EPSPS variability, gene expression, and enzymatic activity in glyphosate-resistant biotypes of Digitaria insularis.

Weed resistance to herbicides is a natural phenomenon that exerts selection on individuals in a population. In Brazil, glyphosate resistance was recently detected in Digitaria insularis. The objective of this study was to elucidate mechanisms of weed resistance in this plant, including genetic variability, allelism, amino acid substitutions, gene expression, and enzymatic activity levels. Most of these have not previously been studied in this species. D. insularis DNA sequences were used to analyze genetic variability. cDNA from resistant and susceptible plants was used to identify mutations, alleles, and 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS) expression, using real-time quantitative reverse transcription-polymerase chain reaction. In addition, EPSPS activity was measured. We found a decrease in genetic variability between populations related to glyphosate application. Substitutions from proline to threonine and tyrosine to cysteine led to a decrease in EPSPS affinity for the glyphosate. In addition, the EPSPS enzymatic activity was slightly higher in resistant plants, whereas EPSPS gene expression was almost identical in both biotypes, suggesting feedback regulation at different levels. To conclude, our results suggest new molecular mechanisms used by D. insularis to increase glyphosate resistance.

Fragmentation of extracellular DNA by long-term exposure to radiation from uranium in aquatic environments.

Persistent harmful scenarios associated with disposal of radioactive waste, high-background radiation areas and severe nuclear accidents are of great concern regarding consequences to both human health and the environment. Of particular concern is the extracellular DNA in aquatic environments contaminated by radiological substances. Strand breaks induced by radiation promote decrease in the transformation efficiency for extracellular DNA. The focus of this study is the quantification of DNA damage following long-term exposure (over one year) to low doses of natural uranium (an alpha particle emitter) to simulate natural conditions, since nothing is known about alpha radiation induced damage to extracellular DNA. A high-resolution Atomic Force Microscope was used to evaluate DNA fragments. Double-stranded plasmid pBS as a model for extracellular DNA was exposed to different amounts of natural uranium. It was demonstrated that low concentrations of U in water (50 to 150 ppm) produce appreciable numbers of double strand breaks, scaling with the square of the average doses. The importance of these findings for environment monitoring of radiological pollution is addressed.

Characterization of chloroplast DNA microsatellites from Saccharum spp and related species.

Microsatellites, or simple sequence repeats (SSRs), and their flanking regions in chloroplast genomes (plastomes) of some species of the family Poaceae were analyzed in silico to look for DNA sequence variations. Comparison of the complete chloroplast DNA sequences (cpDNAs) of sugarcane (Saccharum hybrid cv. SP-80-3280 and S. officinarum cv. NCo310) and related species, Agrostis stolonifera, Brachypodium distachyon, Hordeum vulgare subsp vulgare, Lolium perenne, Oryza nivara, O. sativa subsp indica, O. sativa subsp japonica, Sorghum bicolor, Triticum aestivum, Zea mays, and Z. mays cv. B73, allowed us to examine the organization of chloroplast SSRs (cpSSRs) in genic and intergenic regions. We identified 204 cpSSRs in the sugarcane cpDNA; 22.5% were in genic regions. The ndh, rps, trn, and rpl gene clusters of the chloroplasts had the most repeats. Mononucleotide repeats were the most abundant cpSSRs in these species; however, di-, tri-, tetra-, penta-, and hexanucleotide repeats were also identified. Many base substitutions and deletions/insertions were identified in the cpSSR loci and their flanking regions. Multiple alignments of all cpSSR sequences of Poaceae species made identification of nucleotide variability possible; repeat motifs are not uniformly distributed across the Poaceae plastomes, but are mostly confined to intergenic regions. Phylogeny was determined by maximum parsimony and neighbor-joining inference methods. The cpSSRs of these species were found to be polymorphic. It appears that individual cpSSRs in the Poaceae are stable, at least over short periods of evolutionary time. We conclude that the plastome database can be exploited for phylogenetic analysis and biotechnological development.

Gene expression profile of the plant pathogen Fusarium graminearum under the antagonistic effect of Pantoea agglomerans.

