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PubMed1978

Catecholamine innervation of the basal forebrain. II. Amygdala, suprarhinal cortex and entorhinal cortex.

The catecholamine (CA) innervation of the posterior basal forebrain, the amygdala, suprarhinal cortex and entorhinal cortex, was studied in the rat using biochemical assay and fluorescence histochemistry. The assay studies demonstrate a moderate norepinephrine (NE) content in the amygdala and entorhinal cortex with a lower value for the suprarhinal cortex. Following destruction of the locus coeruleus, the decrease in NE content of these basal forebrain structures indicates that their principal NE innervation is from locus coeruleus. An additional small NE input arises from the medullary NE neuron groups. Ablation of dopamine (DA) cell groups (substantia nigra-ventral tegmental area, SN-VTA) indicates that the DA input to the amygdala arises from the lateral VTA and medial half of the SN. Fluorescence histochemical studies using the glyoxylic acid-Vibratome technique demonstrate the presence of four distinct types of CA neuron terminal plexus in the posterior basal forebrain. These include two different DA fiber types arising in SN-VTA, small NE fibers with small varicosities arising in locus coeruleus and NE fibers with larger varicosities arising in other brainstem NE cell groups. The large NE fibers appear to enter the amygdala via the ansa peduncularis-ventral amygdaloid bundle to innervate the central and basolateral nucleus and the anterior amygdaloid area. The locus coeruleus NE fibers appear to enter the posterior basal forebrain via both the stria terminalis and ansa peduncularis-ventral amygdaloid bundle system to form a moderately dense innervation of the central and basolateral nuclei of the amygdala and a less dense innervation of the other areas. The DA neuron axons are concentrated in the central and basal nuclei and intercalated cell groups. Other areas receive a more diffuse DA input, with the exception of the moderately dense innervation of the suprarhinal cortex and DA "islands" in the ventral-anterrior entorhinal cortex, The DA input to the posterior basal forebrain is complex and heterogeneous and the axonal morphology differs greatly among the terminal fields within the amygdala and adjacent cortical areas.

Amygdala↗

PubMed1995

Expression of vimentin increases in the hippocampus and cerebral cortex after entorhinal cortex lesioning and in response to transforming growth factor beta 1.

Entorhinal cortex lesions (ECL) that damage the perforant path to the dentate gyrus of the hippocampal formation were used to model the regulation of vimentin (VIM) mRNA. ECL increased VIM mRNA in the ipsilateral hippocampus and in the ipsilateral cortex including the wound cavity within 1 day. By in situ hybridization, at 4 days post-ECL, VIM mRNA increased two-fold in the molecular layer of the dentate gyrus. VIM protein was co-localized by immunocytochemistry to astrocytes and microglia/macrophages. Transforming growth factor-beta 1 (TGF-beta 1), which was previously shown to increase in microglia/macrophages of the molecular layer after hippocampal deafferentation by ECL, was investigated as a regulator of VIM expression. Infusions of TGF-beta 1 into the lateral ventricle induced VIM mRNA with dose-dependence, e.g. infusion of 100 ng TGF-beta 1 increased VIM mRNA three-fold. The increase in VIM mRNA was localized by in situ hybridization to astrocytes and microglia in the molecular layer of the dentate gyrus. These findings further implicate TGF-beta 1 as a regulator of cytoskeletal proteins during synaptic reorganization.

Animals↗

PubMed1993

Early areal differentiation of the human cerebral cortex: entorhinal area.

