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PubMed2004

Odors detected by mice deficient in cyclic nucleotide-gated channel subunit A2 stimulate the main olfactory system.

It is believed that odor transduction in the mammalian main olfactory system only involves the cAMP-signaling pathway. Here, we report on odor responsiveness in mice with a disrupted cyclic nucleotide-gated (CNG) channel subunit A2. Several odorants, including putative pheromones, can be detected and discriminated by these mice behaviorally. These odors elicit responses in the olfactory epithelium, main olfactory bulb, and olfactory (piriform) cortex of CNGA2 knock-out mice. In addition, responses to odors detected by CNGA2 knock-out mice are relatively insensitive to inhibitors of the cAMP pathway. These results provide strong evidence that cAMP-independent pathways in the main olfactory system of mammals participate in detecting a subset of odors.

Animals↗
PubMed2005

Recognition of familiar individuals in golden hamsters: a new method and functional neuroanatomy.

The ability to recognize individuals is essential for many aspects of social interaction and social organization, yet we know relatively little about the neural mechanisms underlying this ability. Most laboratory studies of individual recognition in rodents have studied differential responses to familiar versus unfamiliar individuals rather than differential responses to equally well known individuals having different significance for the subject. In experiment 1, we use a new method for studying true individual recognition in which male hamsters first had different experiences with two stimulus males (exposures to one male across a wire-mesh barrier and fights with another male). One day later, losers of fights were tested in a Y-maze for reactions to one of the two familiar males. Subjects tested with the familiar winner avoided this stimulus male, but subjects tested with the familiar, neutral male were attracted to him. Immunohistochemistry for c-Fos and Egr-1 implicate several areas of the brain in individual recognition, particularly the anterior piriform cortex, the CA1 and CA3 regions of anterior dorsal hippocampus, anterior and posterior dentate gyrus, and perirhinal cortex. In experiment 2, temporary inactivation of the CA1 region of anterior dorsal hippocampus by microinfusion of lidocaine eliminated the avoidance of the familiar winner, but a saline control injection had no effect. These results are the first to use a rodent model to characterize neural circuits involved in the recognition of equally well known individuals and the corresponding emotional responses to them.

Animals↗
PubMed2006

A circadian clock in the olfactory bulb controls olfactory responsivity.

Recently, it has been shown that multiple mammalian cell types express daily rhythms in vitro. Although the suprachiasmatic nucleus (SCN) of the hypothalamus is known to regulate a wide range of circadian behaviors, the role for intrinsic rhythmicity in other tissues is unknown. We tested whether the main olfactory bulb (OB) of mice mediates daily changes in olfaction. We found circadian rhythms in cedar oil-induced c-Fos, a protein marker of cellular excitation, in the mitral and granular layers of the OB and in the piriform cortex (PC). These oscillations persisted in constant darkness with a fourfold change in amplitude and a peak approximately 4 h after the onset of daily locomotor activity. Electrolytic lesions of the SCN abolished circadian locomotor rhythms, but not odor-induced c-Fos rhythms in the OB or PC. Furthermore, removal of the OB abolished spontaneous circadian cycling of c-Fos in the PC, shortened the free-running period of locomotor rhythms, and accelerated re-entrainment after a 6 h advance and slowed re-entrainment after a 6 h delay in the light schedule. OB ablation or odorant altered the amplitude of c-Fos rhythms in the SCN and ablation of one OB abolished c-Fos rhythms in the ipsilateral PC, but not in the contralateral OB and PC. We conclude that the OB comprises a master circadian pacemaker, which enhances olfactory responsivity each night, drives rhythms in the PC, and interacts with the SCN to coordinate other daily behaviors.

Analysis of Variance↗
PubMed2004

Coordinate synaptic mechanisms contributing to olfactory cortical adaptation.