The pathogenic fungus Fusarium graminearum is an ongoing threat to agriculture, causing losses in grain yield and quality in diverse crops. Substantial progress has been made in the identification of genes involved in the suppression of phytopathogens by antagonistic microorganisms; however, limited information regarding responses of plant pathogens to these biocontrol agents is available. Gene expression analysis was used to identify differentially expressed transcripts of the fungal plant pathogen F. graminearum under antagonistic effect of the bacterium Pantoea agglomerans. A macroarray was constructed, using 1014 transcripts from an F. graminearum cDNA library. Probes consisted of the cDNA of F. graminearum grown in the presence and in the absence of P. agglomerans. Twenty-nine genes were either up (19) or down (10) regulated during interaction with the antagonist bacterium. Genes encoding proteins associated with fungal defense and/or virulence or with nutritional and oxidative stress responses were induced. The repressed genes coded for a zinc finger protein associated with cell division, proteins containing cellular signaling domains, respiratory chain proteins, and chaperone-type proteins. These data give molecular and biochemical evidence of response of F. graminearum to an antagonist and could help develop effective biocontrol procedures for pathogenic plant fungi.

Stable genetic transformation of tomato plastids and expression of a foreign protein in fruit.

Transgenic chloroplasts offer unique advantages in plant biotechnology, including high-level foreign protein expression, absence of epigenetic effects, and gene containment due to the lack of transgene transmission through pollen. However, broad application of plastid genome engineering in biotechnology has been largely hampered by both the lack of chloroplast transformation systems for major crop plants and the usually low plastid gene expression levels in nongreen tissues such as fruits, tubers, and other storage organs. Here we describe the development of a plastid transformation system for tomato, Lycopersicon esculentum. This is the first report on the generation of fertile transplastomic plants in a food crop with an edible fruit. We show that chromoplasts in the tomato fruit express the transgene to approximately 50% of the expression levels in leaf chloroplasts. Given the generally very high foreign protein accumulation rates that can be achieved in transgenic chloroplasts (>40% of the total soluble protein), this system paves the way to efficient production of edible vaccines, pharmaceuticals, and antibodies in tomato.

Effects of estrogen on neuronal growth and differentiation.

Previous work from our laboratory has shown that in cultures of hypothalamic neurons obtained from male fetuses at embryonic day 16 the axogenic response to estradiol (E2) is contingent upon culture with medium conditioned by astroglia from a target region for hypothalamic axons. E2 also induced increased levels of TrkB that were necessary for the axonal growth to occur. This convergence between estrogenic and neurotrophic signals prompted investigation of the mitogen activated protein kinase (MAPK) cascade. Analysis of the temporal course of MAPK activation showed increased levels of phosphorylated ERK up to 60 min after E2 exposure, with a maximal response at 5-15 min. UO126 (specific inhibitor of MEK 1/2) blocked E2 induced axonal elongation and ERK phosphorylation, confirming the involvement of ERK in the neuritogenic effect of E2. The membrane impermeable construct E2-BSA proved as effective as free E2 to induce axon elongation, suggesting that E2 exerted its effect through a membrane-associated receptor. This possibility received additional support from experiments showing that E2-BSA also increased ERK phosphorylation with the same time course than E2. These results indicate that ERK signaling is necessary for E2 to induce axon growth and this activation is mediated by a membrane bound estrogen receptor.

Cholecystokinin, dopamine D2 and N-methyl-D-aspartate binding sites in the nucleus of the solitary tract of the rat: possible relationship to ingestive behavior.

Receptor autoradiography was used to investigate the distribution of brainstem binding sites for cholecystokinin, dopamine and N-methyl-D-aspartate with particular reference to the nucleus of the solitary tract of the rat, an area involved in the control of ingestive behavior. Binding sites for the A and B subtypes of the cholecystokinin receptor, labeled with [(125)I]cholecystokinin octapeptide sulfate in the presence or absence of antagonists for the devazepide (A) or L-365,260 (B) receptor, were present throughout the caudal rostral extent of the nucleus of the solitary tract, the A type predominating in the commissural, medial and gelatinous part and the B type in the lateral part. In the most rostral part of the medial nucleus of the solitary tract, both A and B receptors were present. Dopamine D2 receptors, labeled with [(125)I]NCQ-298, were found in all parts of the nucleus of the solitary tract. No binding to the dopamine D1 receptor, labeled with [(125)I]SCH-23982, was found in the brainstem. N-Methyl-D-aspartate receptors, labeled with [(3)H]dizocilpine maleate, were also present in the entire caudorostral extent of the nucleus of the solitary tract. Binding to cholecystokinin A receptors was co-distributed with [(125)I]NCQ-298 and [(3)H]dizocilpine maleate binding in the caudal and rostral parts of the nucleus of the solitary tract, and binding to cholecystokinin B receptors overlapped with [(125)I]NCQ-298 and [(3)H]dizocilpine maleate binding in the rostral nucleus of the solitary tract. These results are consistent with the hypothesis that cholecystokinin, dopamine and glutamate interact in the nucleus of the solitary tract in the control of ingestive behavior.

