Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Piriform Cortex”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 667 records · Page 37Linked to original sources

Entorhinal cortex of the mouse: cytoarchitectonical organization.

The present study describes the cytoarchitectonical and chemoarchitectonical organization of the entorhinal cortex of the mouse (C57BL/6J strain). The entorhinal cortex is medially bordered by the parasubiculum, and laterally by the perirhinal cortex; rostrally and medially it is bordered by the piriform cortex, whereas caudally and dorsally it is bordered by the postrhinal cortex. The entorhinal cortex is divided into two main areas, i.e., the lateral entorhinal area (LEA) and the medial entorhinal area (MEA). Both entorhinal areas are further divided into subfields, i.e., LEA is divided into DLE (dorsolateral entorhinal field), DIE (dorsal intermediate entorhinal field), and VIE (ventral intermediate entorhinal field), whereas MEA is divided into CE (caudal entorhinal field) and ME (medial entorhinal field). Cytoarchitectonically, the main difference between LEA and MEA is displayed by layer II neurons: while these are in a dense layer in LEA, they are more dispersed in MEA. Further, in LEA there is a relatively cell-free zone between layers II and III; this zone is not present in MEA. Histochemically, in acetylcholinesterase (AChE)-stained material, MEA is characterized by darker-stained bands in the superficial layer (i.e., layer I) and in the lamina dissecans, in contrast to LEA, which is more evenly stained for AChE. Further, both the border with the perirhinal cortex and the border with the parasubiculum are characterized by dark-stained bands of AChE. The border between the entorhinal cortex and perirhinal cortex is also easily distinguished in parvalbumin-stained material; while the entorhinal cortex is darkly stained, the perirhinal cortex is lightly stained. In contrast, in sections stained for calretinin, the entorhinal cortex is more lightly stained than the parasubiculum, which has a darkly stained superficial layer, and a densely stained group of neurons in layer III.

Animals↗

Changes in [14C]deoxyglucose incorporation into rat brain regions during heat-seeking behavior in the cold environment.

The central nervous structures involved in behavioral thermoregulatory responses during cold exposure were investigated in conscious rats by means of the 2-deoxy-D-[14C]glucose ([14C]-DG) autoradiographic technique. According to autoradiographs, many brain regions with significant increases or decreases in [14C]-DG incorporation were observed during thermoregulatory behavior. When animals were only exposed to cold, significant increases in [14C]-DG incorporation were observed in the caudate putamen, lateral preoptic area, medial forebrain bundle, ventromedial hypothalamus (VMH), posterior hypothalamus, ventroposteromedial thalamus (VPM), dorsomedial thalamus (MD), substantia nigra (SN) and red nucleus (RN). Lower activities were observed in the hippocampus and the medial habenula. However, when animals performed the behavioral thermoregulation (heat seeking behavior) significant increases were noted in the sulcal prefrontal cortex, sensory-motor cortex, and MD, while decreases were noted in the piriform cortex, VMH, VPM, medial habenula, SN and RN, compared with those in the group without the thermoregulatory behavior.

Animals↗

Neuroadaptive changes in NMDAR1 gene expression after extinction of cocaine self-administration.

The aim of the present work was to study the time course effects in levels of mRNA encoding N-methyl-d-aspartate receptor subunit 1 (NMDAR1) after long-term cocaine self-administration (1 mg/kg/ injection) and its extinction using a yoked-box procedure. NMDAR1 content was measured by quantitative in situ hybridization histochemistry in prefrontal cortex, caudate-putamen, nucleus accumbens, olfactory tubercle, and piriform cortex immediately after cessation of the last session of cocaine self-administration (Day 0) and 1, 5, and 10 days after the extinction period. The results show that long-term cocaine self-administration and its extinction alter NMDAR1 gene expression in these forebrain regions, and that the changes depend upon the brain region examined and the type of cocaine administration (contingent, noncontingent, and saline). Compared to saline and noncontingent cocaine administration, contingent cocaine produced an up-regulation in NMDAR1 gene expression on Day 0 in all the brain regions analyzed. NMDAR1 levels of contingent animals decreased progressively in the absence of cocaine, and the decrement persisted 10 days after the extinction of cocaine self-administration behavior in all the forebrain areas, with the exception of olfactory tubercle. In contrast, noncontingent cocaine administration did not produce any change in NMDAR1 gene expression on Day 0, and extinction resulted in an increase of NMDAR1 mRNA content on Days 1 and 5 and returned to control (saline) values on Day 10. These results suggest that an interaction between environmental stimuli and the pharmacological action of cocaine during drug self-administration and its extinction may represent an important factor in the regulation of cocaine effects on NMDAR1 gene expression.

