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PubMed1990

Properties of K-currents in unmyelinated presynaptic axons of brain revealed revealed by extracellular polarisation.

Thin pial surface slices of guinea-pig olfactory cortex contain unmyelinated axons derived from the lateral olfactory tract (LOT). The severed ends of the groups of these axons were drawn into a suction electrode to record the currents resulting from propagated action potentials. On stimulating these unmyelinated axons, a tetrodotoxin-sensitive positive current of 22.5 +/- 3.0 nA was recorded by the suction electrode. The positive current was often followed by a small negative current. A 100 mV positive polarisation applied to the suction electrode revealed a large negative after-current (25.8 +/- 3.5 nA). In contrast, the positive current was slightly reduced by the polarisation. The early phases of the negative after-current induced by the electrode polarisation were blocked by 3,4-diaminopyridine, 4-aminopyridine or 2,3-diaminopyridine (in order of potency). The entire negative after-current was blocked by prolonged (3 h) equilibration in a medium containing 3.5 mmol/l Cs and 1.5 mmol/l K. Tetraethylammonium (TEA) or Ba2+ by themselves had little effect. In aminopyridine, the residual negative after-current was blocked by TEA (10 mmol/l) or 1 mmol/l Ba2+. Muscarinic agonists had no effect on these currents. These experiments show that some axonal currents can be revealed by extracellular polarisation and that these axons rely on an 'A' type of current for the rapid repolarisation of the membrane although slower K-channels are present.

Action Potentials↗

PubMed2006

Acute changes in the neuronal expression of GABA and glutamate decarboxylase isoforms in the rat piriform cortex following status epilepticus.

The piriform cortex (PC) is the largest region of the mammalian olfactory cortex with strong connections to other limbic structures, including the amygdala, hippocampus, and entorhinal cortex. In addition to its functional importance in the classification of olfactory stimuli, the PC has been implicated in the study of memory processing, spread of excitatory information, and the facilitation and propagation of seizures within the limbic system. Previous data from the kindling model of epilepsy indicated that alterations in GABAergic inhibition in the transition zone between the anterior and posterior PC, termed here central PC, are particularly involved in the processes underlying seizure propagation. In the present study we studied alterations in GABAergic neurons in different parts of the PC following seizures induced by kainate or pilocarpine in rats. GABA neurons were labeled either immunohistochemically for GABA or its synthesizing enzyme glutamate decarboxylase (GAD) or by in situ hybridization using antisense probes for GAD65 and GAD67 mRNAs. For comparison with the PC, labeled neurons were examined in the basolateral amygdala, substantia nigra pars reticulata, and the hippocampal formation. In the PC of controls, immunohistochemical labeling for GABA and GAD yielded consistently higher neuronal densities in most cell layers than labeling for GAD65 or GAD67 mRNAs, indicating a low basal activity of these neurons. Eight hours following kainate- or pilocarpine-induced seizures, severe neuronal damage was observed in the PC. Counting of GABA neurons in the PC demonstrated significant decreases in densities of neurons labeled for GABA or GAD proteins. However, a significantly increased density of neurons labeled for GAD65 and GAD67 mRNAs was determined in layer II of the central PC, indicating that a subpopulation of remaining neurons up-regulated the mRNAs for the GAD isoenzymes. One likely explanation for this finding is that remaining GABA neurons in layer II of the central PC maintain high levels of activity to control the increased excitability of the region. In line with previous studies, an up-regulation of GAD67 mRNA, but not GAD65 mRNA, was observed in dentate granule cells following seizures, whereas no indication of such up-regulation was determined for the other brain regions examined. The data substantiate the particular susceptibility of the central PC to seizure-induced plasticity and indicate that this brain region provides an interesting tool to study the regulation of GAD isoenzymes.

Analysis of Variance↗

PubMed2002

Locus coeruleus activation modulates firing rate and temporal organization of odour-induced single-cell responses in rat piriform cortex.