Peripeduncular lesion alters expression of c-fos induced in the female rat brain by male mounting.

In order to investigate the role of the peripeduncular nucleus (PP) in the control of lordosis in female rats, activation of neurons after mounts without intromission was investigated by means of FOS immunoreactivity (FOS-IR). Ovariectomized rats were injected with estradiol and progesterone and submitted to approximately 50 mounts by the male. The vaginal area was covered with masking tape to prevent intromission and vaginocervical stimulation. This limited stimulation produced FOS-IR in the ventrolateral division of the ventromedial hypothalamic nucleus (VMHVL), in the lateral periaqueductal grey (LPAG), in the peripeduncular nucleus (PP), and in the posterior intralaminar thalamic nucleus (PIL). No significant differences were found in the anterodorsal or posterodorsal parts of the medial amygdaloid nucleus, in the medial part of the medial preoptic nucleus, in the dorsomedial periaqueductal grey and in the medial division of the posterointermediate part of the bed nucleus of the stria terminalis. The same experiment was performed in rats with unilateral lesion of the PP. Both VMHVL and LPAG activation were significantly reduced in the ipsilateral PP lesion side, leading to the conclusion that those structures are primary targets for the somatic stimuli that trigger lordotic reflexes and which are relayed in the PP. Taking into account what is known about the function of the target structures, it is proposed that afferences relayed in the PP reaching the VMHVL would contribute to control the long range level of sexual receptivity, whereas stimuli reaching the LPAG would serve to control lordotic responses in a moment to moment fashion.

Glutamate inhibits ingestive behaviour.

Male rats treated with reserpine were motionless and ingested only a few of ten consecutive intraoral injections of a 1 M solution of sucrose. While injection of apomorphine, a dopamine agonist, stimulated locomotion and stereotyped sniffing in reserpinized rats, it did not reactivate ingestive responses. The non-competitive N-methyl-D-aspartate receptor antagonist MK801, however, stimulated locomotion as well as ingestion suggesting involvement of glutamate in the suppressive effect of resperpine on ingestive responses. A series of experiments was therefore undertaken to investigate the possible physiological role of glutamate in feeding. For this purpose, we used Grill's intraoral intake test, in which the rat is infused intraorally with a sucrose solution and the amount ingested measured. In untreated rats, MK801 dose-dependently facilitated ingestion of the sucrose solution and antagonized inhibition of ingestion by cholecystokinin octapeptide. Administration of cholecystokinin octapeptide or ingestion of sucrose increased the concentration of glutamate in the nucleus of the solitary tract, a brain stem relay transmitting sensory information from the gastrointestinal tract to the forebrain. MK801 was found to bind specifically to this brain area and block the elevation of glutamate and dopamine levels which occurred after treatment with cholecystokinin octapeptide in this neural site. Together these data suggest that dopamine and glutamate may interact within the nucleus of the solitary tract in controlling ingestive behaviour.

Neurotrophic factors and estradiol interact to control axogenic growth in hypothalamic neurons.

Previous work from our laboratory has shown that in cultures of hypothalamic neurons obtained from male fetuses at embryonic day 16, the axogenic response to estrogen (E2) is contingent on coculture with target glia or target glia-conditioned media (CM). Neither the estrogen receptor blockers tamoxifen nor ICI 182,780 prevented the axogenic effects of the hormone. Estradiol made membrane-impermeable by conjugation to a protein of high molecular weight (E2-BSA) preserved its axogenic capacity, suggesting the possibility of a membrane effect responsible for the action of E2. Western blot analysis of extracts from homogenates of cultured neurons grown with E2 and CM from target glia had more TrkB than cultures with CM alone or E2 alone. To further investigate the interaction between E2 and the neurotrophin receptors, we used a specific antisense oligonucleotide (AS) to prevent the estradiol-induced increase of TrkB. The effect of E2 was suppressed in cultures in which TrkB was down-regulated by the AS, showing decreased axonal elongation when compared with neurons treated with E2 without AS or with sense TrkB. In cultures grown with AS, the axonal length of E2-treated cultures was not different from cultures without E2. Evidence suggesting cross-talk between E2 and neurotrophic factor(s) prompted investigation of signaling along the MAPK cascade. Immuno blotting of E2-treated cultures showed increased levels of phosphorylated ERK1 and ERK2. UO126 but not LY294002 blocked E2-induced axonal elongation, suggesting that the MAPKs are involved in this response.

