scholarly journals Selective Loss and Selective Sparing of Neurons in the Thalamic Reticular Nucleus following Human Cardiac Arrest

1993 ◽  
Vol 13 (4) ◽  
pp. 558-567 ◽  
Author(s):  
Douglas T. Ross ◽  
David I. Graham
Keyword(s):  
Cardiac Arrest ◽  
Heart Surgery ◽  
Neuronal Damage ◽  
Open Heart Surgery ◽  
Thalamic Reticular Nucleus ◽  
Global Cerebral Ischemia ◽  
Reticular Nucleus ◽  
Thalamic Nuclei ◽  
Attentional Processing ◽  
Thalamic Relay Nuclei

Neurons in the portion of the human thalamic reticular nucleus (RT) associated with the prefrontal cortex and mediodorsal thalamic nuclei were found to be selectively vulnerable to ischemic neuronal damage following relatively short (≤5-min) duration cardiac arrest. In contrast, selective sparing of these RT neurons occurred in cases with longer (>10-min) duration of arrest that was sufficient to produce extensive ischemic neuronal damage throughout the cerebral cortex and thalamic relay nuclei. The selective degeneration of RT neurons appears to require the sustained activity of corticothalamic or thalamocortical projections to the RT following the ischemic insult. Loss of RT neurons associated with the frontal cortex and mediodorsal thalamus may be the biological basis of some types of persisting cognitive deficits in attentional processing experienced by patients following cardiac arrest, open heart surgery, or other forms of brief global cerebral ischemia.

Elective Cardiac Arrest in Open-Heart Surgery: Report of Three Cases

1956 ◽  
Vol 23 (2) ◽  
pp. 105-114 ◽  
Author(s):  
D. B. EFFLER ◽  
L. K. GROVES ◽  
F. M. SONES ◽  
W. J. KOLFF
Keyword(s):  
Cardiac Arrest ◽  
Heart Surgery ◽  
Open Heart Surgery ◽  
Open Heart

scholarly journals Developmental switch in the polarity of experience-dependent synaptic changes in layer 6 of mouse visual cortex

2011 ◽  
Vol 106 (5) ◽  
pp. 2499-2505 ◽  
Author(s):  
Emily Petrus ◽  
Terence T. Anguh ◽  
Huy Pho ◽  
Angela Lee ◽  
Nicholas Gammon ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Critical Period ◽  
Pyramidal Neurons ◽  
Light Exposure ◽  
Visual Deprivation ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Excitatory Synapses ◽  
Thalamic Nuclei ◽  
Developmental Age

Layer 6 (L6) of primary sensory cortices is distinct from other layers in that it provides a major cortical input to primary sensory thalamic nuclei. L6 pyramidal neurons in the primary visual cortex (V1) send projections to the lateral geniculate nucleus (LGN), as well as to the thalamic reticular nucleus and higher order thalamic nuclei. Although L6 neurons are proposed to modulate the activity of thalamic relay neurons, how sensory experience regulates L6 neurons is largely unknown. Several days of visual deprivation homeostatically adjusts excitatory synapses in L4 and L2/3 of V1 depending on the developmental age. For instance, L4 exhibits an early critical period during which visual deprivation homeostatically scales up excitatory synaptic transmission. On the other hand, homeostatic changes in L2/3 excitatory synapses are delayed and persist into adulthood. In the present study we examined how visual deprivation affects excitatory synapses on L6 pyramidal neurons. We found that L6 pyramidal neurons homeostatically increase the strength of excitatory synapses following 2 days of dark exposure (DE), which was readily reversed by 1 day of light exposure. This effect was restricted to an early critical period, similar to that reported for L4 neurons. However, at a later developmental age, a longer duration of DE (1 wk) decreased the strength of excitatory synapses, which reversed to normal levels with light exposure. These changes are opposite to what is predicted from the homeostatic plasticity theory. Our results suggest that L6 neurons differentially adjust their excitatory synaptic strength to visual deprivation depending on the age of the animals.

scholarly journals A thalamic reticular circuit for head direction cell tuning and spatial navigation