The early cytoarchitectonic specialization and area-specific differentiation of the prospective entorhinal cortex were studied in the postmortem human fetal brains (9.5-13.5 postovulatory weeks). At 10 weeks, using the Golgi method, we saw the appearance of area-specific large neurons (promoter neurons) with widely bifurcating apical dendrites situated at the outer margin of the cortical plate of the prospective entorhinal cortex. The analysis of the serial Nissl-stained sections revealed the concomitant appearance of a one-cell-thick layer (monolayer) at the interface between the cortical plate and the marginal zone and multilaminated spread of the deep part of the cortical plate. This is the earliest sign of area-specific cytoarchitectonic differentiation of all pallial regions characterized by the presence of the typical cortical plate. The first subareal differentiation within the entorhinal cortex begins at 13 postovulatory weeks with uneven development of fiber-rich lamina dissecans, which separates two cellular laminae principals (externa and interna), and with the appearance of characteristic cell islands of the prospective layer II. At rostral levels, cell islands begin to develop in the rostromedial entorhinal area at the subpial depths where large promoter neurons reside. At intermediate levels, both lamina dissecans and lamina principalis interna are well delineated. At caudal levels, lamina principalis interna is continuous with the upper subplate zone of the adjacent neocortex. Both area-specific neurons (promoters) and fiber-rich (afferent) strata develop synchronously during the earliest areal differentiation of the cerebral cortex. The precocious lamination of the cortical plate is the crucial event in the histogenesis of the entorhinal cortex.

Afferent Pathways↗

PubMed1999

Excitatory actions of NMDA receptor antagonists in rat entorhinal cortex and cultured entorhinal cortical neurons.

We have characterized excitatory effects of non-competitive NMDA receptor antagonists MK-801, PCP, and ketamine in the rat entorhinal cortex and in cultured primary entorhinal cortical neurons using expression of immediate early gene c-fos as an indicator. NMDA receptor antagonists produced a strong and dose-dependent increase in c-fos mRNA and protein expression confined to neurons in the layer III of the caudal entorhinal cortex. Induction of c-fos mRNA is delayed and it is inhibited by antipsychotic drugs. Cultured entorhinal neurons are killed by high doses of MK-801 and PCP but c-fos expression is not induced in these neurons indicating that this in vitro model does not fully replicate the in vivo effects of PCP-like drugs in the entorhinal cortex. Excitatory effects of the NMDA receptor antagonists may be connected with the psychotropic side effects of these drugs and might become a useful model system to investigate neurobiology of psychosis.

Animals↗

PubMed1984

Inputs from the olfactory bulb and olfactory cortex to the entorhinal cortex in the cat. I. Anatomical observations.

The spatial organization and laminar distribution of projections from the olfactory bulb and the anterior (PPCa) and posterior (PPCp) divisions of the prepiriform cortex to the entorhinal cortex were studied with anterograde (3H-leucine) and retrograde (WGA-HRP) tracing techniques. After 3H-leucine injections into the olfactory bulb transported labeling was seen over the lateral entorhinal area, except its most medial part, and over the rostral part of the medial entorhinal area. The labeling covers exclusively layer Ia. The lateral and medial entorhinal areas are also reached by fibers from the prepiriform cortex. The projection to the medial entorhinal area has not been described previously. Following injections of 3H-leucine into the PPCa transported labeling is present over the entire expanse of the entorhinal cortex and is located over layer Ib with the greatest density in its superficial part. Injections of 3H-leucine into the PPCp give rise to transported labeling over much of the entorhinal cortex. No labeling was found over the most medial parts of the medial subdivision (VMEA) of the lateral entorhinal area and the medial entorhinal area. Labeling occupies layer Ib, especially its middle part, and layers II and III. Both PPCa and PPCp appear to project most heavily to the dorsal (DLEA) and ventral (VLEA) subdivisions of the lateral entorhinal area. From the retrograde experiments it can be inferred that cells of layers II and III of the PPCa project predominantly to the DLEA, whereas those of the PPCp project predominantly to the VLEA. The MEA receives its heaviest projection from layer II of both PPCa and PPCp.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

The distribution of tyrosine hydroxylase-immunoreactive fibers in the human entorhinal cortex.