Pathways conducting amygdaloid influence on feminine sexual behavior in the rat.

In ovariectomized female rats primed with estradiol benzoate and progesterone, electrochemical stimulation of medial amygdaloid nucleus, anterior part ( AMEa ), increased lordotic frequency, but this effect was not found in rats with transection of the stria terminalis (ST) or the ventral amygdalofugal pathways ( VAF ). On the other hand, the decrease in lordotic frequency observed after stimulation of the posterior part of the lateral amygdaloid nucleus (ALp), persisted in animals with transection of the VAF , but was eliminated in animals with section of the ST. The effect of transecting these pathways on the multiunit and field responses evoked in the hypothalamic ventromedial nucleus (VMN) by stimulation of both amygdaloid nuclei was also studied. Responses evoked by AMEa stimulation were smaller or disappeared after lesion of either the ST or the VAF , but responses evoked by ALp stimulation were affected by lesion of the ST only. Findings are interpreted as suggesting that the ST conducts activity originating in AMEa and ALp which affects sexual receptivity in a complementary fashion, whereas VAF contains AMEa originated fibers whose activation increase receptivity. These behavioral effects may be the consequence of modulatory action on VMN neuronal activity.

Gamma aminobutyric acid mediates ventromedial hypothalamic mechanisms controlling the execution of lordotic responses in the female rat.

To study the participation of gamma-aminobutyric acid (GABA) in the control of sexual behavior in the female rat, the effect of GABA and picrotoxin injections in the ventromedial hypothalamic nucleus (VMN) upon lordosis frequency and multiunit spike activity (MUSA) was determined. Infusion of 100 micrograms GABA into conscious rats reduced lordotic responsiveness within 15 min after injection; with a similar time course, the same dose markedly reduced MUSA in urethane anesthetized rats. Forty-five min after injection lordotic responsiveness recuperated to preinjection levels; at this time MUSA showed a rebound increase in neuron firing frequency. The possible relation between ventromedial hypothalamic neuronal activity and capacity for lordotic responses was further tested with injections of a local anesthetic: 1 microliter of 2% Xylocaine infused into the VMN produced similar results, suppressing MUSA and lordotic responsiveness for ca. 45 min beginning immediately after injection. Microinjections of GABA antagonist picrotoxin had the opposite effects: 0.1 microgram increased MUSA and lordotic responsiveness at 5 and 45 min; however at 20 min, when MUSA was at its highest, lordosis frequency was not elevated. Injections of solvent had no consistent effects on either measure. Two conclusions many be tentatively drawn from these data: (a) the VMN is the origin of a neural signal which exerts a moment-to-moment gating control on the execution of lordosis, and (b) the generation and/or the output of this signal is under the control of a GABAergic hypothalamic mechanism which normally exerts an inhibitory effect on the display of lordotic responses.

Ultrastructural changes in the hypothalamic ventromedial nucleus of ovariectomized rats after estrogen treatment.

The changes produced in the hypothalamic ventromedial nucleus (VMN) of ovariectomized rats after administration of 100 microgram estradiol benzoate/kg body weight were studied using light and electron microscopy. Quantitative morphometric studies included number and size of VMN neurons and nuclei, size and density of terminals and synaptic contacts, spine-to-shaft ratio of postsynaptic elements and relative frequency of two types of synaptic vesicles. Evidence was obtained favoring the concept of heterogeneous composition of the VMN: in ovariectomized animals many cells appeared in a state of quiescence, but other neurons showed no major alterations. Estrogen administration to ovariectomized rats produced evidence of metabolic stimulation such as increase in rough surfaced endoplasmic reticulum, condensation of nucleolar material, enlarged Golgi and presence of pleomorphic mitochondria. The number of neurons in the VMN was not modified by estrogen treatment; however, neuron soma and nuclei were larger. In the ventrolateral division of the VMN terminals and synaptic contacts per unit area were increased after estrogen treatment, but synaptic contact length, terminal size and spine-to-shaft ratio were not modified. The possibility that the differences observed may be consequent to changes in synaptic organization of the VMN related to its estrogen-dependent functions is discussed.

Investigation of peripeduncular-hypothalamic pathways involved in the control of lordosis in the rat.