Piriform cortex (PCx) is the primary cortical projection region for olfactory information and has bidirectional monosynaptic connections with olfactory bulb and association cortices. PCx neurons display a complex receptive field, responding to odours rather than their molecular components, suggesting that these neurons are involved in higher order olfactory processing. Neuromodulators, especially noradrenaline (NA), have important influences on sensory processing in other cortical regions and might be responsible for the plasticity observed in PCx during learning. The present study is the first attempt to examine in vivo the actions of NA on sensory responses in the PCx. Stimulation of the noradrenergic nucleus locus coeruleus (LC) was used to induce release of NA in the forebrain in urethane-anaesthetized rats. Extracellular recording of single units was made simultaneously in anterior and posterior PCx. The responses to an odour stimulus were measured over 25 trials. Twenty-five subsequent odour presentations were preceded by stimulation of the ipsilateral LC through a bipolar electrode, previously placed in the LC under electrophysiological control. This priming stimulation modified the activity of 77 of the 135 recorded neurons. For most cells, LC stimulation enhanced cortical responses to odour in terms of both spike count and temporal organization, with some differential effects in anterior and posterior regions. These results are the first to show enhancement of sensory responses in the olfactory cortex by LC activation. Spontaneous activation of LC neurons such as occurs during learning could serve to enhance olfactory perception and promote learning.

Action Potentials↗

PubMed1975

The claustrum in the dog brain.

The structure of the claustrum was studied in the dog brain using Weigert's, Klüver-Barrera's, Manns' and Nissl's methods. It consists of two main parts arranged one above the other. The dorsal part is situated in the depth of the neocortex and extends from the gyrus orbitalis to the gyrus compositus posterior. The ventral part of the claustrum underlying the olfactory cortex continues from the cuadal fragments of the olfactory peduncle to the entorhinal area, where it fuses with its deep layers. The claustrum can be regarded as a fragment of a bigger cellular formation present in different parts of the hemisphere.

Animals↗

PubMed1985

The co-occurrence of a substance P-like peptide and cholecystokinin-8 in a fiber system of turtle cortex.

Single-label and double-label immunohistochemical techniques were used to demonstrate the coexistence of substance P-like immunoreactivity (SPLI) and cholecystokinin-8-like immunoreactivity (CCK-8-LI) in an extensive fiber system within the telencephalic cortex of turtle. All SPLI-containing fibers and terminals of this system contain CCK-8-LI and vice versa. The fibers of this system course from more medial cortical regions to more lateral ones, originating either from neurons in the more medial cortices or from extracortical neurons, the axons of which ascend the medial wall of the cortex. The precise location of the neurons that give rise to this cortical projection system is uncertain, but a hypothalamic location seems most likely at present. The fibers and terminals of this system are found throughout the entire mediolateral and rostrocaudal extent of the telencephalic cortex of turtle and are largely confined to the cell body layer of the cortex. Fewer SPLI/CCK-8-LI-containing fibers are found in pyriform (olfactory) cortex than in the other cortices. Ultrastructural studies indicate that SPLI/CCK-8-LI-containing terminals make asymmetric synapses on cell bodies or their proximal dendrites. Both SPLI and CCK-8-LI are found in large dense core vesicles in these labeled terminals. Labeled terminals also contained numerous small, round, unlabeled vesicles clustered near synaptic release sites and a number of unlabeled large dense core vesicles. Quantification of the percentage of the large dense core vesicles that were labeled in SP-labeled terminals, in CCK-8-labeled terminals, and in terminals labeled for both SP and CCK-8 provided suggestive evidence that SPLI and CCK-8-LI must be contained within the same large dense core vesicles. Radioimmunoassay indicated that the SP/CCK-8-containing system of turtle cortex contains 0.93 +/- 0.090 pg of SP/microgram of cortical tissue protein and 0.31 +/- 0.11 pg of CCK-8/micrograms of cortical tissue protein. The CCK-8-like material in turtle cortex coelutes with CCK-8-sulfate, using gradient elution high pressure liquid chromatography (HPLC). The SP-like material, although immunologically highly similar to undecapeptide SP (Reiner, A., J. E. Krause, K. T. Keyser, W. D. Eldred, and J. F. McKelvy (1984) J. Comp. Neurol. 226: 50-75), does not coelute with undecapeptide SP using gradient elution HPLC.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2002

NMDA receptor-dependent long-term synaptic depression in the entorhinal cortex in vitro.