The entorhinal cortex plays an important role in learning and memory, and it has been implicated as a site of dysfunction in some neuropsychiatric disorders such as schizophrenia. The organization of many components of the neural circuitry of this region, including dopaminergic afferents, has not been studied in detail. Using immunohistochemical techniques, we examined the density and laminar distribution of axons immunoreactive for tyrosine hydroxylase, the rate limiting enzyme in catecholamine biosynthesis, in the entorhinal cortex of eight control human brains. The density of tyrosine hydroxylase-containing axons decreased from rostral to caudal regions of entorhinal cortex. In addition, there was a prominent medial to lateral gradient of increasing fiber density. This gradient extended into the adjacent transentorhinal cortex, which contained the highest density of labeled axons of the regions studied. The laminar distribution of tyrosine hydroxylase-containing fibers also differed among the subdivisions of the entorhinal cortex. A bilaminar pattern of labeled axons in layers deep I-superficial II and in deep layer VI was present in the intermediate and caudal subdivisions of entorhinal cortex. In contrast, the olfactory and rostral subdivisions, as well as portions of the transentorhinal region, contained a trilaminar pattern, with a high density of tyrosine hydroxylase-immunoreactive axons in layers deep I-superficial II, deep III-IV and deep VI. In addition, radially-oriented bands of labeled fibers were observed extending between deep layer I and layer III, particularly in the rostral subdivision of the entorhinal cortex. In summary, tyrosine hydroxylase-containing afferents to the human entorhinal cortex are distributed in a characteristic regional and laminar pattern, and the lateral regions of the entorhinal cortex and the adjacent transentorhinal cortex are particularly densely innervated. These data contribute to the understanding of the normal circuitry of the human entorhinal cortex, and are of potential relevance to the pathophysiology of certain neuropsychiatric disorders, such as schizophrenia.

Adult↗

PubMed1997

Piriform cortex efferents to the entorhinal cortex in vivo: kindling-induced potentiation and the enhancement of long-term potentiation by low-frequency piriform cortex or medial septal stimulation.

The entorhinal cortex receives input from many cortical areas and mediates the flow of information between these sites and the hippocampal formation. Long-term synaptic plasticity in cortical efferents to the entorhinal cortex may contribute to the transmission of neural activity to the hippocampus, as well as the storage of information, but little is known about plasticity in these pathways. We describe here the use of evoked field potential recordings from chronically implanted electrodes in the rat entorhinal cortex to investigate synaptic plasticity in the large piriform (olfactory) cortex projection to the superficial layers of the entorhinal cortex. Both kindling-induced potentiation and long-term potentiation (LTP) were tested. In addition, we attempted to modulate LTP induction by the co-induction of frequency potentiation and by the co-activation of the medial septum. Epileptogenic kindling stimulations of the piriform cortex (1-s, 60-Hz trains 3 times/day for 5 days) were found to result in a reliable potentiation of field responses evoked by piriform cortex test pulses. Non-epileptogenic tetanization of the piriform cortex with 400-Hz 16-pulse trains reliably resulted in LTP effects. These effects could be augmented by embedding brief LTP induction stimuli within 11-pulse, 15-Hz trains that alone produce only frequency potentiation. Co-activating the medial septum with 10-Hz trains, just prior to tetanization of the piriform cortex, augmented LTP of piriform cortex inputs to the entorhinal cortex in an input-specific manner. All potentiation effects were found to last for periods of weeks. These findings demonstrate that both epileptogenic and non-epileptogenic piriform cortex stimulation induces lasting potentiation of population field responses in the entorhinal cortex of the awake rat. The LTP effects were inducible in a graded manner and were sensitive to the temporal context of stimulation. The finding that low-frequency activation of the septum can enhance plasticity in the entorhinal cortex adds to a body of data indicating a role for the medial septum in contributing to theta activity and plasticity in both the entorhinal cortex and hippocampal formation.

Animals↗

PubMed1997

Morphological characteristics of layer II projection neurons in the rat medial entorhinal cortex.