Analysis of Variance↗

Effect of electroacupuncture on the level of preproenkephalin mRNA in rat during penicillin-induced epilepsy.

Our previous studies have shown that seizure induced by injecting penicillin (0.24 mg/2 microliters) into hippocampus could be inhibited by electroacupuncture (EA) probably via decreasing enkephalin content in hippocampus. To determine whether this change reflected the peptide synthesis, preproenkephalin (PPE) mRNA was detected in hippocampus and some other limbic structures during seizure and after EA treatment by in situ hybridization. Four hours after injecting penicillin into hippocampus, PPE mRNA levels were significantly increased by 10 folds in entorhinal cortex, subiculum, CA1 area of hippocampus, amygdaloid nucleus and piriform cortex, whereas EA treatment apparently attenuated the seizure-induced increase of PPE mRNA in the areas mentioned above. The results indicated that EA may regulate the biosynthesis of PPE in hippocampus during seizure by an alteration in gene transcription.

Animals↗

Relationship of mu- and delta-opioid receptors to GABAergic neurons in the central nervous system, including antinociceptive brainstem circuits.

Inhibition of neurons containing gamma-aminobutyric acid (GABA) may underlie some of the excitatory effects of opioids in the central nervous system (CNS). In the present study, we examined the relationship of the cloned mu- and delta-opioid receptors (MOR1 and DOR1, respectively) to GABAergic neurons in brain and spinal cord. This was done by combining immunofluorescent staining for MOR1 or DOR1 with that for GABA or glutamic acid decarboxylase (GAD); fluorescent retrograde tract-tracing was used in some cases to identify neurons with particular projections. In rats, cells double labeled for GABA and MOR1 were observed in layers II-VI of the parietal cortex and in layers II-IV of the piriform cortex. In the hippocampus, double labeling was observed in the dentate gyrus and in regions CA1 and CA3. Double labeling was very prominent in the striatum and in the reticular nucleus of the thalamus; it was also observed in other portions of the diencephalon. However, double labeling for GABA and MOR1 was never observed in the cerebellar cortex. Cells double labeled for GABA and MOR1 were common in the periaqueductal gray (PAG) and the medial rostral ventral medulla (RVM) of both rats and monkeys, suggesting that involvement of GABAergic neurons with supraspinal opioid antinociception may extend to primates. In the RVM of rats, many of those double-labeled neurons were retrogradely labeled from the dorsal spinal cord. In contrast, double-labeled neurons in the PAG were almost never retrogradely labeled from the RVM. No unequivocal examples of double labeling for DOR1 and GAD were found in any region of the CNS that we examined in either rats or monkeys. However, GABAergic neurons were often apposed by DOR1 immunoreactive varicosities. Our findings suggest that activation of mu-opioid receptors directly modulates the activity of GABAergic neurons throughout the CNS, including neurons involved in the supraspinal component of opioid analgesia. In contrast, delta-opioid receptors appear to be positioned to modulate the activity of GABAergic neurons indirectly.

Animals↗

OCD-Like behaviors caused by a neuropotentiating transgene targeted to cortical and limbic D1+ neurons.

To study the behavioral role of neurons containing the D1 dopamine receptor (D1+), we have used a genetic neurostimulatory approach. We generated transgenic mice that express an intracellular form of cholera toxin (CT), a neuropotentiating enzyme that chronically activates stimulatory G-protein (Gs) signal transduction and cAMP synthesis, under the control of the D1 promoter. Because the D1 promoter, like other CNS-expressed promoters, confers transgene expression that is regionally restricted to different D1+ CNS subsets in different transgenic lines, we observed distinct but related psychomotor disorders in different D1CT-expressing founders. In a D1CT line in which transgene expression was restricted to the following D1+ CNS regions-the piriform cortex layer II, layers II-III of somatosensory cortical areas, and the intercalated nucleus of the amygdala-D1CT mice showed normal CNS and D1+ neural architecture but increased cAMP content in whole extracts of the piriform and somatosensory cortex. These mice also exhibited a constellation of compulsive behavioral abnormalities that strongly resembled human cortical-limbic-induced compulsive disorders such as obsessive-compulsive disorder (OCD). These compulsive behaviors included episodes of perseverance or repetition of any and all normal behaviors, repetitive nonaggressive biting of siblings during grooming, and repetitive leaping. These results suggest that chronic potentiation of cortical and limbic D1+ neurons thought to induce glutamatergic output to the striatum causes behaviors reminiscent of those in human cortical-limbic-induced compulsive disorders.