Single shock stimuli applied to the peripeduncular nucleus (PPN) elicited a complex evoked response in the hypothalamic ventromedial nucleus (VMN). An early component and a late component could be distinguished in the evoked response on the basis of their different latency, threshold, site of maximal amplitude, frequency-response characteristics and also because restricted lesions eliminated specifically the short-or the long-latency components. Transection of the dorsal supraoptic pathway immediately in front of the PPN suppressed all the VMN-evoked responses. The same lesion eliminated lordotic responses in ovariectomized rats treated with estradiol benzoate and progesterone. Similar lesions placed more dorsally had no effect on either the sexual behavior or the evoked response. Evidence was obtained suggesting that the short-latency component is generated by activity that reaches the VMN directly through the ventral supraoptic commissure, while the long-latency response involves substations in the amygdala and the bed nucleus of the stria terminalis. The effect of lesions on the performance of lordosis may be attributed to the disruption of ascending and/or descending neural impulses circulating between the PPN and the VMN, with relay stations in the amygdala and the bed nucleus of the stria terminalis.

Estrogen facilitates induction of long term potentiation in the hippocampus of awake rats.

In order to test the hypothesis that circulating levels of estrogen modulate synaptic plasticity in the hippocampus, we have studied the induction of long term potentiation (LTP) in awake rats. Ovariectomized animals, chronically implanted with a recording electrode in the cell body layer of CA1 and a stimulating electrode in stratum radiatum, were used to record evoked field potentials (population spike (PS) and summed EPSP) daily for at least 4 days before injection of sesame oil or 100 microg of estradiol benzoate per kg b.w. (E2). Basal levels of response to single square pulses (0.01 ms pulse width) delivered at 0.05 Hz through the stimulating electrode were recorded daily for 2 days after injection. To induce LTP a high-frequency 'theta pattern' stimulation was administered. Basal recordings at low-frequency stimulation did not change after injection. After high-frequency stimulation all (7/7) E2 injected animals showed LTP whereas only 1/6 oil injected controls did so; the mean increase in amplitude of the PS and slope of the EPSP after high-frequency stimulation were significantly greater in E2 treated rats. Input/output curves did not change significantly after E2 administration. These results show that at low-frequency stimulation, transynaptic responses of pyramidal neurones in CA1 are not affected by changes in levels of circulating estrogen, while synaptic plasticity -- which is at the basis of proposed hebbian associative memory -- is facilitated by estrogen treatment.

Rat organum vasculosum laminae terminalis in vitro: responses to changes in sodium concentration.

Extracellular action potentials were recorded from the organum vasculosum laminae terminalis (OVLT) in rat brain slice preparations; the effect of different concentrations of NaCl on spontaneous firing frequency was studied. From 72 neurons, 67 (93%) were responsive to various perfusion media, while 5 neurons (7%) were not responsive. The change from the standard medium (SM; 124 mM NaCl) to 99 mM, decreased the firing frequency in 24 (65%) and increased it in 13 (35%) out of 37 responsive cells. The change from the SM to 149 mM evoked an increase in the firing rate in 33 (73%) and a decrease in 12 (27%) of 45 responsive neurons; the change to 174 mM, increased the firing rate in 5 (100%) neurons tested. The excitatory effect of increasing [NaCl] in the perfusion medium persisted even in low Ca2+ and high Mg2+ medium. Mannitol (55 mM) added to the SM increased the firing rate of cells; no significant decrease in the firing rate was seen with sodium mannitol 99/55 mM. Ouabain (OUA) (0.1 x 10(-3) mM) added to the SM increased the firing rate in 16 (84%) and decreased it in 3 (16%) out of 19 cells. Diphenylhydantoin (DPH) (1 mM) added to the SM decreased the firing rate in 12 (67%) and increased it in 6 (33%) of 18 cells tested. Hypo- or hypertonic NaCl solutions had no consistent effect on the spontaneous activity of 14 pyramidal cells recorded from the hippocampus (area CA3). The results emphasize the importance of intracellular Na content as a physiological trigger regulating the activity in neurons of the OVLT.

Gangliosides improve synaptic transmission in dentate gyrus of hippocampal rat slices.

The effect of perfusion with gangliosides (1 x 10(-6) M) on the response evoked in the granule cell layer of dentate gyrus by stimulation of perforant path in hippocampal rat slices was studied. Gangliosides induced both a decrease in the frequency threshold of stimulation necessary to generate long-term potentiation (LTP) and greater potentiation than under control conditions. It is proposed that gangliosides improve the mechanisms responsible for synaptic plasticity which generate LTP.

