Biochemical and biological characterization of the venoms of Bothriopsis bilineata and Bothriopsis taeniata (Serpentes: Viperidae).

Snake venom is a complex mixture containing diverse protein components with different structures and functions that are used for prey immobilization and death. Snake venoms from the family Viperidae cause pronounced local and systemic effects, such as pain, edema, hemorrhage and necrosis. Here, we investigated the enzymatic and biological activities of venoms from two Amazonian snakes, Bothriopsis bilineata and Bothriopsis taeniata.

Glucose and lactate utilization by the amygdala of male and female rats.

Gonadal hormones appear to modulate brain energy metabolism, and morphological and functional sexual differences are found in the amygdaloid complex (AC) of rats. Our aim was to study the CO2 production and lipid synthesis, measured by the rate of L-[U-14C]lactate or D-[U-14C]glucose utilization (in pmol x hr(-1) x mg(-1)), by AC slices in vitro of male and female rats. Lactate was more used than glucose as energy substrate (p < 0.

Unique Ca(2+)-activated ATPase in the nervous ganglia of Phyllocaulis soleiformis (Mollusca).

Nucleotide-metabolizing enzymes play important roles in the regulation of intracellular and extracellular nucleotide levels. We studied ATPase activity in the nervous ganglia of Phyllocaulis soleiformis, a terrestrial slug. The ATPase was divalent cation-dependent, with a maximal rate for ATP hydrolysis at pH 6.

Role of hippocampal NO in the acquisition and consolidation of inhibitory avoidance learning.

Nitric oxide (NO), an unconventional neurotransmitter in the brain, has been postulated as a retrograde intercellular messenger necessary for the induction, but not the maintenance phase, of activity-dependent forms of synaptic plasticity in the hippocampus. Here we report on the effects of an inhibitory avoidance learning task on hippocampal NO synthase (NOS) activity and on the effects of intrahippocampal infusion of a NOS inhibitor in the acquisition and consolidation of this task in rats. NOS activity increases by 45% in the hippocampus immediately after training (0 min) but not at 60 min after training.

Memory enhancement by intrahippocampal, intraamygdala, or intraentorhinal infusion of platelet-activating factor measured in an inhibitory avoidance task.

Platelet-activating factor (PAF; 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine), which is thought to be a retrograde messenger in long-term potentiation (LTP), enhances glutamate release and LTP through an action on presynaptic nerve endings. The PAF antagonist BN 52021 blocks CA1 LTP in hippocampal slices, and, when infused into rat dorsal hippocampus pre- or posttraining, blocks retention of inhibitory avoidance. Here we report that memory is affected by pre- or posttraining infusion of the PAF analog 1-O-hexadecyl-2-N-methylcarbamoyl-sn-glycerol-3-phosphocholine (mc-PAF) into either rat dorsal hippocampus, amygdala, or entorhinal cortex.

Experiments suggesting a role for nitric oxide in the hippocampus in memory processes.

Nitric oxide (NO) has been proposed to be involved in the induction of long-term potentiation (LTP) and in other processes. When coupled with weak tetanic stimulation, NO produces a long-term synaptic enhancement on its own. N-Nitroarginine (NO-Arg) inhibits NO-synthase, the enzyme that produces NO, and blocks LTP in hippocampal slices.

Evidence for the involvement of hippocampal CO production in the acquisition and consolidation of inhibitory avoidance learning.

Carbon monoxide (CO), produced through the action of haem oxygenase (HO) isoenzymes, has been recently postulated as a retrograde messenger in the early stages of long-term potentiation (LTP). In the present study, rats submitted to an inhibitory avoidance task there is a significant increase (+76%) in hippocampal HO activity immediately after training (0 min), but not at 60 min post-training. No changes were observed in cerebral cortical and cerebellar HO activity.

Intrahippocampal, but not intra-amygdala, infusion of an inhibitor of heme oxygenase causes retrograde amnesia in the rat.

Zinc protoporhyrin-9 (ZnPP) is an inhibitor of heme oxygenase, the enzyme involved in the biosynthesis of carbon monoxide (CO). CO regulates the activity of glutamatergic synapses and has been proposed to play a role in the early phases of long-term potentiation. The present paper reports on the effect of ZnPP on memory of inhibitory avoidance and of habituation to a novel environment.

Effect of antagonists of platelet-activating factor receptors on memory of inhibitory avoidance in rats.

Platelet-activating factor (PAF) is present in the brain. It enhances glutamate release and long-term potentiation (LTP) through an action on synaptic membrane receptors sensitive to the antagonist, BN 52021, and has been proposed as a retrograde messenger in the genesis of LTP. In addition, PAF has other, metabolic actions mediated by microsomal receptors sensitive to the antagonist, BN 50730.

Intrahippocampal or intraamygdala infusion of KN62, a specific inhibitor of calcium/calmodulin-dependent protein kinase II, causes retrograde amnesia in the rat.

We investigated the effect of a bilateral post-training intracerebral infusion of KN62, a specific inhibitor of calcium/calmodulin-dependent protein kinase II (CaM-II), on memory. This enzyme plays a crucial role in the early phases of long-term potentiation. Male Wistar rats were implanted bilaterally with cannulae aimed at the CA1 region of the dorsal hippocampus or at the junction between the central and the basolateral nuclei of the amygdala.

Chronic ethanol ingestion selectively affects memory modulation in rats.

Post-training treatment alters memory by different mechanisms. Naloxone enhances memory by antagonism of endogenous beta-endorphin-induced state dependency. Epinephrine facilitates consolidation at low doses and generates state dependency at high doses.

Gamma-endorphin affects retrieval of an inhibitory avoidance task.

Rats were trained in a step-down inhibitory avoidance task and retrieval was measured during a test session conducted 24 h after training. The ip administration of a low dose of gamma-endorphin (0.2 micrograms/kg) immediately after training reduced retrieval time from 40.