modulate the autonomic system. Specifically, PVN neurons in the dorsal, ventral and lateral parvocellular regions project to the intermediolateral IML cell column of the thoraco-lumbar spinal cord and pressor region of the rostral ventrolateral medulla RVLM.

In addition to the vasomotor regions, descending projections from the PVN innervate dorsal motor nucleus of the vagus, nTS, nucleus ambiguus, central gray matter, Edinger-Westphal nucleus, pedunculopontine tegmental nucleus, nucleus of the locus coeruleus and parabrachial nucleus Zheng et al. Thus, separate groups of cytoarchitecturally distinct neurons in the PVN project to the posterior pituitary, median eminence, and to autonomic control nuclei in the brainstem and spinal cord, and modulate cardio-sympatho, visceral, respiratory, and behavioral responses Sawchenko ; Sawchenko and Swanson a ; Swanson and Mogenson A schematic diagram showing afferent and efferent neural pathways to and from the PVN.

In addition, PVN neurons project to the rostral ventral respiratory column and hypoglossal nucleus regulating the respiratory drive and genioglossal muscle activity respectively. The A1 and C1, the A2 and C2, as well as the A6 cell groups the locus coeruleus provide almost all of the noradrenergic and adrenergic innervation to the PVN Berk and Finkelstein ; Palkovits et al.

In the magnocellular division of the PVN, noradrenergic fibers terminate only on vasopressin-containing cell bodies, whereas serotonergic and adrenocorticotropic-stained fibers terminate preferentially on oxytocinergic cell bodies. These data indicate differential synaptic control of specific cell types even within the magnocellular subdivision of the PVN.

Angiotensin II acts as a neurotransmitter involved in the regulation of sympathetic activity of the cardiovascular system. In addition, circulating levels of angiotensin II, which increase during hemorrhage or dehydration, act centrally to release vasopressin Malvin et al. However, systemic angiotensin II does not appear to have direct access to the PVN as it neither crosses the blood-brain barrier nor enters the third ventricle by way of the choroid plexus Schelling et al.

However, this activity is blocked by kynurenic acid, a nonselective ionotropic excitatory amino acid EAA receptor antagonist Chen et al. These data indicate that the PVN has: 1 a functionally high level of inhibitory GABAergic tone, 2 tonic excitation from extrinsic synaptic input that is unmasked by GABA A receptor antagonists and 3 neurons with a resting membrane potential below threshold.

Indeed, the PVN has a dense concentration of excitatory glutamatergic nerve terminals Boudaba et al. Thus, blockade of EAA receptors reduces the bicuculline-evoked responses due to interruption of tonic excitation that is revealed on GABAergic inhibition.

Similarly, microinjection of glutamate increases the release of NO Li et al. Thus, a negative feedback, perhaps through NO facilitating GABA release within the PVN, may contribute to the maintenance of the overall balance and tone of sympathetic outflow. The PVN modulates blood flow by multiple direct and indirect pathways to sympathetic preganglionic neurons summarized in Section 2.

Studies conducted nearly fifty years ago showed that decreased hypothalamic function by either electrolytic lesions or thiopental injections depresses ventilation in anesthetized rats Redgate, Kastella and colleagues recorded respiratory-modulated neuronal activity in the anterior hypothalamus, in an area that appears to receive higher-order baroreceptor and chemoreceptor inputs.

Even though the ventilatory reflexes evoked by baroreceptor and chemoreceptor inputs do not depend on an intact hypothalamus, these investigators suggested the hypothalamus shows respiratory-modulated activity and speculated that respiratory and cardiovascular integration may occur in this portion of the hypothalamus in a similar manner to that described for the lower brainstem. In support of this interpretation, Yeh and coworkers showed direct connections between the PVN and phrenic motoneurons, and indirect connections between the PVN and brainstem bulbospinal neurons.

In addition, the activity of PVN changes during phasic respiratory events. Together, these data suggest a link between the PVN and respiratory function Kristensen et al. Activation of PVN alters cardiorespiratory function in parallel.

Electrical stimulation of the PVN in anesthetized rabbits increases respiratory rate and blood pressure Duan et al. Concomitantly, blood pressure and heart rate increased in these rabbits. These studies agree regarding the effect of PVN activation on sympatho-respiratory function. Their differences in the magnitude of the responses could be due to differences between anesthetized and conscious rats, because anesthesia appears to influence PVN-mediated responses Kannan et al.

On the other hand, these differences could also be related to activation of a different population of PVN neurons, and the stimulant used to activate the PVN neurons; for example, glutamate may activate all neurons in the PVN whereas bicuculline only activates those neurons tonically inhibited by GABA. Nevertheless both of these studies demonstrated that PVN-induced modulation on both respiration and blood pressure.