Anterior piriform cortex (aPCX) neurons rapidly filter repetitive odor stimuli despite relatively maintained input from mitral cells. This cortical adaptation is correlated with short-term depression of afferent synapses, in vivo. The purpose of this study was to elucidate mechanisms underlying this nonassociative neural plasticity using in vivo and in vitro preparations and to determine its role in cortical odor adaptation. Lateral olfactory tract (LOT)-evoked responses were recorded in rat aPCX coronal slices. Extracellular and intracellular potentials were recorded before and after simulated odor stimulation of the LOT. Results were compared with in vivo intracellular recordings from aPCX layer II/III neurons and field recordings in urethane-anesthetized rats stimulated with odorants. The onset, time course, and extent of LOT synaptic depression during both in vitro electrical and in vivo odorant stimulation methods were similar. Similar to the odor specificity of cortical odor adaptation in vivo, there was no evidence of heterosynaptic depression between independent inputs in vitro. In vitro evidence suggests at least two mechanisms contribute to this activity-dependent synaptic depression: a rapidly recovering presynaptic depression during the initial 10-20 sec of the post-train recovery period and a longer lasting (approximately 120 sec) depression that can be blocked by the metabotropic glutamate receptor (mGluR) II/III antagonist (RS)-alpha-cyclopropyl-4-phosphonophenylglycine (CPPG) and by the beta-adrenergic receptor agonist isoproterenol. Importantly, in line with the in vitro findings, both adaptation of odor responses in the beta (15-35 Hz) spectral range and the associated synaptic depression can also be blocked by intracortical infusion of CPPG in vivo.

Adaptation, Physiological↗
PubMed2005

High-frequency oscillations are not necessary for simple olfactory discriminations in young rats.

Individual olfactory bulb mitral/tufted cells respond preferentially to groups of molecularly similar odorants. Bulbar interneurons such as periglomerular and granule cells are thought to influence mitral/tufted odorant receptive fields through mechanisms such as lateral inhibition. The mitralgranule cell circuit is also important in the generation of the odor-evoked fast oscillations seen in the olfactory bulb local field potentials and hypothesized to be an important indicator of odor quality coding. Infant rats, however, lack a majority of these inhibitory interneurons until the second week of life. It is unclear if these developmental differences affect olfactory bulb odor coding or behavioral odor discrimination. The following experiments are aimed at better understanding odor coding and behavioral odor discrimination in the developing olfactory system. Single-unit recordings from mitral/tufted cells and local field-potential recordings from both the olfactory bulb and anterior piriform cortex were performed in freely breathing urethane-anesthetized rats (postnatal day 7 to adult). Age-dependent behavioral odor discrimination to a homologous series of ethyl esters was also examined using a cross-habituation paradigm. Odorants were equated in all experiments for concentration (150 ppm) using a flow dilution olfactometer. In concordance with the reduced interneuron population, local field potentials in neonates lacked detectable odor-evoked gamma-frequency oscillations that were observed in mature animals. However, mitral/tufted cell odorant receptive fields and behavioral odor discrimination did not significantly change, despite known substantial changes in local circuitry and neuronal populations, over the age range examined. The results suggest that high-frequency local field-potential oscillations do not reflect processes critical for simple odor discrimination.

Action Potentials↗
PubMed2004

Overexpression of human IGF-II mRNA in the brain of transgenic mice modulates IGFBP-2 gene expression in the medulla oblongata.

The insulin-like growth factors, IGF-I and IGF-II, and their binding proteins play an important role in the growth and development of the central nervous system. In the brain, colocalization of IGFs and IGFBPs often occurs, suggesting that IGFBPs can modulate IGF action. In one strain of our human (h)IGF-II transgenic mice, which carry an hIGF-II transgene driven by the H-2Kb promoter, we found overexpression of hIGF-II in the brain, as measured by Northern blot analysis. To clarify the localization and influence of the hIGF-II transgene on different components of the GH-IGF axis in the brain, we studied the expression pattern of the hIGF-II transgene, endogenous IGF-I and IGF-II, and IGFBP-2, -3 and -5 in the brain of prepubertal 4-week-old mice, using nonradioactive in situ hybridization. We found that the hIGF-II transgene is exclusively expressed in neurons of the piriform cortex, the cerebral cortex, the medulla oblongata and the granular layer of the cerebellum. In general, this pattern is comparable to the expression pattern of endogenous IGF-I, with a few exceptions: there is no expression of IGF-I in the granular layer of the cerebellum, whereas the Purkinje cells of the cerebellum and thalamus both express IGF-I but no hIGF-II transgene. This hIGF-II transgene expression pattern contrasts markedly with endogenous IGF-II expression, which is mainly located in nonneuronal cells such as the meninges and choroid plexus, and in some nuclei of the medulla oblongata. The hIGF-II transgene affects neither endogenous IGF-I and IGF-II expression, nor the expression of IGFBP-3, which is located in the choroid plexus. Although the hIGF-II transgene is expressed in neuronal structures similar to IGF-I and IGFBP-5, it is not able to regulate IGFBP-5 expression, as has previously been reported for IGF-I. In the medulla oblongata, the IGFBP-2 expression level showed 10-fold upregulation by the transgene, suggesting a modulating role for IGFBP-2 at the hIGF-II transgene action in this region.

