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PubMed1995

Differential regulation of adenylate cyclase activity in rat ventral and dorsal hippocampus by rat galanin.

Rat galanin inhibits basal as well as forskolin-stimulated adenylate cyclase activity in rat ventral and dorsal hippocampus. The inhibition of adenylate cyclase activity, both basal and forskolin-stimulated, is characterised by IC50 values being 250-fold lower in ventral hippocampus (IC50 = 1.1 nM) compared to the dorsal hippocampus (IC50 = 270 nM). The maximal inhibition of basal and forskolin-stimulated adenylate cyclase activity in both ventral and dorsal hippocampus in the presence of 10 microM rat galanin is 34-45%. The analysis of the binding data obtained with 125I-labelled Tyr26-porcine galanin as a tracer reveals similar binding constants for rat galanin in both ventral and dorsal hippocampus with 4.8-fold higher concentration of galanin receptors in the ventral hippocampus. Putative galanin receptor subtype differences between the ventral and dorsal hippocampus have been noted by Hedlund et al. (Eur. J. Pharmacol., 224 (1992) 203-205). This study yields further confirmation for the existence of different galanin receptor subtypes or for differential coupling of galanin receptors to the adenylate cyclase in the dorsal versus ventral hippohampus.

Adenylyl Cyclase Inhibitors↗
PubMed1992

5-HT1C receptors mediate phosphoinositide turnover activation in the immature rat hippocampus.

The activation of phosphoinositide turnover in rat cerebral cortex and choroid plexus is triggered by the stimulation of 5-HT2 and 5-HT1C receptors, respectively. To characterize the 5-HT receptor subtype mediating the activation of phosphoinositide turnover in the hippocampus, the potency of several 5-HT agonists and antagonists on total [3H]inositol phosphate formation has been compared in the hippocampus, cerebral cortex and choroid plexus of immature rats. 5-HT, alpha-methyl-5-HT, quipazine, MK-212, mCPP (m-chlorophenylpiperazine) and TFMPP (m-trifluoromethylphenylpiperazine) are less potent and efficient in stimulating phosphoinositide turnover in the hippocampus and cerebral cortex than in the choroid plexus. However, for a number of 5-HT receptor antagonists (ketanserin, spiperone, ritanserin, pizotifen, cyproheptadine, mesulergine, mianserin, methiothepin, methysergide) there is a good correlation (r = 0.82) between their antagonistic potency in the hippocampus and choroid plexus while such correlation is not observed for the hippocampus and cerebral cortex. The specific 5-HT2 receptor antagonist spiperone only partially antagonizes (37% inhibition at 1 microM) the stimulation by 5-HT of phosphoinositide turnover in the hippocampus. These results suggest that in the immature rat hippocampus the activation of phosphoinositide turnover by 5-HT is mainly mediated by the 5-HT1C receptor subtype.

Animals↗
PubMed2005

Kinetic difference of berberine between hippocampus and plasma in rat after intravenous administration of Coptidis rhizoma extract.

In order to investigate the pharmacokinetics of berberine in Coptidis rhizoma extract in rat hippocampus and plasma, a simple and accurate high-performance liquid chromatography method was employed in this study. Berberine was determined using a Hypersil C(18) column with an isocratic mobile phase of acetonitrile-0.05 M potassium dihydrogen phosphate (containing 0.5% triethylamine, pH 3.0) and with UV detection at 236 nm. The lower limit of quantification for berberine in both hippocampus and plasma was 24 ng/ml, and the lowest concentrations of berberine determined in rat hippocampus and plasma samples were 30.7 ng/ml at 48 h and 38.5 ng/ml at 4 h, respectively. The calibration curve for berberine was linear over the concentration range 24--6000 ng/ml. At this concentration range, the overall recoveries (90.6--94.2%) for berberine were determined and the accuracy of intra- and inter-day assays from rat samples were less than 7% RSD. Following intravenous administration of C. rhizoma extract at a dose of 10.2 mg/kg containing 3 mg/kg berberine, berberine in the plasma eliminated rapidly (t(1/2 beta)=1.13 h). However, berberine in the hippocampus increased rapidly (t(1/2 alpha)=0.215 h), peaked at 3.67 h with a concentration of 272 ng/g, and had a slow elimination rate (t(1/2 beta)=12.0 h), which suggests that berberine could have a direct action on neuron and accumulate in the hippocampus. This study first showed the pharmacokinetic characteristics of berberine in rat hippocampus and the kinetic characteristics of berberine are dissimilar in the hippocampus and plasma.

