n(6)-cyclohexyladenosine and Hypoglycemia

Glucose deprivation produced neuronal degeneration of CA1 pyramidal neurons in hippocampal slice cultures. The effects of the adenosine agonist cyclohexyladenosine (CHA) and antagonist cyclopentylxanthine (CPX) on CA1 neuronal loss following hypoglycemia was examined using propidium iodide fluorescence as an indicator of cell death. The intensity of propidium iodide fluorescence in hippocampal area CA1 was quantified using Optimas image analysis software. Following 2 or 3 h of glucose deprivation, CPX significantly enhanced injury in the CA1 region while CHA provided significant protection. These results suggest that adenosine plays an important role in endogenous neuronal protection during hypoglycemic injury, and also supports a role for the use of adenosine agonists as neuroprotective agents.

Topics: Adenosine; Animals; Cell Survival; Glucose; Hippocampus; Hypoglycemia; Nerve Degeneration; Organ Culture Techniques; Pyramidal Cells; Rats; Rats, Sprague-Dawley; Xanthines

Electrophysiological recordings were made from rat hippocampal slices exposed to in vitro ischemic conditions in which the superfused medium is hypoxic and lacking glucose. Under these conditions, the evoked population spike recorded in CA1 is initially depressed and then transiently returns prior to an anoxic depolarization. This transient return in synaptic function under ischemic-like conditions also occurs if the population spike is inhibited by pretreatment with adenosinergic agonists or with the gamma-aminobutyric acid (GABA)B agonist, baclofen.

Topics: Adenosine; Animals; Baclofen; Brain Ischemia; Cell Hypoxia; Electric Stimulation; Electrophysiology; Hippocampus; Hypoglycemia; In Vitro Techniques; Male; Rats; Rats, Inbred Strains; Synapses; Synaptic Transmission