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At least 127 records · Page 7Linked to original sources
PubMed1991

Endogenous opioids released from perforant path modulate norepinephrine actions and inhibitory postsynaptic potentials in guinea pig CA3 pyramidal cells.

The stimulus parameters needed for the release of endogenous opioid peptides were investigated using an in vitro radioligand displacement assay in living guinea pig hippocampal slices. Electrical stimulation of the enkephalin-containing fibers in the perforant path caused the release of endogenous opioid peptides and the subsequent displacement of [3H]-[D-Ala2,N-methyl-Phe4,glyol5]enkephalin binding. High frequency trains of stimuli (10 Hz for 1 sec every 10 sec) were more effective than lower frequency stimulation (1 Hz continuous) at evoking opioid peptide release. Having identified an effective stimulation paradigm able to release endogenous opioids, the electrophysiological effects of endogenous opioids on CA3 pyramidal cells were measured in the guinea pig hippocampal slice preparation. Unlike exogenously applied opioids, stimulated release of endogenous opioid peptides from the perforant path did not significantly reduce inhibitory postsynaptic potential (IPSP) amplitudes recorded in CA3 pyramidal cells. However, perforant path stimulation in the presence of naloxone did cause a dramatic increase in IPSP amplitudes. CA3 pyramidal cells were not directly affected by perforant path stimulation. The naloxone-sensitive increase in IPSPs was delayed 3 min in onset and lasted for several minutes. In addition, the increase in the IPSPs was specifically blocked either by the beta adrenergic antagonist propranolol or by pretreating the animals with reserpine. These findings indicate that endogenous opioids regulate the effects of norepinephrine in the CA3 region of the guinea pig hippocampus. In addition, endogenously released norepinephrine appeared to act on GABAergic interneurons to increase the amplitude of the IPSP recorded in CA3 pyramidal cells.

Animals↗
PubMed1987

Two subtypes of non-pyramidal cells in rat hippocampal formation identified by intracellular recording and HRP injection.

Intracellular recording and injection of horseradish peroxidase in rat hippocampal slice preparations revealed the existence of two physiologically distinct types of non-pyramidal cells: one a fast spiking type and the other a non-fast spiking type. In the CAl pyramidal cell layer and the subgranular zone of the dentate gyrus fast spiking cells were found, while in the border area between the stratum lacunosum-moleculare and the stratum radiatum, non-fast spiking cells were found exclusively. These two types of non-pyramidal cells may play different roles in the functions of hippocampal neuronal networks.

Action Potentials↗
PubMed1989

Pharmacological characterization of muscarinic responses in rat hippocampal pyramidal cells.

Intracellular recording from hippocampal CA1 pyramidal cells was used to characterize the pharmacological properties of muscarinic responses. Results obtained with the M1 antagonist pirenzepine and the M2 antagonist gallamine suggest that an M1 muscarinic receptor is involved in the muscarinic-induced membrane depolarization and blockade of the afterhyperpolarization (AHP). On the other hand, an M2 receptor may be involved in the cholinergic depression of the EPSP and the blockade of the potassium current termed the M-current. Pretreatment of hippocampi with pertussis toxin did not prevent any of the muscarinic responses suggesting that a pertussis toxin-sensitive G-protein is not involved. The M-current, in contrast to the other muscarinic actions, was unaffected by muscarinic agonists which are weak at increasing phosphoinositide (PI) turnover and actually blocked the action of full agonists. This finding suggests that stimulation of PI turnover may be involved in the blockade of the M-current. Although activation of protein kinase C with phorbol esters has little effect on the M-current, intracellular application of inositol trisphosphate did reduce the M-current. We were unable to establish any clear relationship between biochemical effector systems and the muscarinic receptor subtypes.

Animals↗
PubMed1985

Electrophysiological effects of dynorphin peptides on hippocampal pyramidal cells in rat.

Single-unit extracellular recording was carried out in rats to characterize the effects of dynorphin and several structurally related peptides on hippocampal pyramidal cell activity. Dynorphin, applied electrophoretically or by pneumatic pressure, produced a dose-dependent depression of both spontaneous and glutamate-evoked discharge in a majority (63%) of CA1 and CA3 cells tested. In addition, a small number of cells in both cellular fields responded to the peptide with a prolonged elevation in firing. The inhibitory effects of dynorphin were not blocked by naloxone. Moreover, administration of des-tyrosine-dynorphin depressed the firing of pyramidal cells in a manner similar to that of the parent compound. Ethylketocyclazocine produced a mixed pattern of excitatory and inhibitory effects, whereas naloxone-sensitive elevations in firing were most often observed with the application of dynorphin-(1-8). Application of [Leu5]enkephalin produced only facilitations in pyramidal cell firing. The possibility is raised that biologically significant non-opiate actions, in addition to potent opiate-mediated effects, may occur upon release of pro-dynorphin peptides in the hippocampus.