The entorhinal cortex receives inputs from a variety of neocortical regions. Neurons in layer II of the entorhinal cortex originate one component of the perforant path which conveys this information to the dentate gyrus and hippocampus. The current study extends our previous work on the electro-responsive properties of layer II neurons of the medial entorhinal cortex in which we distinguished two categories of layer II neurons based on their electrophysiological attributes (Alonso and Klink [1993] J Neurophysiol 70: 128-143). Here we report on the morphological features of layer II projection neurons, as revealed by in vitro intracellular injection of biocytin. We now report that the two electrophysiologically distinct types of neurons correspond to morphologically distinct types of cells. All neurons (65% of the total cells recorded) that developed sustained, subthreshold, sinusoidal membrane potential oscillations were found to have a stellate appearance. Neurons that did not exhibit oscillatory behavior had either a pyramidal-like (32%) or a horizontal cell morphology (3%). Stellate cells had multiple, thick, primary dendrites. Their widely diverging upper dendritic domain expanded mediolaterally over a distance of around 500 microns close to the pial surface. This mediolateral extent was more than double that of the pyramidal-like cells. Dendrites of stellate cells demonstrated long dendritic appendages, and their dendritic spines had a more complex morphology than those of nonstellates. The stellate cell axons emerged from a primary dendrite and were more than double the thickness (approximately 1.4 microns) of the axons of nonstellate cells. Recurrent axonal collaterization appeared more extensive in axons arising from stellate cells than from pyramidal-like cells.

Animals↗

PubMed1998

The perforant path projection from the medial entorhinal cortex layer III to the subiculum in the rat combined hippocampal-entorhinal cortex slice.

Intracellular recordings were performed to examine the perforant path projection from layer III of the entorhinal cortex to the subiculum in rat combined hippocampal-entorhinal cortex slices. Electrical stimulation in the medial entorhinal cortex layer III caused short latency combined excitatory and inhibitory synaptic responses in subicular cells. In the presence of the GABA(A) antagonist bicuculline and the GABA(B) antagonist CGP-55845 A inhibition was blocked and isolated AMPA- or NMDA receptor-mediated EPSPs could be elicited. After application of the non-NMDA antagonist NBQX and the NMDA antagonist APV excitatory responses were completely blocked indicating a glutamatergic input from the neurons of the medial entorhinal cortex layer III. By stimulation from a close (< 0.2 mm) position in the presence of NBQX and APV and either CGP-55845 A or bicuculline we could record monosynaptic fast GABA(A) or slow GABA(B) receptor-mediated IPSPs, respectively. We compared synaptic responses in subicular cells induced by stimulation in the medial entorhinal cortex layer III with responses elicited by stimulation of afferent fibres in the alveus. The EPSPs of subicular cells induced by stimulation of alvear fibres could be significantly augmented by simultaneous activation of perforant path fibres originating in the medial entorhinal cortex layer III, while delayed activation of alvear fibres after stimulation of the perforant path resulted in a weak inhibition of the alveus evoked EPSPs. Thus, the perforant path projection activates monosynaptic excitation of subicular neurons. Therefore the entorhinal cortex does not only function as an important input structure of the hippocampal formation but is also able to modulate the hippocampal output via the entorhinal-subicular circuit.

Animals↗

PubMed1996

Hyperexcitability of entorhinal cortex and hippocampus after application of aminooxyacetic acid (AOAA) to layer III of the rat medial entorhinal cortex in vitro.