Animals↗
PubMed2005

Pyruvate administered after severe hypoglycemia reduces neuronal death and cognitive impairment.

Hypoglycemia-induced brain injury is a significant obstacle to optimal blood glucose control in diabetic patients. Severe hypoglycemia triggers a cascade of events in vulnerable neurons that may culminate in cell death even after glucose normalization. A key event in this cascade is the activation of poly(ADP-ribose) polymerase-1 (PARP-1). Activated PARP-1 consumes cytosolic NAD, and because NAD is required for glycolysis, hypoglycemia-induced PARP-1 activation may render cells unable to use glucose even when glucose availability is restored. Pyruvate, however, can be metabolized in the absence of cytosolic NAD. Here we tested whether pyruvate could improve the outcome in rats subjected to insulin-induced hypoglycemia by terminating hypoglycemia with either glucose alone or glucose plus pyruvate. In the four brain regions studied--CA1, subiculum, dentate gyrus of the hippocampus, and piriform cortex--the addition of pyruvate reduced neuron death by 70-90%. Improved neuron survival was also observed when pyruvate delivery was delayed for up to 3 h. The improved neuron survival was accompanied by a sustained improvement in cognitive function as assessed by the Morris water maze. These results suggest that pyruvate may significantly improve the outcome after severe hypoglycemia by circumventing a sustained impairment in neuronal glucose utilization resulting from PARP-1 activation.

Animals↗
PubMed1983

Regional cerebral ischemia by occlusion of the posterior communicating artery and the middle cerebral artery in gerbils.

The authors have created an experimental model of regional cerebral ischemia in gerbils that is reproducible and has a low mortality rate. In gerbils, either the posterior communicating artery (PCoA) or the middle cerebral artery (MCA) was occluded, and the distribution of cerebral ischemia from each surgical procedure was compared with that produced by occlusion of the common carotid artery (CCA). In contrast to the widespread cortical and subcortical infarctions seen after occlusion of the CCA, occlusion of the PCoA caused infarction that was restricted to the hippocampus, the piriform cortex, and the posterior part of the thalamus, and occlusion of the MCA resulted in infarction that was restricted to the central part of the cerebral hemisphere and the caudate nucleus and putamen. Intracranial occlusion of the PCoA or MCA in the gerbil resulted in lesions that were reproducible with low mortality rates over a long-term period. Occlusion of the PCoA, MCA, or CCA also produces a model that is suitable for investigation of the postischemic period. A combination of these three experimental models is useful for investigation of regional vulnerability and for the study of regional metabolic differences in cerebral ischemia.

Animals↗
PubMed1989

Neuroanatomical substrates involved in the control of food intake.

Five neural pathways were reviewed regarding their specific role in the control of food intake in birds. The five pathways included the trigeminal sensorimotor system, the visual system/basal ganglia pathway, the gustatory system, the olfactory pathway, and the autonomic nervous system/parasympathetic pathway. The trigeminal system is the pathway best understood among the five systems associated with feeding. It begins with sensory nerves innervating the upper and lower mandibles and buccal cavity and ends with nerves projecting to jaw muscles. The function of the pathway is to control the grasping and mandibulation of pellets or seeds. The visual system includes both the tectofugal and thalamofugal pathways. Both visual pathways interact with the avian paleostriatal complex. The latter is equivalent to the mammalian basal ganglia. The second pathway is important in food recognition as well as in orienting the body with respect to its position in three-dimensional space. The third neural circuit involves the sense of taste. Approximately 300 taste buds have been identified within the buccal cavity of the chicken, suggesting that the gustatory system is better developed than once thought. The fourth pathway involves the olfactory system; as in the visual system, more than one pathway has been identified. The dominant pathway appears to project to the piriform cortex, a structure that may play a role in monitoring essential amino acid contents of the brain. The fifth pathway involves an interaction of the hypothalamus and the dorsal motor nucleus of the vagus. This pathway is important in activating the parasympathetic nervous system and in preparing an organism to feed. All five pathways play different roles in controlling food intake in birds.