Aggression↗

Analysis of the Lynch-Granger model for olfactory cortex.

The behavior of the Lynch-Granger model for layer-II piriform cortex is reviewed, and a simple neural model with similar properties is introduced. This model allows us to understand the observed functionality of the Lynch-Granger model intuitively, and suggests which of the many biological facts introduced into the original model are relevant to this particular behavior.

Computer Simulation↗

Effects of partial decortication on opioid analgesia in the formalin test.

Partially decorticated rats were tested for their response to nociceptive stimulation in the formalin and tail flick tests, and for the effect of morphine on these responses and on motor activity. Undrugged rats showed vigorous responses to nociceptive stimulation in both tests, and exhibited the typical biphasic time course of pain in the formalin test. Morphine 4 and 8 mg/kg produced dose-dependent analgesia in both tests in sham operated rats, and in rats with lesions that removed all or part of the cortex from the midline to the rhinal fissure (excluding the occipital cortex). In rats with lesions that extended deep into the piriform cortex and damaged the amygdala morphine analgesia was eliminated or attenuated. These and other recent findings suggest that analgesia in the formalin test depends on ascending connections to the forebrain, probably the amygdala.

Amygdala↗

Kainic acid induced expression of interleukin-1 receptor antagonist mRNA in the rat brain.

The endogenous interleukin-1 receptor antagonist (IL-1ra), a protein with partial homology with the proinflammatory cytokine interleukin-1beta (IL-1beta), prevents binding of IL-1beta to the signalling receptor. Exogenous IL-1ra has been shown to reduce the neuronal damage occurring after excitotoxic amino acid administration and ischemia. In the present study, in situ hybridization histochemistry was employed to investigate the regulation of endogenous IL-1ra mRNA expression in the rat brain after peripheral administration of kainic acid (10 mg/kg). IL-1ra mRNA expression was markedly induced in the hippocampus, thalamus, amygdala, piriform cortex, perirhinal cortex, entorhinal cortex, and to a lesser extent in the hypothalamus, and parietal and temporal cortex. The expression was first detected at 5 h after the kainic acid administration and it was markedly increased at 24 h. No signal was detected at 4 days after the injection. The majority of the cells expressing IL-1ra mRNA displayed the morphological characteristics of microglia. Expression of IL-1ra mRNA in neurons occurred mainly in the piriform and perirhinal cortex. The distribution pattern of IL-1ra mRNA expressing microglia-like cells was similar to that of cells labelled with ED1, a marker for activated microglia. The induction of IL-1ra mRNA expression may represent an endogenous response to balance IL-1 receptor mediated activity in the brain following kainic acid administration, conceivably to elicit neuroprotective and/or antiinflammatory effects.

Animals↗

GDNF family ligands and receptors are differentially regulated after brain insults in the rat.

Expression of mRNAs for glial cell line-derived neurotrophic factor (GDNF), neurturin (NTN) and their receptors was studied in adult rat brain using in situ hybridization after 40 kindling-evoked, rapidly recurring seizures or 10 min of global forebrain ischaemia. Following seizures, GDNF and NTN mRNAs were elevated in dentate granule cells, and c-Ret mRNA in hilar neurons and non-pyramidal cells in CA1 and CA3 regions. GFRalpha-1 mRNA levels showed more widespread increases in the dentate granule cell layer and hilus, CA1 and CA3 pyramidal layers, basolateral amygdala and parietal cortex. The expression of GFRalpha-2 mRNA increased in the piriform cortex and decreased in the CA1 region and basolateral amygdala. Forebrain ischaemia induced elevated expression of GDNF mRNA in dentate granule cells, GFRalpha-1 mRNA in the dentate granule cell layer, hilus and CA3 pyramidal layer, and GFRalpha-2 mRNA in the parietal cortex. The gene expression patterns observed here suggest that GDNF and NTN may act as target-derived factors, but also in an autocrine or paracrine manner. GFRalpha-1 can be coexpressed with GFRalpha-2 and c-Ret mRNAs in the same hippocampal or thalamic neurons, but other neurons contain GFRalpha-1 alone or together with c-Ret mRNA. The gene expression changes for the ligands, and the receptor components are region-, cell- and insult-specific, and occur independently of each other, mainly within 24 h after seizures or ischaemia. This dynamic regulation of GDNF and NTN circuits primarily at the receptor level may be important for the effectiveness of neuroprotective responses but could also trigger plastic changes, e.g. those underlying the development of epileptic syndromes.