Animals↗
PubMed1992

Inhibitory effects of excitatory amino acids on pyramidal cells of the in vitro turtle medial cortex.

The electroencephalogram of the in vitro brain of the turtle Chrysemys d' orbigny shows spontaneous random large sharp waves (LSWs) which may be compared to interictal spikes. In order to evaluate the role of excitatory amino acids (EAAs)--in particular through the N-methyl-D-aspartate (NMDA) receptor--in the generation of LSWs, the bath application of NMDA and its antagonists 3-((+/-)-2-carboxypiperazin-4y)-propyl-1-phosphonic acid (CPP) and DL-2-amino-5-phosphonovaleric acid (APV), was performed in the whole open hemisphere (WOH) in vitro. Field recordings in WOH showed that both CPP and APV unexpectedly increased LSW amplitude. Consistently, NMDA in the bath suppressed the LSWs. Iontophoretically applied glutamate, kainate and NMDA produced a hyperpolarization of intracellularly recorded medial cortex pyramidal cells both in WOH and in slices. The EAA-induced hyperpolarization was tetrodotoxin (TTX) and bicuculline sensitive and reversed close to -70 mV. It would therefore seem to be due to the activation of gamma-aminobutyric acid (GABA) interneurons. The NMDA could also produce an excitation of pyramidal cells--always following a previous inhibitory phase. In some cases rhythmic bursting discharges or plateau potentials were observed. These NMDA effects were mainly elicited by a direct effect on pyramidal cells. A long-lasting hyperpolarizing response following the NMDA excitatory phase was also observed. This long-lasting response was an intrinsic property of pyramidal cells since it was TTX resistant. This study demonstrates that GABAergic interneurons from the turtle medial cortex can be activated by EAAs, a mechanism that can account for the effects of NMDA antagonists on LSWs.

2-Amino-5-phosphonovalerate↗
PubMed1991

Enhancement of GABA neurotransmission after cerebral ischemia in the rat reduces loss of hippocampal CA1 pyramidal cells.

Increased excitation may be involved in the development of delayed CA1 pyramidal cell death in hippocampus after global cerebral ischemia. Therefore we investigated the possible neuroprotective effect of the GABA uptake inhibitor, R-(-)-1-(4,4-(3-methyl-2-thienyl)-3-butenyl)-3-piperidine carboxylic acid (No-328), in a rat cerebral ischemia model of delayed CA1 pyramidal cell death. No-328 in doses of 36 mg/kg given 30 min before, and 1, 24, 48 and 72 h after ischemia significantly reduced the CA1 neuron loss. Doses of 50 mg/kg of No-328 given immediately before, 24 h and 48 h after ischemia, also reduced the CA1 neuron loss significantly. Furthermore, we demonstrated that postischemic treatment with diazepam (4 x 15 mg/kg) significantly reduced the CA1 neuron loss. However, postischemic treatment with several doses (5 x 12 mg/kg) of the GABA analog, 4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol (THIP), offered no CA1 neuron protection when given alone, but when administrated together with diazepam (4 x 15 mg/kg) it significantly reduced the CA1 neuron loss. We conclude that enhancement of postischemic GABA neurotransmission, during the first 2-3 days after ischemia, may reduce the ischemic CA1 damage through a continuous increase in hippocampal GABA extracellular levels (No-328), or through an increase in sensitivity to GABA neurotransmission (diazepam).

Animals↗
PubMed1983

Geniculocortical synapses involving apical dendrites of layer V pyramidal cells in area 17 of the albino rat visual cortex: a combined Golgi/EM study.

