Cyclic nucleotides in the amygdala of the kindled rat.

The basolateral amygdala of rats was stimulated once daily until three successive fully kindled seizures were elicited. Twenty-four hours after the last seizure the rats were sacrificed by focused microwave irradiation to the head. Tissues from homolateral and contralateral amygdala and cerebral cortex were assayed for cAMP and cGMP content. No significant changes in cyclic nucleotides were measured in the kindled animals. These studies indicate that long term changes in the steady-state level of total tissue cyclic nucleotides do not occur concomitant with the persistently altered excitability associated with kindling of the amygdala.

Evidence against a role of acetaldehyde in electroencephalographic signs of ethanol-induced intoxication.

Acetaldehyde, the proximate metabolite of ethanol, when injected intravenously in rats produced electroencephalogram (EEG) changes similar to those observed after ethanol administration; that is, low doses activated the cortical EEG and higher doses caused activation followed by synchronization. However, when acetaldehyde was administered as a continuous infusion to simulate production of ethanol-derived acetaldehyde, only synchronization occurred, and then only at the higher doses. At low infusion dosage when the EEG was unaffected, concentrations of acetaldehyde in the blood were equal to or greater than those which occur during intoxication. Thus, acetaldehyde by itself cannot account for ethanol-induced EEG synchronization.

Ethanol-induced regional and dose-response differences in multiple-unit activity in rabbits.

Multiple-unit activity (MUA), recorded simultaneously from many brain areas, was used to detect the existence ahd location of "target sites" for ethanol action in rabbits with chronically implanted electrodes in 14 areas. Each of 12 rabbits received intraperitoneal injection of 300, 600, 900, and 1200 mg/kg of 20% ETOH and a saline control injection given in random order with at least a 4-day interval between injections. Large amounts of MUA data, recorded continuously for a 2-min pre-injection control period and a 15-min post-injection period, were quantified by a sensitive and unique technique. MUA changes did not correlate with alcohol-induced changes in the corresponding EEG for the same locus. Whereas visual inspection of the EEG did not disclose any regional differences in response to ethanol, both temporal and topographical differences in ethanol effect on MUA were observed. There were 14 histologically verified brain areas with adequate sample size for statistical evaluation of MUA response. At high doses, all brain areas were affected. Included among the brain areas which were least affected by low doseas were the caudate nucleus, septum, fornix, and medial forebrain bundle. Those areas that met the criteria for target sites of responding quickly (less than 5 min) to low doses (300 mg/kg) were: cerebellar cortex, cerebral cortex, hippocampus, lateral and medial geniculate nuclei, midbrain reticular formation, and pyriform cortex. In conjunction with the preliminary study [Brain Res. 70, 361 (1974], the data indicate that the most ethanolsensitive tissue is found in the various kinds of cortex, cerebellar and cerebral (both paleocortex and neocortex).

EEG evaluation of humaneness of asphyxia and decapitation euthanasia of the laboratory rat.

The relative humaneness of asphyxia and decapitation was objectively evaluated in rats by EEG monitoring. EEG activation (low voltage, fast activity) was considered to indicate discomfort, pain, and affective responses to euthansia. Such activation was present 37.3 plus or minus 7.5 sec after asphyxia and 13.6 plus or minus 4,6 sec after decapitation. Decapitation was also characterized by an immediate large, and relatively long-lasting, ultra-slow voltage, detected by non-polarizable scalp electrodes. Isoelectric activity (death) occurred 69.4 plus or minus 9.9 sec after onset of asphyxia and 27.2 plus or minus 4.4 sec after decapitation.