1. Injection of aminooxyacetic acid (AOAA) into the entorhinal cortex in vivo produces acute seizures and cell loss in medial entorhinal cortex. To understand these effects, AOAA was applied directly to the medial entorhinal cortex in slices containing both the entorhinal cortex and hippocampus. Extracellular and intracellular recordings were made in both the entorhinal cortex and hippocampus to study responses to angular bundle stimulation and spontaneous activity. 2. AOAA was applied focally by leak from a micropipette or by pressure ejection. Evoked potentials increased gradually within 5 min of application, particularly the late, negative components. Evoked potentials continued to increase for up to 1 h, and these changes persisted for the remainder of the experiment (up to 5 h after drug application). 3. Paired pulse facilitation (100-ms interval) was also enhanced after AOAA application. Increasing stimulus frequency to 1-10 Hz increased evoked potentials further, and after several seconds of such stimulation multiple field potentials occurred. When stimulation was stopped at this point, repetitive field potentials occurred spontaneously for 1-2 min. These recordings, and simultaneous extracellular recordings in different layers, indicated that spontaneous synchronous activity occurred in entorhinal neurons. Intracellularly labeled cortical pyramidal cells depolarized and discharged during spontaneous and evoked field potentials. 4. The effects of AOAA were blocked reversibly by bath application of the N-methyl-D-aspartate (NMDA) receptor antagonist D-amino-5-phosphonovalerate (D-APV; 25 microM) or focal application of D-APV to the medial entorhinal cortex. 5. Simultaneous extracellular recordings from the entorhinal cortex and hippocampus demonstrated that spontaneous synchronous activity in layer III was often followed within several milliseconds by negative field potentials in the terminal zones of the perforant path (stratum moleculare of the dentate gyrus and stratum lacunosum-moleculare of area CA1). The extracellular potentials recorded in the dentate gyrus corresponded to excitatory postsynaptic potentials and action potentials in dentate granule cells. However, extracellular potentials in area CA1 were small and rarely correlated with discharge in CA1 pyramidal cells. 6. The results demonstrate that AOAA application leads to an NMDA-receptor-dependent enhancement of evoked potentials in medial entorhinal cortical neurons, which appears to be irreversible. The potentials can be facilitated by repetitive stimulation, and lead to synchronized discharges of entorhinal neurons. The discharges invade other areas such as the hippocampus, indicating how seizure activity may spread after AOAA injection in vivo. These data suggest that AOAA may be a useful tool to study longlasting changes in NMDA receptor function that lead to epileptiform activity and neurodegeneration.

Aminooxyacetic Acid↗

PubMed1995

CA3 neuronal degeneration follows chronic entorhinal cortex lesions.

Entorhinal cortex lesions are a common experimental paradigm to study memory function and neural plasticity after hippocampal deafferentation. The long term consequences of such lesions are of particular interest both in the context of these models and because pathological changes of Alzheimer's disease destroy entorhinal cortex projection neurons. We used stereological counting techniques to assess the structural integrity of the hippocampal formation 0.5-28 months after entorhinal lesion in the rhesus monkey. Surprisingly, 18-28 months after lesion the number of CA3 neurons was decreased by 57%, while neuron numbers in other subfields did not change. These results suggest that delayed transsynaptic neural degeneration can occur long after brain injury.

Animals↗

PubMed1994

Current density analysis of outward currents in acutely isolated rat entorhinal cortex cells.

Entorhinal cortex stellate and pyramidal cells were acutely isolated from juvenile rats. Using the whole-cell configuration of the patch-clamp method outward potassium currents were recorded. A fast transient A-current and a sustained outward current could be measured in both stellate and pyramidal cells. The A-current density was significantly larger in pyramidal cells than in stellate cells. In contrast, stellate cells possessed a larger current density of the delayed rectifier current as well as the Ca2+ activated K+ current than pyramidal cells. Moreover, superficial stellate cells exhibited large delayed rectifier currents and only small A-currents while entorhinal cortex deep layer pyramidal cells displayed larger A-currents than delayed rectifier currents.

Animals↗

PubMed1984

Inputs from the olfactory bulb and olfactory cortex to the entorhinal cortex in the cat. II. Physiological studies.

Field potentials and unit activity elicited by electrical stimulation of the olfactory bulb (OB) and anterior and posterior prepiriform cortex (PPCa and PPCp) were measured extracellularly in the entorhinal cortex (EC) of the cat. Different topographic distributions of the amplitude and peak latency of average evoked potentials (AEPs) were obtained depending on the stimulated area. The maximal evoked activity in the EC showed a gradient in a latero-medial direction with the extremes corresponding to the stimulation of OB and PPCp respectively. Analysis of firing patterns of units in the EC in response to stimulation of the OB, PPCa and PPCp showed that an appreciable number of units responded to stimulation of different areas, mainly PPCa and PPCp. It was found that the pathways being stimulated differed in conduction velocities with the PPCp-EC being the slowest. Most responding units lay in layer I and II of the EC. The AEPs to PPCa- and PPCp-stimulation presented different types of depth profiles. Stimulation of the PPCa evoked an initial surface-negative depth-positive potential whereas the PPCp evoked a different type of AEP with an initial positive component at the surface and negative in depth. It is assumed that the stimulated fibres have their active synapses at different levels within the superficial layers of the EC. The possibility of direct influence of olfactory inputs on the hippocampus mediated by one synapse in the EC is discussed.