Animals↗

The reinforcing properties of nicotine are associated with a specific patterning of c-fos expression in the rat brain.

Rats were trained for nicotine intravenous infusions in a self-administration paradigm. The effect of nicotine self-administration on regional brain activity was studied by mapping changes of c-fos expression. Specific nicotine effects were determine by comparing the patterning of Fos-like immunoreactivity (Fos-Ll) in nicotine self-administering rats with that in three different control groups. Controls included rats exposed to the same manipulation as nicotine self-administering rats who received intravenous saline instead of nicotine. In addition, two groups of untrained sham-operated rats exposed daily to the same operant boxes were included: one group had the same food restriction used in the operant training, the other was fed ad libitum. Nicotine self-administration, exposure to saline and food restriction increased Fos-Ll in 43, 33 and three brain regions, respectively, when compared with the control group fed ad libitum. Computer-assisted image analysis of Fos-Ll profiles performed on 16 relevant limbic and sensory structures showed that in saline-treated rats a significant (P < 0.01) increase of Fos-Ll profiles was observed in medial prefrontal cortex, lateral septum, core and ventral shell of nucleus accumbens, claustrum, amygdaloid nuclei, paraventricular thalamic nucleus and lateral geniculate nucleus. A significant (P < 0.01) further increase produced by nicotine was found in medial prefrontal cortex and ventral shell of nucleus accumbens. Interestingly, cingulate and piriform cortex, superior colliculus and medial terminal nucleus of the accessory optic tract were specifically activated by nicotine but not saline. These results show that nicotine self-administration activates sensory structures, as well as limbic structures involved in natural rewarding pathways. The results suggest the involvement of restricted terminal regions of the mesocorticolimbic dopaminergic system in the maintenance of nicotine self-administration.

Analysis of Variance↗

Neonatal gamma-ray irradiation impairs learning and memory of an olfactory associative task in adult rats.

Adult neonatally gamma-irradiated rats were compared with control animals in a non-spatial olfactory associative task using two different procedures. Irradiation induced a clear reduction in the total mean area of the olfactory bulbs and hippocampus but not of the orbital prefrontal cortex, diagonal band and cell layers of the entorhinal and piriform cortex. The gamma-irradiation affected the granule cells of the olfactory bulbs and differentially altered the cell layers of the subfields of the ammonic fields and the dorsal and ventral blades of the dentate gyrus. In the CA1 ammonic field, dorsal and ventral blades of the dentate gyrus, the cellular loss was significant in comparison with control adult rats. The behavioural data indicated that irradiated rats were deeply disturbed in learning the odour-reward association, and substantially impaired in a reversal experiment, but not in the discrimination of the odours per se. The cellular loss in the olfactory bulbs, in the CA1 and in the ventral blade of the gyrus dentatus was positively correlated with the deficit in behavioural performance. The data support the findings that the hippocampal system participates in the odour-reward associations and facilitates the long-term storage of associations after learning is achieved in this olfactory associative task.

Animals↗

Hippocampal damage and kainic acid injection induce a rapid increase in mRNA for BDNF and NGF in the rat brain.