The entorhinal cortex receives a large projection from the piriform (primary olfactory) cortex and, in turn, provides the hippocampal formation with most of its cortical sensory input. Synaptic plasticity in this pathway may therefore affect the processing of olfactory information and memory encoding. We have recently found that long-term synaptic depression (LTD) can be induced in this pathway in vivo by repetitive paired-pulse stimulation but not by low-frequency (1 Hz) stimulation with single pulses. Here, we have used field potential recordings to investigate the stimulation parameters and transmitter receptors required for the induction of LTD in the rat entorhinal cortex in vitro. The effectiveness of low-frequency stimulation (900 pulses at 1 or 5 Hz) and repeated delivery of pairs of stimulation pulses (30-ms interpulse interval) was assessed. Only repeated paired-pulse stimulation resulted in lasting LTD, and a low-intensity paired-pulse stimulation protocol that induces LTD in vivo was only effective in the presence of the GABA(A) receptor antagonist bicuculline (50 microM). LTD could also be induced in normal ACSF, however, by increasing the number of pulse-pairs delivered and by increasing the stimulation intensity during LTD induction. The induction of LTD was blocked by constant bath application of the N-methyl-d-aspartate (NMDA) glutamate receptor antagonist d-2-amino-5-phosphonovalerate (50 microM), indicating that LTD is dependent on NMDA receptor activation. However, LTD was not blocked by the group I/II mGluR antagonist (RS)-alpha-ethyl-4-carboxyphenylglycine (500 microM) or by bicuculline (50 microM). The induction of LTD in the entorhinal cortex in vitro is therefore dependent on intense stimulation that recruits activation of NMDA receptors, but does not require concurrent activation of mGluRs or inhibitory synaptic inputs.

2-Amino-5-phosphonovalerate↗

PubMed1993

Synaptic events that generate fast oscillations in piriform cortex.

Prominent, odor-evoked, fast (40-60 Hz) oscillations have been reported in the olfactory bulb and piriform (primary olfactory) cortex of both awake-behaving and anesthetized animals. The present study used current source-density analysis to examine the origin of the fast oscillations evoked by single weak shocks to afferent fibers. These shock-evoked oscillations closely resemble those evoked by odor. The results revealed that each cycle of the oscillatory field potential was generated by a stereotyped series of membrane currents similar to those previously characterized in the nonoscillatory response to strong afferent fiber shocks. Each cycle began with a strong inward current in layer la identified as an EPSC mediated by afferent fibers in distal apical dendrites of pyramidal cells. This afferent input was followed by a strong inward current in layer Ib identified as an EPSC mediated by intrinsic association fibers in middle apical dendritic segments. These excitatory events were followed by a smaller inward current at the depth of pyramidal cell somata (layers II and superficial III) that may be the depolarizing Cl(-)-mediated IPSC previously identified in the strong-shock response. Based on an analysis of the timing of the EPSCs it was concluded that the weak shock-evoked oscillation is generated in the olfactory bulb and that the resulting periodic activity in afferent fibers drives the oscillation in the piriform cortex.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗

PubMed2004

The potion's magic.

During remembering, a perception of the past is constructed that includes sensory details of the original episode. In this issue of Neuron, Gottfried and colleagues provide evidence for selective piriform activation during recognition of visual cues previously paired with scents. These data provide evidence of sensory-specific reactivation of olfactory cortex during remembering.

Auditory Cortex↗

PubMed2002

Central olfactory connections in the microsmatic marmoset monkey (Callithrix jacchus).