Animals↗
PubMed2005

Activation of dopaminergic neurotransmission in the medial prefrontal cortex by N-methyl-d-aspartate stimulation of the ventral hippocampus in rats.

Many behavioral functions-including sensorimotor, attentional, memory, and emotional processes-have been associated with hippocampal processes and with dopamine transmission in the medial prefrontal cortex (mPFC). This suggests a functional interaction between hippocampus and prefrontal dopamine. The anatomical substrate for such an interaction is the intimate interconnection between the ventral hippocampus and the dopamine innervation of the mPFC. The present study yielded direct neurochemical evidence for an interaction between ventral hippocampus and prefrontal dopamine transmission in rats by demonstrating that subconvulsive stimulation of the ventral hippocampus with N-methyl-d-aspartate (NMDA; 0.5 mug/side) activates dopamine transmission in the mPFC. Postmortem measurements revealed that bilateral NMDA stimulation of the ventral hippocampus, resulting in locomotor hyperactivity, increased the homovanillic acid/dopamine ratio, an index of dopamine transmission, in the mPFC; indices of dopamine transmission in any of five additionally examined forebrain regions (amygdala, nucleus accumbens shell/core, lateral prefrontal cortex, caudate putamen) were unaltered. In vivo microdialysis measurements in freely moving rats corroborated the suggested activation of prefrontal dopamine transmission by demonstrating that unilateral NMDA stimulation of the ventral hippocampus increased extracellular dopamine in the ipsilateral mPFC. The suggested influence of the ventral hippocampus on prefrontal dopamine may be an important mechanism for hippocampo-prefrontal interactions in normal behavioral processes. Moreover, it indicates that aberrant hippocampal activity, as found in neuropsychiatric diseases, such as schizophrenia and mood disorders, may contribute to disruption of certain cognitive and emotional functions which are extremely sensitive to imbalanced prefrontal dopamine transmission.

Animals↗
PubMed2006

Changes in cholinergic function in the frontal cortex and hippocampus of rat exposed to ethanol and acetaldehyde.

Our previous microdialysis study demonstrated that both ethanol (EtOH) and acetaldehyde (ACe) decrease in vivo acetylcholine (ACh) release in the medial frontal cortex of freely moving rats. To better understand the mechanisms of EtOH and ACe's effects on the cholinergic system in the brain, choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) expression was examined at 40 and 240 min after a dose of EtOH (1 g/kg) in the rat frontal cortex and hippocampus. The control group was treated with 0.9% saline, and other groups received EtOH or cyanamide (CY, 50 mg/kg, a potent aldehyde dehydrogenase inhibitor) and 60 min later by EtOH intraperitoneally. Reverse-transcription polymerase chain reaction (RT-PCR) analysis revealed that ChAT mRNA levels were decreased by 72.8% and 71.6% in the EtOH and CY+EtOH groups, respectively, at 40 min after EtOH injection compared with saline in the frontal cortex. The hippocampal ChAT levels were reduced by 76.5% and 53.0% in the EtOH and CY+EtOH groups, respectively, at this time. CY+EtOH-induced depletion in ChAT mRNA levels was markedly higher than EtOH in the hippocampus. A similar decrease pattern of ChAT was observed at protein levels as determined by Western blot, but the reduced ChAT levels were significantly higher in the CY+EtOH group as compared with the EtOH group both in the frontal cortex and hippocampus. At 240 min after EtOH injection, the EtOH group had no effect on ChAT at mRNA levels, as compared with saline, whereas CY+EtOH group induced a significant decrease in ChAT mRNA expression to 62.0% and 65.5% in the frontal cortex and hippocampus, respectively. These data were consistent with the results of the Western blot analysis. AChE expression at mRNA levels was not changed at either 40 or 240 min after EtOH dosing in either of these groups in the frontal cortex and hippocampus. Within 40 and 240 min, a statistically significant difference in ChAT expression at mRNA and protein levels was found in the EtOH and CY+EtOH groups both in the frontal cortex and hippocampus. The data obtained from this study demonstrate that EtOH and ACe concentrations decreased ChAT expression at 40 and 240 min after EtOH administration in the frontal cortex and hippocampus, and this result suggests that reduced ChAT expression is strongly related to a decrease in ACh release in the rat brain.