Animals↗
PubMed1999

Electroconvulsive therapy as an anticonvulsant: a possible role of neuropeptide Y (NPY).

Seizure threshold increases during a series of electroconvulsive therapy (ECTs). Based on assumptions that the effect of ECT may be related to its anticonvulsant effect we were interested in identifying transmitters that are activated by the treatment and play an anticonvulsant role. Animal studies reveal that neuropeptide Y (NPY) neurotransmission is increased by repeated electroconvulsive shock (ECS), and NPY has been found to inhibit glutamate-mediated synaptic transmission in the rat hippocampus. The increase of NPY gene expression in highly sensitive areas of the rat hippocampus (dentate gyrus) and piriform cortex accompanied by a reduction of NPY binding sites in the same regions after ECS supports this notion. Further studies have shown that NPY exerts a seizure-suppressing activity of NPY after kainic acid injections in vivo. Taken together the present series of experiments in rats strongly points to the seizure suppressing properties of NPY and suggests that this peptide may be involved in the seizure threshold increase during effective ECT in humans.

Animals↗
PubMed1999

Distribution and intracellular localization of a mouse homologue of Ca2+/calmodulin-dependent protein kinase Ibeta2 in the nervous system.

Ca2+/calmodulin-dependent protein kinases (CaMKs) are believed to play important roles in the development and function of the nervous system. We report here the identification and expression of mouse CaMKIbeta (mCaMKIbeta), in particular mCaMKIbeta2, an isoform of mCaMKIbeta. During embryogenesis, the mCaMKIbeta2 gene is expressed mainly in the nervous system, including brain, spinal cord, trigeminal ganglion, and retina. Within the CNS, the expression of mCaMKIbeta2 is detected in the mantle zone, but not in the ventricular zone, suggesting its possible involvement in the differentiation of neurons. In the adult brain, mCaMKIbeta2 transcripts are detected at high levels in the anterior olfactory nuclei, piriform cortex, septal nuclei, bed nuclei of the stria terminalis, hippocampal pyramidal cells, dentate granule cells, amygdala, hypothalamic nuclei, parabrachial nucleus, and nucleus of the solitary tract. The distinct gene expression pattern suggests that mCaMKIbeta2 may also be involved in different mature neuronal functions from other CaMKs. In addition, mCaMKI/beta2 proteins are localized to the cytoplasm and nuclei, but not to nucleoli, suggesting that mCaMKIbeta2 proteins might be involved in the cytoplasmic and nuclear signal transduction of the nervous system.

Amino Acid Sequence↗
PubMed1999

Systemic injection of lidocaine induced expression of c-fos mRNA and protein in adult rat brain.

Both direct and indirect environmental stress to the brain can increase the expression of transcription factor c-fos in various populations of neurons. In this study, we examined whether the intraperitoneal injections of lidocaine at doses inducing convulsions within 10 min, increased the level of c-fos mRNA and protein in forebrain areas. In in situ hybridization using [35S]UTP-labeled antisense c-fos, cRNA increased c-fos mRNA levels through the hippocampal formation, piriform cortex, septum, caudate-putamen, neostriatum, and amygdala within 2 hr. In parallel with the mRNA expression, c-fos protein immuno-reactivity was also observed in the same forebrain areas. In contrast to the seizure activity and wide-spread neuronal degeneration following kainate treatment, injections of lidocaine did not produce neuronal death within three days. The present study indicates that lidocaine induces convulsions and c-fos expression without causing neurotoxicity.

Animals↗
PubMed2000

Postural and anticonvulsant effects of inhibition of the rat subthalamic nucleus.