Using the combined Golgi/EM technique (Fairén et al. 1977) we have investigated whether apical dendrites of layer V pyramidal cells with different diameters receive different numbers of geniculocortical synapses. An electrolytic lesion was made in the lateral geniculate nucleus (LGN) of albino rats. After a survival time of two days degenerating boutons of LGN afferents onto visual cortex (area 17) were identified by electron microscopy. Postsynaptic layer V pyramidal cells marked by Golgi impregnation were studied. The location of nine identified pyramids was determined by light microscopy. The diameter of the apical dendrites - ranging from 0.9 to 2.5 mum - was measured on electron micrographs. The dendrites of eight out of the nine pyramids make synaptic contacts with geniculocortical afferents in layer IV and lower layer III. The degenerative geniculocortical terminals were mostly of the electron dense type; one times the electron lucent type was observed. These axon terminals synapse mainly with asymmetrical synaptic junctions on spines. Occasionally synaptic contacts were found on dendritic shafts. Most degenerating synapses are localized on the pyramidal cell with the thinnest apical dendrite. There was also an other thin apical dendrite, which did not receive any degenerating bouton. All out of one apical dendrites of different size are involved in geniculocortical synapses without giving any preference to dendrites of a defined diameter.

Animals↗
PubMed1992

GABAB receptor-mediated inhibitory postsynaptic potentials evoked by electrical stimulation and by glutamate stimulation of interneurons in stratum lacunosum-moleculare in hippocampal CA1 pyramidal cells in vitro.

Following micropressure application of glutamate (500 microM) in stratum lacunosum-moleculare (L-M), inhibitory postsynaptic potentials (glut-IPSPs) were recorded in CA1 pyramidal cells. These glut-IPSPs were blocked by tetrodotoxin (1 microM) and, thus, were probably generated by the activation of local interneurons. The effects of pharmacological antagonists on glut-IPSPs and on electrically-evoked early and late IPSPs were assessed in the same cells during the same application of the antagonist. Local application of the GABAB antagonist 2-OH saclofen (1-4 mM) reduced both glut-IPSPs and late IPSPs but not early IPSPs. In contrast, the GABAB antagonist phaclofen (20 mM) reduced late IPSPs but not early IPSPs but not early IPSPs or glut-IPSPs. Early IPSPs were blocked by the GABAA antagonists bicuculline and picrotoxin but late IPSPs and glut-IPSPs were not. Repetitive electrical stimulation depressed early and late IPSPs as well as glut-IPSPs, suggesting that interneurons activated with glutamate were also stimulated electrically. Thus, interneurons in str. lacunosum-moleculare appear to inhibit pyramidal cells via a GABAB receptor-mediated IPSP. The discrepancy in the pharmacological profile of the GABAB glut-IPSPs and of the GABAB late IPSPs may suggest the presence of two GABAB mechanisms in CA1 pyramidal cells.

Animals↗
PubMed1988

Nerve cells with irregular processes: demonstration of anisotropic core geometry of a pyramidal cell.

An analytical, recursive method has been developed to demonstrate the anisotropic electrotonic geometry of nerve cells containing varicose or spiny dendrites. The procedure has been based on the distribution of the core geometry of dendrites into modules which consist of module elements where the physical length is much shorter than the actual space constant. The unambiguous representation of the anisotropic core geometry has been possible by plotting the decomposed geometries separated under the condition of the unidirectional spread of the wave front of dendritic potentials. This decomposition has revealed the bidirectional, "smoothed" core geometries as a function of irregular distribution of varicosities or spines. The shape of decomposed core geometries may change according to the position of the input site. The shaping of core geometry reflects the electrotonic effectiveness of a synaptic site to any arbitrary locations which may lead to considerable savings in computations on synaptic effects. The detailed, computer-reconstructed geometry of the apical dendritic field of the pyramidal cell has been analysed by the proposed method. The frequency-dependence of input impedances has been compared between the original and the transformed core geometries assuming that the current is injected into the soma. The significance of dendritic irregularities in the impedance matching has been studied when the shaping of the core geometry has been induced by laminar inputs. The proposed approach may be useful in comparing the input dependence of the receptive fields of different non-smooth cells. The mismatch of the core geometries induced by the opposite travelling waves from the same anatomical location has also been studied and the possible control of the preferred, direction-sensitive activities will be discussed. The important differences between the compartmental modelings based on the known isotropic treatment of dendrites and the more realistic anisotropic approach will be illustrated.

Animals↗
PubMed1992

Enhanced calcium uptake by CA1 pyramidal cell dendrites in the postischemic phase despite subnormal evoked field potentials: excitatory amino acid receptor dependency and relationship to neuronal damage.