Acetaldehyde↗
PubMed2005

Differential effects of vigabatrin and zonisamide on the neuropeptide Y system in the hippocampus of seizure prone gerbil.

Changed neuropeptide Y (NPY) system in the hippocampus has been reported in various experimental epileptic models. However, there have been little data concerning the alteration in the NPY system in the epileptic hippocampus following treatment of anti-epileptic drugs (AEDs). In the present study, therefore, we performed analyses of effects of vigabatrin (VGB) and zonisamide (ZNS) treatment on the NPY system in the hippocampus of the seizure sensitive (SS) gerbils. In SS gerbil, NPY immunoreactivity in the hippocampus was lower than that in seizure resistant gerbil. Following VGB treatment, the number of NPY immunoreactive neurons and NPY mRNA expression were increased in the hilus and the hippocampus proper. In contrast, ZNS treatment markedly elevated only the density of NPY immunoreactive fibers in the dentate gyrus, not in the hippocampus proper, as compared with saline-treated animals. These patterns were observed in the dose-dependent manners. These findings suggest that AEDs treatments may distinctly affect the NPY system in the SS gerbil hippocampus.

Animals↗
PubMed2005

Actions at GABA(A) receptors in the hippocampus may mediate some antiseizure effects of progestins.

Progestins can have antiseizure effects; however, the mechanisms and sites of action of these effects are not well-understood. Whether progesterone's actions at GABA(A) receptors in the hippocampus are important for its antiseizure effects was investigated. In Experiment 1, ovariectomized rats were administered sesame oil vehicle or a regimen of progesterone (500 microg sc, which produces physiological concentrations in plasma and the hippocampus), followed 2.5 hours later by administration of saline vehicle or a regimen of bicuculline (1 mg/kg, sc), a GABA(A) receptor antagonist, which does not produce any intrinsic effects on seizures. Progesterone, compared with vehicle, significantly increased the latency to, and decreased the number of, pentylenetetrazole-induced tonic seizures and increased GABA-stimulated chloride flux. Co-administration of bicuculline attenuated progesterone's antiseizure effects and decreased GABA-stimulated chloride flux in the hippocampus. Bicuculline did not alter ictal behavior compared with vehicle. In Experiment 2, ovariectomized rats were subcutaneously administered sesame oil or progesterone (500 microg), followed 2.5 hours later by bilateral infusions of bicuculline (100 ng) or vehicle (saline) into the hippocampus. Infusion of bicuculline into the hippocampus of progesterone-primed rats significantly increased ictal activity, compared with that induced by progesterone administration alone, but alone did not alter seizures compared with that produced by saline infusions into the hippocampus. These data suggest that actions of progesterone at GABA(A) receptors in the hippocampus are important for progesterone's antiseizure effects.

Analysis of Variance↗
PubMed2004

Neural aromatization accelerates the acquisition of spatial memory via an influence on the songbird hippocampus.

Circulating estrogens affect the neural circuits that underlie learning and memory in several vertebrates via an influence on the hippocampus. In the songbird hippocampus local estrogen synthesis due to the abundant expression of aromatase may modulate hippocampal function including spatial memory performance. Here, we examined the effect of estradiol, testosterone, and dihydrotestosterone on the structure and function of the songbird hippocampus. Adult male zebra finches were castrated, implanted with one of these steroids or a blank implant, and trained on a spatial memory task. The rate of acquisition and overall performance on this task was recorded by direct observation. The size and density of cells in the hippocampus and its volume were measured. Estradiol-treated birds learned the task more rapidly than any other group. Although testosterone- and blank-implanted birds did learn the task, we found no evidence of learning in dihydrotestosterone-implanted subjects. Cells in the rostral hippocampus were larger in estradiol- and testosterone-treated birds relative to other groups. A corresponding decrease in the density of cells was apparent in estradiol-implanted subjects relative to all other groups. These data suggest that estradiol may accelerate the acquisition of a spatial memory task and increase the size of neurons in the rostral hippocampus. Since testosterone-mediated changes in acquisition and cell size were similar to those of estradiol, but not dihydrotestosterone, we conclude that neural aromatization of testosterone to estrogen is responsible for effects on the structure and function of the songbird hippocampus.