Our studies have identified two phenotypes of PVN neurons projecting to sympatho-respiratory sites in the brainstem. Most of the labelled neurons projecting to both cardiorespiratory sites were identified in the dorsal, ventral and medial parvocellular region of the PVN, regions of the PVN that are involved in autonomic control. The co-localization of axons with the neurotransmitter and receptors in these regions support that the hypothesis that vasopressin and oxytocin may be released and act as neurotransmitters in respiratory and vasomotor control nuclei Andreatta-Van Leyen et al.

Microinjections of these ligands increased respiration, blood pressure and heart rate Kc et al. Taken together, these data suggest that vasopressin and oxytocin-containing PVN neurons can affect respiratory and cardiovascular functions. Arrow indicates time of injection. AU, Arbitrary units.

As indicated earlier, PVN activation increases sympatho-respiratory activity, the mechanisms that are involved in initiating and limiting the evoked responses may depend on nitric oxide NO. Furthermore as a control experiment, these responses were not observed in the presence of an inactive isomer, D-NMMA Zhang et al.

The sympatho-excitatory response to L-NAME as well as the sympathoinhibitory response to sodium nitroprusside was attenuated by bicuculline Zhang and Patel, Note, microinjection of sodium nitroprusside into the PVN significantly decreased RSND, arterial blood pressure, and heart rate at the highest dose.

These responses were eliminated by blockade of the GABA system. An interaction between NO and GABA is dynamic and may precipitate sympathoexcitation during stressful situations, such as exposure to chronic intermittent hypoxic CIH or maternal separation.

Further, chronic stress alters the efficacy of GABA A receptors in rat hypothalamic-pituitary-adrenocortical axis Cullinan and Wolfe, However, the sympathoinhibitory effect of NO may not be limited by evoking a GABA release, but also by inhibiting release of excitatory neurotransmitters such as glutamate and angiotensin II Bains and Ferguson, ; Martin and Haywood, Activation of V 1A receptor signalling increases blood pressure and respiration Kc et al.

This is consistent with the results of Yang et al. Thus, these physiological studies complement the neuroanatomical studies indicating that under normal conditions, vasopressin may not provide an effective tonic drive to the RVLM region, at least in anesthetized animal whereas after conditioning with CIH the upregulation of receptor results in effective tonic drive to the RVLM.

Arrows indicate BIC injection. Pretreatment with d CH2 5VDAVP, a specific vasopressin antagonist, partially reduces the blood pressure response to intracerebrovascular injection of angiotensin II, suggesting vasopressin contributes to the central angiotensin II pressure responses Unger et al. Angiotensin II receptor blocker when microinjected into the RVLM region partially decreases the blood pressure Tagawa and Dampney, whereas vasopressin antagonist blunts the blood pressure responses Kc et al.

One possibility of this observed difference between these two studies could be due to unilateral verses bilateral microinjection of the blocker in the RVLM. This unilateral injection may have caused angiotensin II to evoke release of vasopressin as indicated earlier causing only partial decrease in the blood pressure response.

It appears that the excitability of RVLM-spinal vasomotor neurons depends on a number of chemically discrete synaptic inputs. Future studies with microdialysates and chemical detection using HPLC would provide valuable information about an equipotencial or differential role of vasopressin, angiotensin II or other neurotransmitters involved mediating these responses.

The PVN integrates chemosensory afferent signals Schlenker, Hypoxia stimulates carotid bodies, which via the carotid sinus nerves activate the commissural nuclei of the solitary tract nTS Swanson and Sawchenko, , and evokes an increase in sympatho-respiratory motor activity via respiratory sites Koshiya and Guyenet, In unanesthetized rats, bilateral lesions of the PVN prevent potassium cyanide KCN from evoking the chemoreflex in spite of an intact brainstem network Olivan, Similarly in anesthetized rats, the pressor, sympathoexcitatory and respiratory responses to KCN are dependent, in part, on the PVN Reddy et al.

Furthermore, the role of the PVN in mediating chemoreflex may be specific for hypoxic but not for hypercapnic stimulation. The PVN neurotransmission blockade with lidocaine has no effect on hypercapnia-induced central chemoreflex responses indicating that the PVN is not needed for modulating cardiopulmonary and RSNA responses to hypercapnia.

In summary, the role of the PVN may be selective for processing sympathoexcitatory and ventilatory responses evoked by the peripheral but not central chemoreflex. PVN neurons exhibit marked biochemical plasticity in response to stress Boudaba et al. Indeed, a decrease in GABAergic mechanisms in the PVN is related to the pathogenesis of a variety of clinical manifestations related to increased sympathetic nerve activity Haywood et al. Conceivably, bicuculline microinjection in the PVN induces release of glutamate which could increase sympathetic nerve activity Li et al.

However, changes in the other excitatory neurotransmitters such as glutamate Herman et al. Kc and HL to T. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

National Center for Biotechnology Information , U. Respir Physiol Neurobiol. Author manuscript; available in PMC Nov Prabha Kc 1 and Thomas E. Dick 2. Thomas E. Author information Copyright and License information Disclaimer.

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