Animals↗

PubMed1993

[3H]phorbol ester binding sites and neuronal plasticity in the hippocampus following entorhinal cortex lesions.

Entorhinal cortex lesioning (ECL) produces a loss of more than 80% of the synapses in the outer molecular layer of the hippocampus. However, the loss of synapses is transient. Beginning a few days after denervation, new synapses are formed, virtually replacing the lost inputs within 2 months. Synaptic remodelling induced by ECL is associated with specific modifications of neurotransmitters, hormones and growth factors. Particularly, protein kinase C (PKC) plays important functional roles in receptor-mediated transmembrane signal transduction. PKC is also involved in various aspects of synaptic plasticity, such as cellular growth and differentiation. To investigate further the potential roles of PKC in synaptic plasticity observed in the ECL model, [3H]phorbol 12,13-dibutyrate ([3H]PDBu) binding, a putative marker of PKC, was examined at different times post-lesion. [3H]PDBu binding sites transiently decreased bilaterally at 2 and 8 days post-lesion (20%) in different laminae and sub-fields of the rostral hippocampus but returned to control values at 14 and 30 days post-lesion. In caudal portion of the hippocampus, [3H]PDBu binding was also decreased at 2 days post-lesion but only on the contralateral side. Interestingly, [3H]PDBu binding sites in the cortex increased by up to 30% in the contralateral side while no significant change was observed in the ipsilateral side at any time post-lesion. It is known that PKC can be regulated by different systems following alterations of neuronal and glial activity. We suggest that these could be involved in the response of PKC and [3H]PDBu binding sites following ECL. Moreover, PKC seemed to be modified in different brain areas in neuronal inputs from the entorhinal cortex and the subsequent reinnervation process.

Acetylcholinesterase↗

PubMed1993

Relationships between stress protein induction and NMDA-mediated neuronal death in the entorhinal cortex.

The entorhinal cortex (EC) appears to be one of the earliest regions to express cellular pathology in aging and Alzheimer's disease. The relationships between cellular stress protein responses and the temporal and spatial aspects of cell death induced by N-methyl-D-aspartate (NMDA) was investigated in this anatomical region. Low doses of NMDA were infused stereotactically into the medial EC of the rat. At intervals starting from 0.5 h up to 7 days after a 1.25-microliters EC infusion of 15 mM NMDA, 30 mM NMDA, or saline, the expression of ubiquitin (Ub), 72-kDa heat shock protein (HSP 72), and c-Fos was determined in relation to neuronal death. Volumes of entorhinal Ub- and HSP 72-like immunoreactivity peaked between 18 and 48 h after either 15 or 30 mM NMDA infusions. After 15 mM NMDA infusions, maximal volumes of HSP 72- and Ub-like immunoreactivity in the EC at 48 h were similar to the subsequent maximal volume of neuronal loss in the EC seen after 96 hours. After infusion of 30 mM NMDA, the final EC volume of neuronal loss seen at 7 days after NMDA corresponded to 70-80% of the maximal HSP-Ub stress protein response seen at 2 days, implying that a population of HSP 72- and Ub-immunopositive cells survived the NMDA insult. C-Fos expression as determined by immunoreactivity for the nuclear phosphoprotein (Fos) indicated neuronal activation at NMDA infusion sites, in the perirhinal cortex, hippocampus, and other sites throughout the injected hemisphere. In the EC, c-Fos immunoreactivity returned to baseline levels by 8 h, well before the dramatic increases in HSP 72 and Ub volumes. Our results demonstrate that HSP 72 and Ub expression in vivo precedes and correlates with, but does not necessarily lead to, neuronal death following glutamate receptor-mediated toxicity in the EC.

Analysis of Variance↗

PubMed1991

Astrocytic apolipoprotein E mRNA and GFAP mRNA in hippocampus after entorhinal cortex lesioning.