The subthalamic nucleus (STN) plays a crucial role as a regulator of basal ganglia outflow by providing excitatory glutamatergic input into the two output nuclei of the basal ganglia, substantia nigra pars reticulata (SNpr), and entopeduncular nucleus. This study examined the effects of suppressing activity in the STN of the awake, behaving rat. Specifically, we evaluated the effects of unilateral and bilateral focal inhibition of STN on posture, locomotion, and susceptibility to limbic motor seizures. Unilateral microinjection of a GABA(A) receptor agonist (muscimol, 200 pmol) into STN produced a site-dependent contralaterally directed postural asymmetry without locomotor activation. This effect differed from responses produced by the same dose of muscimol placed into SNpr, which included locomotor activation in addition to contralaterally directed postural asymmetry. Locomotor activation and postural asymmetry were obtained also after blockade of glutamate transmission in SNpr by the unilateral application of kynurenate (100 nmol). Our observation that STN inhibition did not induce the locomotor activation characteristic of SNpr inhibition suggests that there are glutamatergic inputs to SNpr, other than those from STN, that are responsible for controlling locomotion. Bilateral, but not unilateral, injection of muscimol (200 pmol) into STN protected against limbic motor seizures evoked either by intravenous bicuculline or by focal application of bicuculline into anterior piriform cortex (area tempestas). These results demonstrate that focal inhibition of STN reproduces the postural asymmetry and anticonvulsant actions that are obtained with the inhibition of SNpr. This provides behavioral support for the concept that STN contributes a crucial tonic excitatory (glutamatergic) drive to the rat SNpr.

Animals↗
PubMed2001

Expression of the Per1 gene in the hamster: brain atlas and circadian characteristics in the suprachiasmatic nucleus.

Recent progress in study on the molecular component of mammalian clocks has claimed that mammals and Drosophila share the similar fundamental clock oscillating system. In the present study, we investigated expression of Per1, the first gene of the mammalian homolog of the Drosophila clock gene period, in the hamster brain, and we also examined its circadian expression pattern in the mammalian clock center, the suprachiasmatic nucleus (SCN). In situ hybridization using isotope-labeled cRNA probes revealed a wide and region-specific distribution of Per1 in the hamster brain and spinal cord. High levels of Per1 were found in the internal granular layer of the granular cells of the olfactory bulb, anterior olfactory nuclei, tenia tecta, olfactory tubercle, piriform cortex, suprachiasmatic nucleus, and gyrus dentatus of hippocampus. Moderate levels of expression were detected in many brain regions including the granular layer of the cerebellum, anterior paraventricular thalamic nucleus, caudate-putamen, inferior colliculus, pontine nuclei, inferior olive, and nucleus of the solitary tract. We examined the circadian profile of hamster Per1 mRNA in the SCN in constant darkness and found that Per1 expression showed a peak at subjective day (circadian time [CT] 4) and formed a trough at subjective night (CT16-CT20). A brief exposure of light at CT16 could acutely induce large quantities of Per1 mRNA in the hamster SCN, except for its dorsomedial subdivision. These findings suggest that the characteristics of Per1 gene expression in the mammalian circadian center (showing a peak in the daytime and a trough in the nighttime and a rapid inducibility by light) are common among mammalian species. Lastly, in hamster brain, Per1 gene is also inducible in extra-SCN brain nuclei, since light at night also elicited Per1 mRNA in neurons of the hypothalamic paraventricular nucleus.

Animals↗
PubMed2001

Systemic toxicity from repeated cutaneous contact with 2,4-pentanedione.

2,4-Pentanedione (2,4 PD; CAS Number 123-54-6) is an industrial chemical with potential for skin contact. Repeated exposure studies by peroral and inhalation routes have shown central neurotoxicity and possible effects on the immune system. To determine the likelihood for systemic toxicity by cutaneous contact with 2,4-PD, a short-term repeated skin contact study was conducted in New Zealand white rabbits. The planned protocol was for dosing, with 0.5, 1.0 and 1.5 ml undiluted 2,4-PD by 6 h occlusive contact/d for 9 d; these were equivalent to dosages of 244, 975 and 1463 mg/kg/d. A dosage-related skin irritation was seen macroscopically and by light microscopy, which was minimal at the low dosage. Mortalities occurred at the mid (1/6 males, 3/6 females) and high dosages (5/12 males, 7/12 females), with deaths between the 2nd and 5th dosing day. In view of these mortalities and signs, dosing of the mid and high dose animals was discontinued, and survivors were kept to the end of the dosing period. Signs at the mid and high dosage included hypoactivity, tremors, convulsions, uncoordinated movements and prostration, and appeared between the 2nd and 4th dose. Body weight gain and food consumption were reduced for the mid and high dosage groups. Increased hemoglobin, hematocrit and erythrocyte counts may have been associated with dehydration, and increased heterophil count with cutaneous inflammation. Several serum biochemical changes reflected cutaneous irritation, and high creatine kinase activity was probably a consequence of convulsions. Immune effects included decreased lymphocyte counts and lymphoid necrosis in spleen and thymus. Central neuropathology in the mid and high dosages was seen as hemorrhages and neuronal degeneration, the latter principally in piriform cortex, globus pallidus and hippocampus. No peripheral neuropathy was present. 244 mg/kg/d was the no-effects dosage for systemic toxicity. This study confirmed a potential for systemic toxicity, principally central neurotoxicity, from percutaneous absorption of 2,4-PD.

