scholarly journals Frequency-dependent disynaptic inhibition in the pyramidal network: a ubiquitous pathway in the developing rat neocortex

2009 ◽  
Vol 587 (22) ◽  
pp. 5411-5425 ◽  
Author(s):  
Thomas K. Berger ◽  
Rodrigo Perin ◽  
Gilad Silberberg ◽  
Henry Markram
Keyword(s):  
Frequency Dependent ◽  
Rat Neocortex ◽  
Disynaptic Inhibition ◽  
Developing Rat

Hypoxia preferentially destroys GABAergic neurons in developing rat neocortex explants in culture

1988 ◽  
Vol 100 (2) ◽  
pp. 332-340 ◽  
Author(s):  
H.J. Romijn ◽  
J.M. Ruijter ◽  
P.S. Wolters
Keyword(s):  
Gabaergic Neurons ◽  
Rat Neocortex ◽  
Developing Rat

scholarly journals Coupling between neurons of the developing rat neocortex

1983 ◽  
Vol 3 (4) ◽  
pp. 773-782 ◽  
Author(s):  
BW Connors ◽  
LS Benardo ◽  
DA Prince
Keyword(s):  
Rat Neocortex ◽  
Developing Rat

Hypoxia-Induced Dysfunction in Developing Rat Neocortex

1997 ◽  
Vol 78 (3) ◽  
pp. 1212-1221 ◽  
Author(s):  
Heiko J. Luhmann ◽  
Thomas Kral
Keyword(s):  
Spreading Depression ◽  
Age Groups ◽  
Field Potential ◽  
Oxygen Deprivation ◽  
Synaptic Function ◽  
Adult Age ◽  
Enhanced Sensitivity ◽  
Anoxic Depolarization ◽  
Rat Neocortex ◽  
Developing Rat

Luhmann, Heiko J. and Thomas Kral. Hypoxia-induced dysfunction in developing rat neocortex. J. Neurophysiol. 78: 1212–1221, 1997. Neocortical slices from young [postnatal day (P) 5–8], juvenile (P14–18), and adult (>P28) rats were exposed to long periods of hypoxia. Field potential (FP) responses to orthodromic synaptic stimulation, the extracellular DC potential, and the extracellular Ca2+concentration ([Ca2+]o] were measured simultaneously in layers II/III of primary somatosensory cortex. Hypoxia caused a 42 and 55% decrease in the FP response in juvenile and adult cortex, respectively. FP responses recorded in slices from young animals were significantly more resistant to oxygen deprivation as compared with the juvenile ( P < 0.01) and adult age group ( P < 0.001) and declined by only 3% in amplitude. In adult cortex, hypoxia elicited, after 7 ± 4.5 min (mean ± SD), a sudden anoxic depolarization (AD) with an amplitude of 14 ± 6 mV and a duration of 0.89 ± 0.28 min at half-maximal amplitude. Although the AD onset latency was significantly longer in P5–8 (12.5 ± 4.9 min, P < 0.001) and P14–18 (8.7 ± 3.2 min, P < 0.002) cortex, the amplitude and duration of the AD was larger in young (45.7 ± 7.6 mV, 2.19 ± 0.71 min, both P < 0.001) and juvenile animals (29.9 ± 9.1 mV, P < 0.001, 0.96 ± 0.26 min, P > 0.05) when compared with the adults. The hypoxia-induced [Ca2+]odecrease was significantly ( P < 0.002) larger in young cortex (1,115 ± 50 μM) as compared with the adult (926 ± 107 μM). Prolongation of hypoxia after AD onset for >5 min elicited in young and juvenile cortex a long-lasting AD with an amplitude of 40.5 mV associated with a decrease in [Ca2+]oby >1 mM. On reoxygenation, only slices from these age groups showed spontaneous repetitive spreading depression in 3 out of 26 cases. In adults, the same protocol caused a significantly ( P < 0.05) smaller and shorter AD and never a spreading depression. However, recovery in synaptic transmission after this long-term hypoxia was better in young and juvenile cortex, indicating a prolonged or even irreversible deficiency in synaptic function in mature animals. Application of ketamine caused a 49% reduction in the initial amplitude of the AD in juvenile cortex but did not significantly affect the AD in slices from adult animals. These data indicate that the young and juvenile cortex tolerates much longer periods of oxygen deprivation as compared with the adult, but that a sufficiently long hypoxia causes severe pathophysiological activity in the immature cortex. This enhanced sensitivity of the immature cortex is at least partially mediated by activation of N-methyl-d-aspartate receptors.

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