2019 ◽  
Author(s):  
Gil Vantomme ◽  
Zita Rovó ◽  
Romain Cardis ◽  
Elidie Béard ◽  
Georgia Katsioudi ◽  
...  
Keyword(s):  
Spatial Navigation ◽  
Sensory Information ◽  
Search Strategies ◽  
Retrosplenial Cortex ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Head Direction ◽  
Thalamic Nuclei

SummaryTo navigate in space, an animal must refer to sensory cues to orient and move. Circuit and synaptic mechanisms that integrate cues with internal head-direction (HD) signals remain, however, unclear. We identify an excitatory synaptic projection from the presubiculum (PreS) and the multisensory-associative retrosplenial cortex (RSC) to the anterodorsal thalamic reticular nucleus (TRN), so far classically implied in gating sensory information flow. In vitro, projections to TRN involved AMPA/NMDA-type glutamate receptors that initiated TRN cell burst discharge and feedforward inhibition of anterior thalamic nuclei. In vivo, chemogenetic anterodorsal TRN inhibition modulated PreS/RSC-induced anterior thalamic firing dynamics, broadened the tuning of thalamic HD cells, and led to preferential use of allo-over egocentric search strategies in the Morris water maze. TRN-dependent thalamic inhibition is thus an integral part of limbic navigational circuits wherein it coordinates external sensory and internal HD signals to regulate the choice of search strategies during spatial navigation.

Hypothermic Reperfusion after Cardiac Arrest Augments Brain-Derived Neurotrophic Factor Activation

2002 ◽  
Vol 22 (7) ◽  
pp. 843-851 ◽  
Author(s):  
Brian J. D'Cruz ◽  
Kristofer C. Fertig ◽  
Anthony J. Filiano ◽  
Shawn D. Hicks ◽  
Donald B. DeFranco ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Neurotrophic Factor ◽  
Mild Hypothermia ◽  
Neuronal Damage ◽  
Brain Derived Neurotrophic Factor ◽  
Global Cerebral Ischemia ◽  
Ischemia And Reperfusion ◽  
Bdnf Signaling ◽  
The Many ◽  
Asphyxial Cardiac Arrest

Induction of mild hypothermia improves neurologic outcome after global cerebral ischemia. This study measured levels of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in hippocampal tissue of rats after resuscitation from 8 minutes of normothermic, asphyxial cardiac arrest. After resuscitation, rats were maintained either at normal temperature (37°C) or cooled to mild hypothermia (33°C, beginning 60 minutes after resuscitation). After 12 or 24 hours, neurotrophin levels in hippocampus were measured by immunoblotting. Ischemia and reperfusion increased hippocampal levels of BDNF. Induction of hypothermia during reperfusion potentiated the increase in BDNF after 24 hours, but not after 12 hours. Levels of NGF were not increased by postresuscitation hypothermia. Hypothermia also increased tissue levels and tyrosine phosphorylation of TrkB, the receptor for BDNF. Increased BDNF levels were correlated with activation of the extracellularly regulated kinase (ERK), a downstream element in the signal transduction cascade induced by BDNF. In contrast to the many deleterious processes during ischemia and reperfusion that are inhibited by induced hypothermia, increasing BDNF levels is a potentially restorative process that is augmented. Increased activation of BDNF signaling is a possible mechanism by which mild hypothermia is able to reduce the neuronal damage typically occurring after cardiac arrest.

scholarly journals A METHOD FOR CONTROLLED CARDIAC ARREST AS AN ADJUNCT TO OPEN HEART SURGERY

1956 ◽  
Vol 32 (5) ◽  
pp. 604-611
Author(s):  
W. Glenn Young ◽  
Will C. Sealy ◽  
Ivan W. Brown ◽  
Wilmer C. Hewitt ◽  
Henry A. Callaway ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Heart Surgery ◽  
Open Heart Surgery ◽  
Open Heart

scholarly journals Neuronal Death in the CNS Autonomic Control Center Comes Very Early after Cardiac Arrest and Is Not Significantly Attenuated by Prompt Hypothermic Treatment in Rats

Cells ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 60
Author(s):  
Ji Hyeon Ahn ◽  
Tae-Kyeong Lee ◽  
Hyun-Jin Tae ◽  
Bora Kim ◽  
Hyejin Sim ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Cardiac Arrest ◽  
Survival Rate ◽  
Mortality Rate ◽  
Motor Neurons ◽  
Neuronal Death ◽  
Neuronal Damage ◽  
Autonomic Control ◽  
Reticular Nucleus ◽  
Fluoro Jade B