The mammalian primary olfactory system consists of a set of different telencephalic structures, including paleo-, archi-, periarchi- and mesocortical components. We present the first characterisation of the normal and connectional anatomy of the primary olfactory cortex of the common marmoset, a microsmatic simian species increasingly used in primate research. The centrifugal and centripetal bulbar projections were determined by injections of the anterograde and retrograde tracer wheat germ agglutinin-conjugated horseradish peroxidase and fluorescent dyes into the ipsilateral main olfactory bulb. The efferent projections of the marmoset bulb are organised entirely ipsilaterally and are established via a rudimentary medial olfactory tract and the dominant lateral olfactory tract. Target areas are the anterior olfactory nucleus, the entire prepiriform cortex, ventral tenia tecta, periamygdaloid cortex and the rostral part of the entorhinal cortex. The bulbar axons predominantly terminate in the outer part of layer I. The anterior olfactory nucleus receives a weak additional input within layer II and III, which is not found in macrosmatic rodents. Further anterograde labelling was found in the endopiriform nucleus deep under the prepiriform cortex and within an anterolateral strip of the olfactory tubercle. However, control injections into the olfactory tubercle suggest that the marmoset olfactory tubercle receives a bisynaptic olfactory input only. Retrograde labelling after bulb injections revealed that, except for the olfactory tubercle, all primary olfactory cortices contributed to an ipsilateral bulbopetal feedback projection. Like in rodents, the only bulbopetal projection organised bilaterally in the marmoset is maintained by the anterior olfactory nucleus. With few exceptions, the projections of the marmoset olfactory brain are organised similarly to that of the macaque monkey or those of macrosmatic species.

Animals↗

PubMed1975

Water contents of various regions of the feline nervous system.

A systematic analysis of the regional water content of the feline nervous system was made. In general, areas rich in grey matter contained about 10-15% more water than white matter areas. Percentage water values were lowest for cranial and peripheral nerves and highest for cerebral cortex, cerebellar cortex, olfactory bulb and other grey matter regions. Values for cerebral cortex varied from about 81.5% for suprasplenic gyrus to over 84% for frontal gyrus. It is suggested that the effective concentrations of dissolved substances in various regions of the nervous system might be influenced greatly by these differences in water content.

Animals↗

PubMed2004

Bilateral microinjections of vigabatrin in the central piriform cortex retard amygdala kindling in rats.

The piriform cortex (PC) is the largest region of the mammalian olfactory cortex with strong connections to limbic structures, including the amygdala, hippocampus, and entorhinal cortex. Various previous studies in rodents suggest that the PC might be very important in the development and maintenance of limbic kindling, i.e. a widely used model of temporal lobe epilepsy. GABAergic inhibition in the transition zone between the anterior and posterior PC, termed here central PC, seems to be particularly involved in the processes leading to progression of kindled seizures. This prompted us to study whether elevation of GABA levels in this subregion of the PC by bilateral microinjection of vigabatrin is capable of suppressing amygdala kindling. Rats were stimulated once daily until fully kindled (stage 5) seizures had developed. Vigabatrin (10 microg) was injected 24 h before the first stimulation as well as 6 h before the 5th and 10th stimulation, which approximately doubled the number of stimulations required for kindling development compared with controls. This marked retardation of kindling acquisition was predominantly due to a significant inhibition of the progression from stage 1 to stage 2 and stage 3 to stage 4 seizures, demonstrating that microinjection of vigabatrin into the central PC markedly inhibits the progression and secondary generalization of focal seizures emanating from the amygdala.

Amygdala↗

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↗

PubMed2002

Slit1 and slit2 proteins control the development of the lateral olfactory tract.

The development of olfactory bulb projections that form the lateral olfactory tract (LOT) is still poorly understood. The septum and the olfactory cortex have been shown to secrete diffusible factors repelling olfactory axons in vitro and are likely to cause the axons to avoid the septum region in vivo. Slit2, a member of the Slit gene family, has been proposed to be this septal factor based on its expression in the embryonic septum and its ability to repel and collapse olfactory axons. However, this issue is still controversial, and recent in vitro studies have questioned the role of the septum and Slit proteins in organizing LOT projections. We therefore decided to examine directly the role of Slit proteins in mediating olfactory axon guidance in vivo using mice with targeted deletions in the Slit1 and Slit2 genes. When olfactory bulb explants are cocultured with septum from Slit1- and/or Slit2-deficient mice, the septum repulsive activity for olfactory bulb axons is progressively abolished in a gene dose-dependent manner. Anterograde tracing of olfactory bulb axons showed that the LOT develops normally in Slit1 or Slit2 single-deficient mice but is completely disorganized in Slit1/Slit2 double-deficient embryos, with many axons reaching the midline and entering the septum region. Therefore, our study showed that the septum chemorepellent is a combination of Slit1 and Slit2 and that these molecules play a significant role in olfactory bulb axon guidance in vivo.