Modulation of the proestrous surge of luteinizing hormone by electrochemical stimulation of the amygdala and hippocampus in the unanesthetized rat.

The roles played by the amygdala and hippocampus in controlling the release of pituitary luteinizing hormone (LH) were studied in the freely moving rat. Monopolar stainless steel electrodes were implanted into the corticomedial (CM) amygdala, basolateral (BL) amygdala and dorsal hippocampus of female rats. When the animal had recovered from surgery and shown two consecutive 4-day estrous cycles, a chronic atrial cannula was introduced during the afternoon of diestrus II. On the following day (proestrus) electrochemical stimulation (ECS) was applied (20--50 micronA anodal DC 120 sec) bilaterally to the amygdala or hippocampus and blood samples were taken every 90 min from 12.00 to 21.00 h for radioimmunoassay (RIA) of LH. Next day, uterine tubes were examined for ova as evidence of ovulation. ECS of the amygdala exerted two divergent influences on LH release. Stimulation of the BL amygdala at 13.45 h, just before the critical period (14.00--16.00 h), was effective in delaying and reducing the LH surge, whereas ECS of the CM amygdala at 12.00 h resulted in an early synchronization in the timing of the LH curves. All of the rats in both groups ovulated, in contrast to the results of applying ECS to the dorsal hippocampus; there the LH surge and ovulation were completely blocked in 7 out of 9 rats. Thus, in the freely moving rat, the hippocampus can exert a potent inhibitory influence on LH release whereas the amygdala plays a modulatory role in the process.

PIP: Modulation of the proestrous surge of luteinizing hormone (LH) by electrochemical stimulation of the amygdala and hippocampus in the unanesthetized female rat was investigated. Monopolar stainless steel electrodes were implanted into the corticomerdial (CM) amygdala, basolateral (BL) amygdala, and dorsal hippocampus of the rats. Following recovery from surgery and 2 consecutive 4-day estrous cycles, a chronic atrial cannula was introduced during the afternoon of Diestrous 2. On the following day (proestrus) electrochemical stimulation (ECS) was applied (20-50 mcA anodal direct current 120 seconds) bilaterally to the amygdala or hippocampus and blood samples were taken every 90 minutes from 1200 to 2100 hours for radioimmunoassay of LH. The next day uterine tubes were examined for ova as evidence of ovulation. ECS of the amygdala exerted 2 divergent influences on LH release. Stimulation of the BL amygdala at 1345 hours just before the critical period (1400-1600 hours) was effective in delaying and reducing the LH surge, whereas ECS of the CM amygdala at 1200 hours resulted in an early synchronization in the timing of the LH curves. All of the rats ovulated in contrast to the results of applying ECS to the dorsal hippocampus. It is concluded that in the freely moving rat the hippocampus can exert a potent inhibitory influence on LH release whereas the amygdala plays a modulatory role in the process.

The learning capacity of high or low performance rats is related to the hippocampus NMDA receptors.

The hippocampal synaptic plasticity of rats with an inborn high (HP) or low (LP) learning capacity to perform in a shuttle box is closely related to their percentage of conditioned responses (Crs). HP rats show less sensitivity to the blocking effect of 2-aminophosphonopentanoic acid (AP5) on the generation of long-term potentiation (LTP) than do LP rats. Results described in the present report are indicative of an increased density of N-methyl-D-aspartate (NMDA) receptors in HP rats compared to control and LP rats. We postulate that the differential pharmacological sensitivity of LTP in these rats is a reflection of this biochemical difference. Also, from these results we suggest that the learning capacity may be related to the density of glutamate NMDA receptors of HP, LP and control rats.

Correlation between threshold to induce long-term potentiation in the hippocampus and performance in a shuttle box avoidance response in rats.

The relationship between the learning ability of normal rats and the facility to induce long-term potentiation (LTP) in the same animals was investigated. Behavioral performance was measured in a shuttle box avoidance paradigm, using a buzzer as conditioned stimulus. Three days later animals were sacrificed; frequency threshold necessary to induce LTP was determined in transverse hippocampal slices taken from these animals and maintained in vitro. A linear regression analysis on the behavioral and electrophysiological data showed a negative correlation (Spearman rank correlation coefficient rs = -0.705; P less than 0.001) between percent of conditioned responses in the shuttle box and threshold frequency necessary to induce LTP in gyrus dentatus in response to tetanic stimulation of the perforant path. It is concluded that learning ability of normal rats in a shuttle box avoidance paradigm is correlated with hippocampal synaptic plasticity.