Autonomic dysfunction in the central nervous system (CNS) can cause death after recovery from a cardiac arrest (CA). However, few studies on histopathological changes in animal models of CA have been reported. In this study, we investigated the prevalence of neuronal death and damage in various brain regions and the spinal cord at early times after asphyxial CA and we studied the relationship between the mortality rate and neuronal damage following hypothermic treatment after CA. Rats were subjected to 7–8 min of asphyxial CA, followed by resuscitation and prompt hypothermic treatment. Eight regions related to autonomic control (the cingulate cortex, hippocampus, thalamus, hypothalamus, myelencephalon, and spinal cord) were examined using cresyl violet (a marker for Nissl substance) and Fluoro-Jade B (a marker for neuronal death). The survival rate was 44.5% 1 day post-CA, 18.2% 2 days post-CA and 0% 5 days post-CA. Neuronal death started 12 h post-CA in the gigantocellular reticular nucleus and caudoventrolateral reticular nucleus in the myelencephalon and lamina VII in the cervical, thoracic, lumbar, and sacral spinal cord, of which neurons are related to autonomic lower motor neurons. In these regions, Iba-1 immunoreactivity indicating microglial activation (microgliosis) was gradually increased with time after CA. Prompt hypothermic treatment increased the survival rate at 5 days after CA with an attenuation of neuronal damages and death in the damaged regions. However, the survival rate was 0% at 12 days after CA. Taken together, our study suggests that the early damage and death of neurons related to autonomic lower motor neurons was significantly related to the high mortality rate after CA and that prompt hypothermic therapy could increase the survival rate temporarily after CA, but could not ultimately save the animal.

scholarly journals Early Thalamic Injury After Resuscitation From Severe Asphyxial Cardiac Arrest in Developing Rats

2021 ◽  
Vol 9 ◽  
Author(s):  
Hoai T. Ton ◽  
Katherine Raffensperger ◽  
Michael Shoykhet
Keyword(s):  
Cardiac Arrest ◽  
Microglial Activation ◽  
Neuronal Degeneration ◽  
Ischemic Injury ◽  
Selective Vulnerability ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Severity Of Injury ◽  
Hypoxic Ischemic Injury ◽  
Asphyxial Cardiac Arrest

Children who survive cardiac arrest often develop debilitating sensorimotor and cognitive deficits. In animal models of cardiac arrest, delayed neuronal death in the hippocampal CA1 region has served as a fruitful paradigm for investigating mechanisms of injury and neuroprotection. Cardiac arrest in humans, however, is more prolonged than in most experimental models. Consequently, neurologic deficits in cardiac arrest survivors arise from injury not solely to CA1 but to multiple vulnerable brain structures. Here, we develop a rat model of prolonged pediatric asphyxial cardiac arrest and resuscitation, which better approximates arrest characteristics and injury severity in children. Using this model, we characterize features of microglial activation and neuronal degeneration in the thalamus 24 h after resuscitation from 11 and 12 min long cardiac arrest. In addition, we test the effect of mild hypothermia to 34°C for 8 h after 12.5 min of arrest. Microglial activation and neuronal degeneration are most prominent in the thalamic Reticular Nucleus (nRT). The severity of injury increases with increasing arrest duration, leading to frank loss of nRT neurons at longer arrest times. Hypothermia does not prevent nRT injury. Interestingly, injury occurs selectively in intermediate and posterior nRT segments while sparing the anterior segment. Since all nRT segments consist exclusively of GABA-ergic neurons, we asked if GABA-ergic neurons in general are more susceptible to hypoxic-ischemic injury. Surprisingly, cortical GABA-ergic neurons, like their counterparts in the anterior nRT segment, do not degenerate in this model. Hence, we propose that GABA-ergic identity alone is not sufficient to explain selective vulnerability of intermediate and posterior nRT neurons to hypoxic-ischemic injury after cardiac arrest and resuscitation. Our current findings align the animal model of pediatric cardiac arrest with human data and suggest novel mechanisms of selective vulnerability to hypoxic-ischemic injury among thalamic GABA-ergic neurons.

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