Animals↗

PubMed1980

Chronic haloperidol or fluphenazine: effects on dopamine metabolism in brain, cerebrospinal fluid and plasma of Cercopithecus aethiops (vervet monkey).

Chronic treatment with haloperidol for 3 to 5 weeks (0.5 mg/kg, daily) resulted in significant increases of homovanillic acid (HVA) content in dorsal and orbital frontal cortex and in cingulate cortex. No change in HVA was seen in the olfactory cortex, basal ganglia, cisternal cerebrospinal fluid or plasma of animals chronically treated with haloperidol. Treatment with a single weekly dose of fluphenazine decanoate (5 mg/kg) for 3 weeks resulted in increased HVA levels in all the above brain regions, cisternal cerebrospinal fluid and plasma. Moreover, the fluphenazine-treated group had a significantly higher incidence of extrapyramidal side effects than the haloperidol-treated group. It is concluded that chronically increased dopamine metabolite production in the basal ganglia but not in cortex is reflected by increases in the HVA level of cerebrospinal fluid and plasma and is accompanied by severe extrapyramidal side effects.

Animals↗

PubMed1991

Higher olfactory processes: perceptual learning and memory.

The past year has seen several important findings emerge from studies of higher olfactory processes. The identification of synaptic long-term potentiation in the olfactory cortex, induced via repetitive burst stimulation at the theta rhythm, and physiological activity patterns associated with learning, some of which mimic long-term potentiation induction patterns, have suggested relationships between rhythmic activity, behavioral learning and synaptic plasticity. In addition, the construction of computational models of the olfactory bulb and cortex have generated testable behavioral and physiological predictions which have been supported by experimental evidence.

Animals↗

PubMed1987

Development of a dopamine- and cyclic adenosine 3':5'-monophosphate-regulated phosphoprotein (DARPP-32) in the prenatal rat central nervous system, and its relationship to the arrival of presumptive dopaminergic innervation.

The development of a dopamine- and adenosine 3':5'-monophosphate-regulated phosphoprotein with an apparent Mr of 32,000 (DARPP-32) has been investigated in the central nervous system of the prenatal and newborn rat by immunocytochemical methods. DARPP-32 first appears in the rat brain at day 14 of gestation, in the anlage of the primary olfactory cortex and the caudate nucleus. Over the next few days, the number of immunoreactive cell bodies in these 2 areas, and in the olfactory tubercle and frontal cortex, increases rapidly. By the day of birth, most of the brain regions that will ultimately contain DARPP-32-positive somata already display a disposition toward DARPP-32-like immunoreactivity similar to that observed in the adult animal. In addition to the nuclei mentioned above, DARPP-32-containing cell bodies also appear over the intervening period in the olfactory nucleus, nucleus accumbens, central amygdaloid nucleus, lateral funiculus, and the choroid plexus and ependymal layers of the third, fourth, and lateral ventricles and the Sylvian aqueduct. Many of these immunoreactive cells disappear during subsequent postnatal maturation. DARPP-32-immunoreactive fibers were also observed in the prenatal and newborn rat CNS. As in the adult, the processes were observed in known target areas of the DARPP-32-containing neurons, namely, the globus pallidus, ventral pallidum, internal capsule, and substantia nigra. The ontogeny of tyrosine hydroxylase (TH)-like immunoreactivity was analyzed simultaneously. Of particular interest was the observation that the arrival within a given brain region of the presumed dopaminergic, TH-containing innervation, part of whose postsynaptic function is putatively mediated by DARPP-32, was preceded by at least 2 d by the appearance of the DARPP-32-containing cells. Moreover, the subsequent reorganization of the DARPP-32-positive somata within the caudate nucleus into distinct clumps also predated by 1 or 2 d the aggregation of the TH fibers into the same microzones. The development of DARPP-32-like immunoreactivity is mostly complete by the day of birth, and is consistent with its playing a role in mediating some of the postsynaptic actions of dopamine pathways. The appearance of this protein does not seem to be dependent on the presence of a dopaminergic innervation.

Animals↗

PubMed1999

Treatment with estrogen and progesterone affects relative levels of brain-derived neurotrophic factor mRNA and protein in different regions of the adult rat brain.

Quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) were used to examine the effects of acute estrogen and progesterone replacement on relative levels of brain-derived neurotrophic factor (BDNF) mRNA and protein in different regions of the adult rat brain. Adult ovariectomized animals were killed 53 h after receiving estrogen (E53), 53 h after receiving estrogen and 5 h after receiving progesterone (E53P), or 72 h after receiving estrogen and 24 h after receiving progesterone (E72P). Ovariectomized controls were killed 53 and 72 h after receiving vehicle. Tissues from the hippocampus, pyriform cortex, olfactory bulbs, septum, and nucleus basalis/ventral pallidum were dissected. Tissues from the right hemisphere were processed for quantitative RT-PCR analysis of BDNF mRNA, and tissues from the left hemisphere were processed for the detection and quantification of BDNF protein by ELISA. The results demonstrate significant increases in BDNF mRNA in the pyriform cortex of E53- and E53P-treated animals, as well as an increase in BDNF protein in the pyriform cortex of E72P-treated animals, relative to controls. Significant increases in BDNF mRNA were likewise detected in the hippocampus of E53- and E72P-treated animals, but were accompanied by a significant decrease in BDNF protein in the hippocampus of E53P- and E72P-treated animals relative to controls. No significant changes in BDNF mRNA or protein were detected in the olfactory bulbs, frontal cortex, or nucleus basalis/ventral pallidum following hormone treatment; however, an increase in BDNF protein was detected in the septum of E53-treated animals. This may indicate an increase in the retrograde transport of BDNF from the hippocampus to the septum, which could help account for the decrease in BDNF protein detected in the hippocampus following hormone treatment. These findings demonstrate that hormone replacement significantly affects relative levels of BDNF mRNA and protein within specific regions of the brain. These effects may, in turn, contribute to the effects of estrogen replacement on hippocampal connectivity and cognitive processes that have recently been reported.

Age Factors↗

PubMed1994

Modulation of associative memory function in a biophysical simulation of rat piriform cortex.

1. Associative memory function was analyzed in a realistic biophysical simulation of rat piriform (olfactory) cortex containing 240 pyramidal cells and 58 each of two types of inhibitory interneurons. Pyramidal cell simulations incorporated six different intrinsic currents and three different synaptic currents. We investigated the hypothesis that acetylcholine sets the appropriate dynamics for learning within the network, whereas removal of cholinergic modulation sets the appropriate dynamics for recall. The associative memory function of the network was tested during recall after simulation of the cholinergic suppression of intrinsic fiber synaptic transmission and the cholinergic suppression of neuronal adaptation during learning. 2. Hebbian modification of excitatory synaptic connections between pyramidal cells during learning of patterns of afferent activity allowed the model to show the basic associative memory property of completion during recall in response to degraded versions of those patterns, as evaluated by a performance measure based on normalized dot products. 3. During learning of multiple overlapping patterns of afferent activity, recall of previously learned patterns interfered with the learning of new patterns. As more patterns were stored this interference could lead to the exponential growth of a large number of excitatory synaptic connections within the network. This runaway synaptic modification during learning led to excessive excitatory activity during recall, preventing the accurate recall of individual patterns. 4. Runaway synaptic modification of excitatory intrinsic connections could be prevented by selective suppression of synaptic transmission at these synapses during learning. This allowed effective recall of single learned afferent patterns in response to degraded versions of those patterns, without interference from other learned patterns. 5. During learning, cholinergic suppression of neuronal adaptation enhanced the activity of cortical pyramidal cells in response to afferent input, compensating for decreased activity due to suppression of intrinsic fiber synaptic transmission. This modulation of adaptation led to more rapid learning of afferent input patterns, as demonstrated by higher values of the performance measure. 6. During recall, when suppression of excitatory intrinsic synaptic transmission was removed, continued cholinergic suppression of neuronal adaptation led to the spread of excessive activity. More stable activity patterns during recall could be obtained when the cholinergic suppression of neuronal adaptation was removed at the same time as the cholinergic suppression of synaptic transmission. 7. A realistic biophysical simulation of the effects of acetylcholine on synaptic transmission and neuronal adaptation in the piriform cortex shows that these effects act together to set the appropriate dynamics for learning, whereas removal of both effects sets the appropriate dynamics for recall.

Acetylcholine↗