Entorhinal cortex lesions (ECL) that damage the perforant path to the hippocampus induce rapid increases of apolipoprotein E (apo E) mRNA in the hippocampus. Apo E mRNA was localized in astrocytes by in situ hybridization in combination with immunocytochemistry for glial fibrillary acidic protein (GFAP). Unilateral ECL also increased hippocampal GFAP mRNA, with increases preceding those of apo E mRNA. The apo E mRNA and GFAP mRNA responses were transiently bilateral in non-denervated zones. The timing of response in apo E mRNA to deafferentation supports suggestions that apo E has roles in membrane remodelling during responses to neuron injury.

Animals↗

PubMed1990

Functional reciprocal connections of the rat entorhinal cortex and subicular complex with the medial frontal cortex: an in vivo intracellular study.

We used in vivo intracellular recording techniques in the rat in order to determine the properties of projections from the medial frontal cortex to the entorhinal cortex and subicular complex. Three main results were obtained. (1) A high proportion (65%) of neurons within the medial frontal cortex were antidromically activated at short latency (0.4-1.9 ms) by electrical stimulation of the entorhinal cortex or subicular complex. This provided physiological evidence for fast direct projections from the medial frontal cortex to the entorhinal cortex and subicular complex. (2) Clear excitatory postsynaptic potentials (EPSPs) were evoked in 8% of the cells within the entorhinal cortex, subicular complex, or adjacent cortices after electrical stimulation of the medial frontal cortex. (3) The most salient synaptic response was inhibition, as shown by the presence of inhibitory postsynaptic potentials (IPSPs) in 50% of the cells sampled. Similar results were obtained for the reciprocal pathway: 56% of the sampled cells in the entorhinal cortex or subicular complex responded with antidromic spikes to stimulation of the medial cortex; 4% of medial frontal neurons responded to stimulation of the entorhinal cortex or subicular complex with clear EPSPs, and 48% with IPSPs. The latencies of most synaptic responses, 15-25 ms, were inconsistent with monosynaptic activation. This suggests that oligosynaptic relays amplified the signal within or en route to their targets, and/or that cells with more slowly propagating axons were also present but not sampled by the intracellular electrodes. Finally, responsive fast-spiking cells (candidate inhibitory neurons) were encountered within target structures. The results provide evidence that these distant cortical regions are functionally connected in a reciprocal manner, and that both principal and inhibitory neurons are excited by this projection system.

Animals↗

PubMed1997

Morphological and electrophysiological characterization of layer III cells of the medial entorhinal cortex of the rat.

Entorhinal cortex layer III cells send their axons into hippocampal area CA1, forming the less well studied branch of the perforant path. Using electrophysiological and morphological techniques within a slice preparation, we can classify medial entorhinal cortex layer III cells into four different types. Type 1 and 2 cells were projection cells. Type 1 cells fired regularly and possessed high input resistances and long membrane time constants. Electrical stimulation of the lateral entorhinal cortex revealed a strong excitation by both N-methyl-D-aspartate and non-N-methyl-D-aspartate receptor-mediated excitatory postsynaptic potentials. Type 2 cells accommodated strongly, had lower input resistances, faster time constants and featured prominent synaptic inhibition. Type 1 and 2 cells responded to repetitive synaptic stimulation with a prolonged hyperpolarization. We identified the two other, presumed local circuit, cell types whose axons remained within the entorhinal cortex. Type 3 cells were regular firing, had high input resistances and slow membrane time constants, while type 4 cells fired at higher frequencies and possessed a faster time constant and lower input resistance than type 3 neurons. Type 3 cells presented long-lasting excitatory synaptic potentials. Type 4 neurons were the only ones with different responses to stimulation from different sites. Upon lateral entorhinal cortex stimulation they responded with an excitatory postsynaptic potential, while a monosynaptic inhibitory postsynaptic potential was evoked from deep layer stimulation. In contrast to type 1 and 2 neurons, none of the local circuit cells could be antidromically activated from deep layers, and prolonged hyperpolarizations following synaptic repetitive stimulation were also absent in these cells. Together, the complementing morphology and the electrophysiological characteristics of all the cells can provide the controlled flexibility required during the transfer of cortical information to the hippocampus.

2-Amino-5-phosphonovalerate↗