In situ hybridization and Northern blots were used to study expression of mRNAs for members of the nerve growth factor family in the rat brain following an excitatory stimulus. One hour after a unilateral needle insertion or saline injection into the dorsal hippocampus, the level of brain-derived neurotrophic factor (BDNF) mRNA increased markedly in granular neurons of the dentate gyrus and in the piriform cortex ipsilateral to the injection. The same treatment also increased the level of NGF mRNA in granular neurons of the ipsilateral dentate gyrus. The rapid increase in BDNF and NGF mRNA after a needle insertion or injection of saline was transient and preceded by an increase in c-fos mRNA in the same brain regions. In contrast to a needle insertion per se or a saline injection, 7 h after a unilateral injection of kainic acid into the dorsal hippocampus, the level of BDNF mRNA was dramatically increased in the ipsilateral hippocampus, as well as in the ipsilateral frontoparietal, piriform and perihinal cortex, the amygdaloid complex, claustrum, and ventromedial hypothalamus. A less pronounced increase was also seen in these brain areas on the contralateral side. Northern blots revealed that the level of BDNF mRNA increased 5- and 40-fold in the contra- and ipsilateral hippocampus, respectively, compared to sham-operated control animals. In contrast to BDNF and NGF, the level of hippocampus-derived neurotrophic factor/neurotrohin-3 (HDNF/NT-3) mRNA was not altered by either needle insertion or injection of saline or kainic acid.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Expression of ODC and its regulatory protein antizyme in the adult rat brain.

Ornithine decarboxylase and its inhibitor protein, antizyme are key regulators of polyamine biosynthesis. We examined their expression in the adult rat brain using in situ hybridization and immunocytochemistry. Both genes were widely expressed and their expression patterns were mostly overlapping and relatively similar. The levels of antizyme mRNA were always higher than those of ornithine decarboxylase mRNA. The highest expression for both genes was detected in the cerebellar cortex, hippocampus, hypothalamic paraventricular and supraoptic nuclei, locus coeruleus, olfactory bulb, piriform cortex and pontine nuclei. Ornithine decarboxylase and antizyme mRNAs appeared to be localized in the nerve cells. ODC antibody displayed mainly cytoplasmic staining in all brain areas. Antizyme antibody staining was mainly cytoplasmic in the most brain areas, although predominantly nuclear staining was detected in some areas, most notably in the cerebellar cortex, anterior olfactory nucleus and frontal cortex. Our study is the first detailed and comparative analysis of ornithine decarboxylase and antizyme expression in the adult mammalian brain.

Animals↗

The metabotropic glutamate 5 receptor antagonist 3-[(2-methyl-1,3-thiazol-4-yl)ethynyl]-pyridine reduces ethanol self-administration in multiple strains of alcohol-preferring rats and regulates olfactory glutamatergic systems.

The metabotropic glutamate 5 receptor (mGlu5) receptor has been implicated as having a role in pain modulation, anxiety, and depression, as well as drug-seeking behavior. In the present study, we examined the effect of the selective mGlu5 receptor antagonist 3-[(2-methyl-1,3-thiazol-4-yl)ethynyl]-pyridine (MTEP) on operant ethanol self-administration by two strains of rats, the Fawn-Hooded (FH) rat and the inbred alcohol-preferring (iP) rat. MTEP (2 mg/kg i.p.) caused a significant reduction in responding for ethanol by both strains of rats; however, in the iP rats, MTEP also induced apparent sedation at this dose, although still reduced alcohol responding at lower doses. Chronic MTEP (2 mg/kg/day) caused a significant reduction in ethanol consumption by FH rats in a two-bottle preference test; however, chronic treatment with this dose had no effect on anxiety-like behavior or depressive-like behavior in FH rats, suggesting the dose used was subthreshold for anxiolytic or antidepressive-like effects. Finally, repeated dosing with MTEP (2 mg/kg i.p.) caused significant reductions in expression of the mRNA encoding the NR1 subunit of the N-methyl-D-aspartate receptor and the GluR2 subunit of the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptor in the cingulate cortex. A significant decrease in NR1 expression also occurred in the piriform cortex. Chronic MTEP also caused a significant decrease in mGlu5 gene expression and a significant increase in dopamine transporter and dopamine D(2)-like receptor binding within the olfactory tubercle. Collectively, these data suggest that MTEP can reduce alcohol-seeking behavior in different rodent models of alcoholism, and this effect is associated with regulation of cortical glutamate systems, particularly those in olfactory-related regions.

Alcohol Drinking↗

Expression of hepatoma-derived growth factor family members in the adult central nervous system.