Analysis of Variance↗
PubMed2000

Permanent and temporary inactivation of the hippocampus impairs T-maze footshock avoidance acquisition and retention.

The hippocampus is widely recognized as playing an important role in learning and memory. Lesions of the hippocampus can disrupt spatial navigational learning and memory and injection of drugs into the hippocampus can affect both spatial navigational and nonspatial tasks. In the current studies we tested the effects of bilateral of electrolytic lesions and reversible inactivation of the hippocampus on acquisition and retention of T-maze footshock avoidance conditioning. Electrolytic lesions, which destroyed 31+/-0.04% of the hippocampus, significantly impaired acquisition and retention for T-maze footshock avoidance. No differences were found in motivation to avoid shock, open field activity, or foot shock sensitivity between lesion and control groups. Temporary inactivation of the hippocampus with lidocaine administered immediately before training disrupted acquisition and retention for T-maze footshock avoidance. Temporary hippocampal inactivation performed just prior to retention testing and post-training inactivation in mice trained to first avoidance had no effect on retention. However, temporary post-training inactivation in 'undertrained' (enough trials to remember 1 week later if treated with saline, but not allowed to make the avoidance response) mice impaired retention. The current findings indicate that the hippocampus plays an important role in learning and memory processing in the aversive T-maze paradigm.

Animals↗
PubMed2002

Functional effects of chronic electroconvulsive shock on serotonergic 5-HT(1A) and 5-HT(1B) receptor activity in rat hippocampus and hypothalamus.

The aims of this work were to determine the influence of chronic electroconvulsive shock (ECS) on presynaptic 5-HT(1A) receptor function, postsynaptic 5-HT(1A) receptor function in hippocampus and hypothalamus, and presynaptic 5-HT(1B) receptor function in hippocampus and hypothalamus. This represents part of an on-going study of the effects of ECS on serotonergic receptor activity in selected brain areas which may be relevant to the effects of electroconvulsive therapy (ECT) in humans. Chronic ECS reduced the ability of the 5-HT(1A) receptor agonist 8-hydroxy-2(di-n-propylamino)tetraline (8-OH-DPAT) (0.2 mg/kg s.c.) to decrease 5-HT levels in hypothalamus as shown by in vivo microdialysis, indicative of a reduction in sensitivity of presynaptic 5-HT(1A) autoreceptors. The ability of the 5-HT(1B) receptor antagonist GR 127935 (5 mg/kg s.c.) to increase 5-HT levels in both hippocampus and hypothalamus was unaffected by chronic ECS. 8-OH-DPAT (0.2 mg/kg s.c.) increased cyclic AMP levels in hippocampus measured by in vivo microdialysis approximately 2-fold. The degree of stimulation of cyclic AMP formation was not altered by chronic ECS. However the cyclic AMP response to forskolin (50 micro M) administered via the microdialysis probe, which was approximately 4-fold of basal in sham-treated rats, was almost completely abolished in ECS-treated rats. Since this indicates that either adenylate cyclase catalytic unit activity or Gs protein activity is reduced in the hippocampus after chronic ECS, the lack of change in 8-OH-DPAT-induced cyclic AMP formation may be taken as possible evidence of an increase in sensitivity of postsynaptic 5-HT(1A) receptors in the hippocampus by chronic ECS. Chronic ECS increased basal plasma levels of corticosterone, ACTH and oxytocin. The ACTH response to s.c. injections of 0.2 mg/kg or 0.5 mg/kg 8-OH-DPAT was reduced by chronic ECS. Postsynaptic 5-HT(1A) receptor activity in the hypothalamus, in contrast to the hippocampus, thus appears to be desensitized after chronic ECS. We conclude that chronic ECS has regionally specific effects on both pre- and post-synaptic 5-HT(1A) receptors, but, in contrast to some antidepressant drugs, does not affect presynaptic 5-HT(1B) receptor activity.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2002

Enhancing effects of estrogen on inhibitory avoidance performance may be in part independent of intracellular estrogen receptors in the hippocampus.