After 6-12 h of recovery from transient cerebral ischemia, the pyramidal cells of the hippocampal CA1 region take up excessive amounts of calcium upon electrical stimulation, which has been suggested to be important for the development of delayed neuronal death. The aim of this study was to further characterize this enhanced calcium uptake with respect to time-course of development, relationship to neuronal damage, and amplitude of evoked field potentials as well as the dependency on N-methyl-D-aspartate (NMDA) and non-NMDA receptors. Adult Wistar rats were used and calcium-sensitive microelectrodes were placed in the stratum radiatum of the CA1 hippocampus for recording of the extracellular calcium concentration ([Ca2+]ec) during 20 min of ischemia and for 6 h of reflow. High-frequency stimulation of the perforant pathway elicited burst firing in CA1 and a transient decrease in [Ca2+]ec which reflects neuronal uptake. Shifts in [Ca2+]ec could not be evoked 0-1 h after ischemia. However, from 1-2 h burst firing could be evoked and the accompanying shift in [Ca2+]ec increased thereafter in amplitude with prolonged reflow, exceeded preischemic levels after 4 h, and reached 250 +/- 116% (mean +/- SD) of control after 6 h of reflow (p less than 0.05). The extracellular reference potential shift during electrical stimulation and the amplitude of evoked field potentials were still subnormal after 6 h [85 +/- 25% and 83 +/- 25%, respectively (mean +/- SD)]. There was a significant correlation between the degree of stimulated calcium uptake at 6 h postischemia and the extent of CA1 damage evaluated 7 days after the ischemic insult (r = 0.849; p less than 0.001). The shifts in [Ca2+]ec were reduced by the NMDA antagonist MK-801 (0.5-2 mg/kg, i.v.) to approximately 50% of the initial level during both control and postischemic conditions (p less than 0.01). The non-NMDA antagonist 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo[F]quinoxaline (NBQX) (42 +/- 13 mg/kg, i.p.; mean +/- SD) decreased the amplitude of the evoked field potentials (to 30 +/- 28% of control, p less than 0.05) and completely abolished the evoked shifts in [Ca2+]ec. In conclusion, the uptake of calcium into CA1 pyramidal cells during electrical stimulation was enhanced already 4 h after ischemia in spite of the fact that other measures of excitability were subnormal. This calcium uptake correlated to the extent of CA1 pyramidal cell damage and was dependent on both NMDA and non-NMDA receptor activation.

Analysis of Variance↗
PubMed1992

Neuropathology of the chronic epileptic syndrome induced by intrahippocampal tetanus toxin in rat: preservation of pyramidal cells and incidence of dark cells.

A few nanograms of tetanus toxin injected into a rat hippocampus causes a chronic epileptic syndrome characterized by brief seizures that recur intermittently for about 6 weeks. Cognitive and other behavioural impairments persist after the seizures and other epileptic electrographic activity have remitted, and may be permanent. Our previous studies suggested that the behavioural changes following seizure remission were an indication of functional impairment associated with decreased neuronal excitability rather than with neuronal loss. The conclusion that neurons were preserved relied on qualitative histological observations and, indirectly, on electrophysiological measurements of the amplitudes of antidromic population spikes. Recently, gross histopathology has been described in a quantitative histological study of rats 7-10 days after they had received rather higher doses of intrahippocampal tetanus toxin. Here we report a quantitative histological study of hippocampi from rats which had gained remission from seizures induced by low doses of tetanus toxin. Adult Sprague Dawley rats received unilateral injections of 3-4 ng (about 6-8 mouse LD50) tetanus toxin, or vehicle, into the dorsal hippocampus. The first experiment confirmed that postsynaptic evoked responses recorded from pyramidal cells were depressed 10-19 weeks after injection. Unexpectedly, there also was a decrease of 20% in the antidromic response from CA3a contralateral to the injection. However, cell counts in these hippocampi revealed no change in pyramidal cell numbers. The second experiment used rats from two breeding colonies, prepared for histology 7 weeks after injection. Hippocampal pyramidal cell numbers were within the normal range in all but three of the 24 rats that had received tetanus toxin. These three had lesions of the CA1 pyramidal layer contralateral to the injection. The lesions were of the order of 2 mm in diameter, and were associated with glial proliferation. When these three cases were excluded, there remained a small increase in glial density in CA1 of the toxin-injected rats. In addition, toxin-injected rats from one of the colonies were susceptible to a pathology known as acidophylic or dark cell change. These occurred in 11 of 18 toxin-injected rats from this colony, in all divisions of the pyramidal layer, in both the injected and the contralateral hippocampus (where parallel studies revealed independent secondary epileptic foci). We conclude that loss of pyramidal neurons is not necessary for the persistent behavioural changes in this model.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1983

[Relation between lipofuscin content and organelle density in pyramidal cells of laminae III and V of area 10 (Brodmann) of the cerebral frontal lobe of humans of different ages].

