Biomedical subjects
Publications and source records attributed to C G Mallari.
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This research tested morphine and naloxone effects on evoked EEG and unit activity in 3 opiate-relevant brain areas in response to electrical stimulation of the olfactory bulb in acute, unanesthesized rat preparations. Stimulation evoked clear EEG responses in the amygdala (Amyg) and sometimes in the other areas (caudate and central grey); morphine (15 mg/kg) depressed the Amyg response in some rats, but enhanced it in others, and naloxone usually reversed both kinds of effect. Stimulation caused excitatory unit impulse reponses in the Amyg, and morphine unexpectedly increased the magnitude of the stimulus-evoked excitation; naloxone reversed this enhancement. In control rats, naloxone often decreased the Amyg evoked response. Stimulus-evoked increases in unit activity in the caudate and central grey, when they did occur, were depressed by morphine, but naxoxone had no consistent reversing effect. Both the EEG and unit data indicate that morphine excites, or disinhibits, certain neurons associated with the olfactory-Amyg pathway. There was also some evidence that this pathway contains endorphinergic elements.
Previous studies have indicated that morphine alters nerve impulse activity differently in various brain areas of intact animals. Because morphine has profound effects on visceral organs and on the spinal cord, cervically transected preparations, in which hypothermia was prevented, were used for recording spontaneous impulse activity before and for 30 min after morphine simultaneously from six regions of the brain: caudate (Cau), midbrain reticular formation (MBRF), central grey (CG), cingulate cortex (CC), hippocampus (Hip), and substantia nigra (SN). Morphine (5 and 15 mg/kg, i.p.) caused a naloxone-preventable depression of impulse activity in most brain areas. The depression was, however, especially pronounced in the CG, more so with the lower than the higher dose; naloxone completely blocked the low-dose effect. The MBRF responded with increased impulse activity after 5 mg/kg, but with depression after 15 mg/kg; naloxone blocked both responses. Activity in both the Hip and CC was depressed by the low dose of morphine, but not by the high dose; naloxone blocked the depression. Both doses of morphine generally depressed the variance in impulse activity, with a clear preferential depression of CG variance; naloxone blocked the CG variance effect, but not that of other brain areas.
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).