Estradiol (E(2)) can have classical actions via intracellular estrogen receptors (ERs) in the dorsal hippocampus, as well as effects independent of ERs ('non-genomic' mechanisms). These experiments investigated whether E(2)'s cognitive enhancing effects in the inhibitory avoidance task require actions at ERs in the dorsal hippocampus. Ovariectomized (ovx) rats were administered E(2) (s.c. or to the dorsal hippocampus), an E(2) conjugate (E(2):BSA), or vehicle and/or an ER antagonist, tamoxifen (10 mg/kg s.c.) or ICI 182,780 (10 microg intrahippocampally), or vehicle for 2 days prior to training (Day 3) and testing (Day 4) in the inhibitory avoidance task. Exp 1: crossover latencies in the inhibitory avoidance task were significantly increased in ovx rats with s.c. E(2) silastic capsules or s.c. injections of 1000 or 10 microg E(2) compared to vehicle-administered rats. Exp 2: bilateral inserts of E(2) to the dorsal hippocampus significantly increased crossover latencies compared to vehicle. Exp 3: s.c. tamoxifen, the ER antagonist, did not block the increased crossover latencies produced by 10 microg E(2) s.c. (compared to vehicle). Exp 4: s.c. tamoxifen did not block the increased crossover latencies produced by intrahippocampal E(2) (compared to vehicle). Exp 5: ICI 182,780 was unable to attenuate the increased crossover latencies produced by intrahippocampal E(2). Exp 6: E(2):BSA administered to the dorsal hippocampus significantly enhanced performance on the inhibitory avoidance task compared to control implants to the hippocampus. The ability of systemic and intrahippocampal E(2) to similarly enhance inhibitory avoidance performance suggests that actions of E(2) in the dorsal hippocampus are sufficient to enhance cognitive performance. Further, that neither tamoxifen nor ICI 182,780 blocked E(2)'s enhancing effects on inhibitory avoidance and that E(2):BSA was able to enhance performance suggest that non-genomic mechanisms may in part mediate E(2)'s cognitive enhancing performance in this task.

Animals↗
PubMed2003

Excitatory effects of motilin in the hippocampus on gastric motility in rats.

Intestinal motilin is known to stimulate gastrointestinal motility. Recently, it was shown that the motilin gene and the motilin receptor are expressed in various regions of the brain. We studied whether motilin can activate pathways in the rat hippocampus to stimulate gastric motility. Gastric motility was monitored in conscious rats, whereas extracellular electrical activity recordings of the hippocampus were performed on anaesthetized rats to measure the influence of microinjection of motilin and CCK-8 into the hippocampus and into the cerebral ventricles. We found that neurons in the CA3 region of the hippocampus are sensitive to gastric distension, and that injection of motilin into the hippocampus increased the amplitude of gastric contractions by 35.3+/-6.8%, while CCK-8 injection inhibited motility by -27.3+/-6.8%. The hippocampal motilin-induced stimulation of gastric motility (30.6+/-5.5%) was completely abolished by subdiaphragmal vagotomy (-2.8+/-4.4%) but unaffected by the intravenously applied receptor blockers atropine, phentolamine and propranolol. In vivo extracellular recordings of gastric distension-responsive CA3 neurons revealed that intracerebroventricular administration of motilin increased firing while CCK-8 inhibited firing. These opposite effects of motilin and CCK-8 fit with the nature of the actions of these gut-brain peptides on gastric motility. Our findings suggest that the stimulation of gastric motility by motilin administered in the hippocampus reflects the existence of a functional interaction between the hippocampus and a vago-vagus reflex running via a noncholinergic and nonadrenergic efferent pathway.

Action Potentials↗
PubMed1998

Microinjection of GABA-A agonist muscimol into the dorsal but not the ventral hippocampus impairs non-mnemonic measures of delayed non-matching-to-position performance in rats.

