Effect of ischaemia & aglycaemia on the synaptic transmission in neonatal rat spinal cord in vitro.
OBJECTIVE
In vitro models of anoxia have revealed severe changes in neuronal functions after ischaemia but not after aglycaemia, although hypoglycaemia produced severe neuronal dysfunctions sometimes leading to coma. The present study was therefore undertaken to examine and compare the effects of aglycaemia with that of ischaemia on synaptic transmission in vitro.


METHODS
Spinal cord from the neonatal rat was isolated, hemisected and placed in a chamber perfused with standard physiological solution. The stimulation of a dorsal root elicited monosynaptic (MSR) and polysynaptic (PSR) reflex potentials in the segmental ventral root. The effects of suprefusing glucose free medium (aglycaemia) and superfusing glucose free and O2 free medium (ischaemia) were examined on these reflexes.


RESULTS
Superfusion of aglycaemic solution did not alter the magnitude of MSR or PSR in the first 15 min and subsequently there was a time-dependent depression of the reflexes (P < 0.05). The ischaemic solution depressed the reflexes in a time-dependent manner from the very beginning. The 50 per cent depression of the reflexes occurred around 25 and 15 min, for aglycaemia and ischaemia, respectively. In the presence of Mg2+, the aglycaemia-induced depression of MSR was completely blocked but the ischaemic response was attenuated partially as the reflex was abolished by 80 min.


CONCLUSIONS
The results of the present study indicate that the aglycaemia and ischaemia depressed the synaptic transmission to the same extent though there were differences in their onset and progress. Aglycaemia involves N-methyl-D-aspartate (NMDA) receptor-dependent (Mg2+ sensitive) mechanism, while ischaemia-induced depression involves other mechanisms in addition to NMDA.
Jha
Archana
A
Department of Physiology, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India.
Dasgupta
S
S
Deshpande
S B
SB
D000818:Animals; D000831:Animals, Newborn; D015687:Cell Hypoxia / Q000502:physiology; D005947:Glucose / Q000378:metabolism; D005998:Glycine / Q000494:pharmacology*; D000860:Hypoxia; D007511:Ischemia; D008274:Magnesium / Q000378:metabolism / Q000494:pharmacology; D016202:N-Methylaspartate / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism; D010477:Perfusion; D051381:Rats; D013116:Spinal Cord / Q000473:pathology*; D013126:Spinal Nerve Roots / Q000473:pathology; D013569:Synapses; D009435:Synaptic Transmission; D013997:Time Factors
D016202:N-Methylaspartate; D008274:Magnesium; D005947:Glucose; D010100:Oxygen; D005998:Glycine