BACKGROUND: Hepatoma-derived growth factor (HDGF) belongs to a polypeptide family containing five additional members called HDGF related proteins 1-4 (HRP-1 to -4) and Lens epithelial derived growth factor. Whereas some family members such as HDGF and HRP-2 are expressed in a wide range of tissues, the expression of others is very restricted. HRP-1 and -4 are only expressed in testis, HRP-3 only in the nervous system. Here we investigated the expression of HDGF, HRP-2 and HRP-3 in the central nervous system of adult rats on the cellular level by immunohistochemistry. In addition we performed Western blot analysis of various brain regions as well as neuronal and glial cell cultures. RESULTS: HDGF was rather evenly expressed throughout all brain regions tested with the lowest expression in the substantia nigra. HRP-2 was strongly expressed in the thalamus, prefrontal and parietal cortex, neurohypophysis, and the cerebellum, HRP-3 in the bulbus olfactorius, piriform cortex and amygdala complex. HDGF and HRP-2 were found to be expressed by neurons, astrocytes and oligodendrocytes. In contrast, strong expression of HRP-3 in the adult nervous system is restricted to neurons, except for very weak expression in oligodendrocytes in the brain stem. Although the majority of neurons are HRP-3 positive, some like cerebellar granule cells are negative. CONCLUSION: The coexpression of HDGF and HRP-2 in glia and neurons as well as the coexpression of all three proteins in many neurons suggests different functions of members of the HDGF protein family in cells of the central nervous system that might include proliferation as well as cell survival. In addition the restricted expression of HRP-3 point to a special function of this family member for neuronal cells.

Age Factors↗

5-HT concentration in cat's brain.

Endogenous concentrations of TRP, 5-HT and 5-HIAA were determined in the different cortical and subcortical areas of adult cat's brain, using ion-exchange chromatography and spectrofluorimetric methods. Tryptophan is homogeneously distributed in all structures of the brain. 5-HT is mainly accumulated in the brain stem, hypothalamus and caudate nucleus, but also in cortical areas as olfactory and piriform gyrus. The ratio 5-HIAA/5-HT shows that 5-HT utilization is higher in the structures containing small amounts of 5-HT. Using the radioenzymatic assay described by Saavedra et al. (1973), the rostrocaudal distribution of 5-HT content was determined in olfactory and piriform cortex. Important concentrations of 5-HT were detected in the prepiriformis and anterior amygdaloidea areas. Using the same assay and microdissection on frozen frontal slices of the brain, the distribution of 5-HT concentration throughout the different layers of cortical areas was studied. Piriform, olfactory and sigmoid cortex present high concentrations in the superficial layers, including the molecular one. These results were confirmed by uptake studies, made on crude homogenates from frozen tissue, suggesting that 5-HT is mainly contained in the most external cortical terminals.

Animals↗

Parallel-distributed processing in olfactory cortex: new insights from morphological and physiological analysis of neuronal circuitry.

A working hypothesis is proposed for piriform cortex (PC) and other olfactory cortical areas that redefines the traditional functional roles as follows: the olfactory bulb serves as the primary olfactory cortex by virtue of encoding 'molecular features' (structural components common to many odorant molecules) as a patchy mosaic reminiscent of the representation of simple features in primary visual cortex. The anterior olfactory cortex (that has been inappropriately termed the anterior olfactory nucleus) detects and stores correlations between olfactory features, creating representations (gestalts) for particular odorants and odorant mixtures. This function places anterior olfactory cortex at the level of secondary visual cortex. PC carries out functions that have traditionally defined association cortex--it detects and learns correlations between olfactory gestalts formed in anterior olfactory cortex and a large repertoire of behavioral, cognitive and contextual information to which it has access through reciprocal connections with prefrontal, entorhinal, perirhinal and amygdaloid areas. Using principles derived from artificial networks with biologically plausible parallel-distributed architectures and Hebbian synaptic plasticity (i.e. adjustments in synaptic strength based on locally convergent activity), functional proposals are made for PC and related cortical areas. Architectural features incorporated include extensive recurrent connectivity in anterior PC, predominantly feedforward connectivity in posterior PC and backprojections that connect distal to proximal structures in the cascade of olfactory cortical areas. Capabilities of the 'reciprocal feedforward correlation' architecture that characterizes PC and adjoining higher-order areas are discussed in some detail. The working hypothesis is preceded by a review of relevant anatomy and physiology, and a non-quantitative account of parallel-distributed principles. To increase the accessibility of findings for PC and to advertise its substantial potential as a model for experimental and modeling analysis of associative processes, parallels are described between PC and the hippocampal formation, inferotemporal visual cortex and prefrontal cortex.

Animals↗