Anatomical studies of afferent and efferent connections suggest that the hippocampus may have more than one information processing role that varies along the septo-hippocampal axis. The present study was conducted to test whether a distinct functional specialization for the dorsal versus ventral extents of the hippocampus could be detected. The effects of a GABA-A receptor agonist, muscimol, microinjected into either the dorsal or ventral hippocampus on an operant, spatial delayed non-matching-to-position (DNMTP) task were measured. A decrease in the number of trials completed per session and disruption of several DNMTP discrimination parameters were produced by muscimol microinjection into the dorsal hippocampus but not into the ventral hippocampus. Muscimol injected into either site did not impair the measure of working memory, delayed choice accuracy. These results are consistent with the view that hippocampal function varies along the septo-temporal axis, and that the dorsal hippocampus is relatively more critical to visual discrimination performance than the ventral hippocampus.

Animals↗
PubMed2003

Pretreatment of donor cells with FGF-2 enhances survival of fetal hippocampal CA3 cell transplants in the chronically lesioned young adult hippocampus.

The lesioned CA3 region of the young adult hippocampus is very conducive for robust survival and integration of fetal hippocampal CA3 cell grafts when transplanted at an early postlesion delay of 4 days. However, similar CA3 cell grafts placed at 45 days postlesion display significantly diminished cell survival, implying that the receptivity of the lesioned young adult host hippocampus to grafts decreases considerably with a prolonged postlesion transplantation delay. We hypothesize that decreased cell survival in grafts placed into the chronically lesioned hippocampus is due to a reduced level of host neurotrophic factors that support fetal hippocampal cells; hence, pretreatment and grafting of donor fetal CA3 cells with fibroblast growth factor-2 (FGF-2) considerably enhances graft neuronal integration into the chronically lesioned young adult hippocampus. We employed the optical fractionator cell counting method and rigorously quantified the number of surviving cells and neurons derived from 5'-bromodeoxyuridine-labeled Embryonic Day 19 CA3 cell grafts pretreated and transplanted with FGF-2 into the lesioned CA3 region of the young adult rat hippocampus, at a delay of 60 days after a unilateral intracerebroventricular administration of the kainic acid. For comparison, we also analyzed the survival of standard fetal CA3 cell grafts (i.e., without FGF-2 treatment) after similar transplantation. Pre treatment and transplantation of CA3 cell grafts with FGF-2 resulted in a robust yield of surviving cells (115% of injected cells) and neurons (100% of injected cells) from grafts. In contrast, standard CA3 cell grafts exhibited a reduced yield of surviving cells (29%) and neurons (25%). Thus, the yield of neurons from fetal hippocampal CA3 cell grafts placed into the chronically lesioned young adult hippocampus can be greatly enhanced by a simple pretreatment and grafting of donor fetal CA3 cells with FGF-2. These results have significance toward advancement of clinically feasible cell grafting strategies for repair of the damaged young adult hippocampus, particularly at extended periods after the injury or the onset of neurodegenerative diseases.

Animals↗
PubMed1997

Calcium-sensing receptor in the rat hippocampus: a developmental study.

The extracellular Ca2+ (Ca2+(o))-sensing receptor (CaR) plays a key role in maintaining near constancy of Ca2+(o) in mammals through its presence in parathyroid gland and kidney. The CaR is also present in brain, and although its role(s) in the brain is not known, it is possible that small changes in Ca2+(o) modify essential physiological and pathological processes, since calcium is crucial for numerous neuronal functions. Northern analysis has revealed that the CaR mRNA is present in hippocampus and several other regions of the brain. The hippocampus is an important site for learning and memory, but the relevance of the CaR to these processes is unknown. Long-term potentiation (LTP), a putative in vitro analog of memory, can only be induced after 7-10 days postnatally in rat hippocampus. Therefore, in the present study we determined the time course for the developmental expression of the CaR in rat hippocampus to assess its relationship to the development of other important hippocampal functions, such as the capacity for induction of LTP. Northern and Western analyses showed that CaR mRNA and protein were expressed at low levels at 5 days postnatally but then increased markedly at 10 days. A high level of receptor expression, due primarily to an increase in a 7.5 kb transcript, persisted until 30 days, when it gradually decreased by 3-fold to reach the adult level of expression. In situ hybridization histochemistry and immunohistochemistry revealed CaR mRNA and protein in pyramidal cells of all the layers of hippocampus and in granule cells of the dentate gyrus. The results show that CaR expression rises at a time when LTP can first be induced in hippocampus and persists at high levels during the time when brain development is proceeding most rapidly. Further studies are needed to determine the role of the CaR in the development of important aspects of the function of hippocampus and other regions of brain, including LTP.