The areal portion of the lipofuscin granules and mitochondria contained in ultrathin sections, the length of rough endoplasmic reticulum (RER) and the numerical density of ribosomes were determined in the pyramidal cells of layers III and V of area 10 (Brodmann) of the frontal brains of six newly died persons of different ages. This revealed considerable differences in lipofuscin contents and numerical density of organelles between the pyramidal cells and greater values, on an average, for the pyramidal cells of layer III. The comparison of averages for the single brains did not show the continuity nor the age dependence of changes but rather the individual variability of these processes. The expected decrease of the density of organelles with increasing lipofuscin contents was found more frequently only at extremely high values of lipofuscin contents. It becomes evident that even under the conditions of lipofuscin accumulation the permanently necessary physiological renewal of cell structures involved in metabolism is guaranteed over a longer period of time and that their full performance is almost completely unimpaired during this phase.

Adult↗
PubMedDate not supplied

The action of thallium on the excitability of CA1 pyramidal cells in hippocampal slices.

The effect of thallium ions on central neuronal activity was investigated in hippocampal slice preparations from guinea pigs and rats using extra- and intracellular recording techniques. Thallium induced a reversible and concentration-dependent reduction of the orthodromically evoked compound action potential of CA1 pyramidal cells with only weak effects on either afferent fiber activity, postsynaptic potentials or antidromically evoked responses. The membrane potential and input resistance of the pyramidal cells were not impaired by thallium. In contrast, variations in the maintained spike activity and spontaneously occurring inhibitory postsynaptic potentials were observed. It is concluded, that in contrast to its presynaptic action in the peripheral nervous system, thallium has a predominant postsynaptic target site in the hippocampal slice preparation. It is suggested that the neurotoxic action of thallium is not mediated by an interaction with specific ion channels of the cell membrane, but rather by an unspecific influence on the intracellular metabolism of the CA1 pyramidal cell.

Action Potentials↗
PubMed1990

Organization of intrahippocampal projections originating from CA3 pyramidal cells in the rat.

The distribution of intrahippocampal projections arising from the CA3 region of the rat hippocampus was investigated using in vitro and in vivo methods. In the in vitro hippocampal slice preparation, single CA3 pyramidal cells were intracellularly labeled with horseradish peroxidase (HRP), and the three-dimensional organization of the axonal plexus was analyzed by using a computer-aided digitizing system. As many as eight primary collaterals originated from the principal axon of CA3 pyramidal cells and these commonly bifurcated further and innervated stratum oriens and stratum radiatum of CA3 and CA1. Within the 400 microns slice, the summed length of all visible collaterals per neuron ranged from 2.6 mm to approximately 12.5 mm. While the CA3 principal axon tended to be relatively smooth, the axonal collaterals bore numerous varicosities that electron microscopy confirmed to be presynaptic boutons. These varicosities occurred, on average, once every 7 microns of collateral length. The distribution of axonal collaterals differed depending on the location of the parent pyramidal cell. Only rarely could CA3 collaterals be followed in the slice to their terminations within CA1. To study the topographic organization of CA3 projections both to other levels of CA3 and to CA1, the anterograde tracer, Phaseolus vulgaris leucoagglutinin (PHA-L) was injected into various transverse and septotemporal levels of CA3. Immunohistochemical visualization of the lectin was conducted in dissected and "extended" hippocampi to facilitate analysis of the topographic distribution of projections along the long or septotemporal axis. Projections from all portions of CA3 reached widespread regions of CA3, CA2, and CA1, but only a few fibers entered the subicular complex and there were no projections to the entorhinal cortex. There were also some CA3 and CA2 projections to the hilus of the dentate gyrus, but these did not enter the granule cell or molecular layers. The CA3 projections to CA1 were organized according to several distinctive and consistent gradients that can generally be summarized as follows. 1. CA3 cells located close to the dentate gyrus (proximal CA3), while projecting both septally and temporally, tended to project more heavily to levels of CA1 located septal to the injection site. CA3 cells located closer to CA1, in contrast, projected more heavily to levels of CA1 located temporally to the injection site. 2. At, or close to, the septotemporal level of the injection, cells located proximally in CA3 gave rise to collaterals that tended to terminate more superficially in stratum radiatum than did those arising from mid and distal levels of CA3.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1982

Baclofen selectively inhibits transmission at synapses made by axons of CA3 pyramidal cells in the hippocampal slice.

The effects of baclofen, an antispastic drug, on excitatory transmission were tested by bath application to the hippocampal slice preparation. (+/-)-Baclofen (20 microM) strongly depressed extracellularly recorded synaptic responses to stimulation of projections that originate from CA3 hippocampal pyramidal cells. Responses to stimulation of four other excitatory pathways were little affected and the amplitudes of presynaptic fiber potentials and antidromic responses were unaltered. When tested on the Schaffer collateral-commissural-CA1 pyramidal cell synapse. (-)-baclofen depressed the amplitude of the extracellular excitatory postsynaptic potential with an IC50 of 3.7 microM and was 180 times more potent than (+)-baclofen. gamma-Aminobutyric acid, 3-aminopropanesulfonic acid and imidazole-4-acetic acid also inhibited transmission at this site. Baclofen could suppress the response completely, and its action was unaffected by bicuculline. In contrast, imidazole-4-acetic acid could suppress the response by a maximum of only 75%, and its action was highly sensitive to bicuculline. gamma-Aminobutyric acid and 3-aminopropanesulfonic acid could suppress the response completely, and their actions were relatively weakly antagonized by bicuculline. These results are consistent with the hypothesis that baclofen inhibits excitatory transmission by interacting with a bicuculline-insensitive gamma-aminobutyric acid receptor. These receptors may be located on one type of glutamatergic/aspartergic synaptic terminal, exemplified by axon terminals of CA3 hippocampal pyramidal cells. Synapses made by these axons may therefore serve as models for studying the mechanism of action of baclofen.

Action Potentials↗
PubMed1986

Effects of histamine on hippocampal pyramidal cells of the rat in vitro.

The actions of bath applied histamine on CA1 pyramidal cells were investigated in hippocampal slices of the rat. Histamine caused a) a slight depolarization but no significant change in resting membrane conductance; b) an abbreviation of long afterhyperpolarizations after single action potentials, bursts of action potentials or TTX resistant spikes; c) a loss of accommodation of firing. In the presence of TEA or barium, histamine prolonged and increased the size and number of the slow TTX resistant spikes. A depolarizing plateau which follows such spikes was also increased by histamine, but the population spike was increased. The frequency of spontaneous chloride dependent potentials, which reflect interneurone firing, was also increased. These effects considerably outlasted histamine application and were mimicked by the H2-agonist impromidine but not the H1-agonist thiazolethylamine, and blocked by the H2-antagonists cimetidine and metiamide but not the H1-antagonists mepyramine or the beta-antagonist propranolol. It is concluded that histamine, by activating H2-receptors, antagonizes a calcium mediated potassium conductance in hippocampal pyramidal cells without affecting calcium current. By this mechanism histaminergic afferent fibres could effectively regulate cortical responsiveness by selectively potentiating large excitatory inputs of target neurones.

Animals↗
PubMed1988

Water-maze learning and effects of cholinergic drugs in mouse strains with high and low hippocampal pyramidal cell counts.

Morphological differences have been found in inbred strains of mice in the number and volume of pyramidal cells in Ammon's horn of the hippocampus. Among the mouse strains surveyed, NZB/BINJ (NZB) and C57BL/10J (B10) are most divergent in both total volume and total number of neurons. These genetically derived differences were exploited to determine hippocampal involvement in the acquisition of a spatial water maze. Genetic differences in hippocampal cell number were related to the acquisition of this spatial task. Mice with small numbers of hippocampal pyramidal cells, the B10 strain, acquired a water-maze task more slowly than either NZB mice or (NZBxNZW) F1 (NZBWF) animals. In addition, strain differences in responsivity to cholinergic manipulations were found. B10 mice were more sensitive than NZB or NZBWF mice to both the disruptive effects of scopolamine and the facilitory effects of physostigmine on swim maze learning. Although other inherited differences undoubtedly exist between these strains as is apparent in other mouse lines, these data suggest a prominent role for the hippocampus in the learning of spatially oriented behavior. Furthermore, this behavior appears to be responsive to cholinergic manipulations.

Animals↗