Aging↗
PubMed2002

Histaminergic neurons of the ventral hippocampus and the baso-lateral amygdala of the rat: functional interaction on memory and learning mechanisms.

The possibility of a functional interaction between the amygdala and the ventral hippocampus on learning of a conditioned avoidance response when both brain structures are chemically stimulated with histamine was studied in rats. Adult male rats were stereotaxically implanted under ether anaesthesia with guide cannulae into the baso-lateral amygdala and the ventral hippocampus. Seventy-two hours after the implant, rats were microinjected with: 1 microl saline solution into both structures (SAL+SAL group); 9 or 90 nmol doses of histamine into both structures (HA+HA groups); 9 or 90 nmol histamine into the hippocampus and saline into the amygdala (HA+SAL groups); saline into the hippocampus and 9 or 90 nmol histamine into the amygdala (SAL+HA groups). Five minutes following the injection, rats were subjected to a learning task in eight consecutive trials, consisting of avoiding an electric shock applied to the feet of the animal when an ultrasonic tone of 40 kHz is on for 30 s. Results show that histamine applied in any dose into both amygdala and hippocampus was able to significantly increase the escape latency and impair the efficacy of learning. Chemical stimulation with histamine of only hippocampus or amygdala affected selectively the escape latency. Results suggest that there is a functional interaction between histamine-sensitive neurons of the amygdala and hippocampus during processing of a learning task.

Acoustic Stimulation↗
PubMed2003

Age-related working memory impairment is correlated with increases in the L-type calcium channel protein alpha1D (Cav1.3) in area CA1 of the hippocampus and both are ameliorated by chronic nimodipine treatment.

The hippocampus is critical for spatial memory formation in rodents. Calcium currents through L-type voltage-sensitive calcium channels (L-VSCCs) are increased in CA1 neurons of the hippocampus of aged rats. We have recently shown that expression of the calcium conducting L-VSCC subunit alpha(1D) (Ca(v)1.3) is selectively increased in area CA1 of aged rats. We and others have speculated that excessive Ca(2+) influx through L-VSCC may be detrimental to memory formation. Therefore, we investigated the relationship between age-related working memory decline and alpha(1D) protein expression in the hippocampus. In addition, we studied the effects of chronic treatment with the L-VSCC antagonist nimodipine (NIM) on age-related working memory deficits and alpha(1D) expression in the hippocampus. Here we report that age-related increases in alpha(1D) expression in area CA1 correlate with working memory impairment in Fischer 344 rats. Furthermore, we demonstrate that chronic NIM treatment ameliorates age-related working memory deficits and reduces expression of alpha(1D) protein in the hippocampus. The present results suggest that L-VSCCs participate in processes underlying memory formation and that increases in L-VSCC protein and currents observed with aging may play a role in age-related memory decline. Furthermore, the amelioration in age-related memory decline produced by NIM treatment may be mediated, at least in part, by reductions in the abnormally high levels of alpha(1D) protein in the aged hippocampus. These findings may have implications for patients with Alzheimer's disease, who show increased L-VSCC protein expression in the hippocampus, and for patients receiving chronic treatment with L-VSCC antagonists.

Aging↗
PubMed2002

Differences in hippocampal mitotic activity within the dorsal and ventral hippocampus following flurothyl seizures in mice.

To date, there is little information regarding the regional division (dorsal and ventral) of hippocampal mitotic activity at either baseline or following seizures. To determine the regional distribution of hippocampal mitotic activity, animals were given seizures followed by injections of 5-bromo-2'-deoxyuridine (label for mitotic cells). Our results indicate that the baseline and seizure-induced levels of mitotic activity (neurogenesis) are greater in the dorsal hippocampus as compared to the ventral hippocampus. Moreover, seizures were able to significantly increase mitotic activity in both dorsal and ventral hippocampus with a greater proportional increase from baseline in the ventral hippocampus as compared to the dorsal hippocampus. These results suggest that the amount of mitotic activity differs between the dorsal and ventral hippocampus and suggests that seizure activity is capable of differentially driving mitotic activity in the dorsal and ventral hippocampus.

Animals↗