Administration, Cutaneous↗
PubMed1997

Behavior and activities in the central nervous system after activation of L-type calcium channels in mice.

The distribution of the immediate early gene c-fos expression in the mouse central nervous system after subcutaneous injection of Bay K 8644 was observed immunohistochemically. Half an hour after injection, c-fos protein (FOS) was expressed in the piriform cortex, sensorimotor cortex, caudate putamen, thalamic paraventricular nucleus and striate cortex, etc. Intense FOS immunoreactive (FOS-ir) cells were seen during 2-4 h after injection. The results suggested that the distribution of FOS-ir cells after subcutaneous injection of Bay K 8644 was coincident with that of L-type calcium channels in the different areas of the CNS. After Bay K 8644 injection, mice appeared seizure-like behavior. The percentage of cells double-labelled by FOS and CaBP immunoreactivities in the observed regions was about 60.2-72.8% in CaBP-ir cells. It suggested that most CaBP-ir cells may have L-type calcium channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed2001

Oxytocin in the medial amygdala is essential for social recognition in the mouse.

Oxytocin (OT) knock-out mice fail to recognize familiar conspecifics after repeated social exposures, despite normal olfactory and spatial learning abilities. OT treatment fully restores social recognition. Here we demonstrate that OT acts in the medial amygdala during the initial exposure to facilitate social recognition. OT given before, but not after, the initial encounter restores social recognition in OT knock-out mice. Using c-Fos immunoreactivity (Fos-IR) as a marker of neuronal activation in this initial encounter, we found similar neuronal activation in the wild-type (WT) and OT knock-out mouse in olfactory bulbs, piriform cortex, cortical amygdala, and the lateral septum. Wild-type, but not OT knock-out mice exhibited an induction of Fos-IR in the medial amygdala. Projections sites of the medial amygdala also failed to show a Fos-IR induction in the OT knock-out mice. OT knock-out, but not WT, mice showed dramatic increases in Fos-IR in the somatosensory cortex and the hippocampus, suggesting alternative processing of social cues in these animals. With site-specific injections of OT and an OT antagonist, we demonstrate that OT receptor activation in the medial amygdala is both necessary and sufficient for social recognition in the mouse.

Amygdala↗
PubMed1975

The telencephalon of the sea catfish Galeichthys felis.

The sea catfish is a relatively abundant teleost fish. Its placement on the phylogenetic scale remains in question, although its brain resembles grossly those of some of the other teleosts which also possess pedunculated olfactory bulbs. The forebrain of Galeichthys felis consists of two hemispheres which lack lateral ventricles. They are joined at the midline by a thin membrane ventromedially and by the hippocampal and anterior commissures. The telencephalic hemispheres are overlaid by a single, ventrolaterally attached membrane which is continuous rostrally with the roofs of the olfactory ventricles. Six basic nuclear regions are evident in the telencephalon of the sea catfish: a dorsomedial, a ventromedial, a ventral, a lateral, a dorsal and a central. Dorsomedially, the primordial hippocampal formation is divided into an anterior continuation, a primordial dentate gyrus, a primordial cornu ammonis and a primordial subiculum. Ventromedially, the precommissural septum consists of the medial septal nucleus (pars dorsalis and pars ventralis), the lateral septal nucleus and the nuclei of the hippocampal and anterior commissure. Ventrally, the medial and the lateral zones and the medial island constitute the tuberculum olfactorium. The primordial general pallium comprises the dorsal area. Laterally, the primordial piriform cortex and the prepiriform region overlie the relatively large primordial amygdaloid complex, which includes an anterior anygdaloid nucleus, a primordial corticomedial amygdaloid nucleus and a primordial basolateral amygdaloid nucleus. The hyperstriatum, the neostriatum, and paleostriatum augmentatum and the paleostriatum primitivum constitute the central region. Basic fiber systems in Galeichthys felis which are homologous to those of higher vertebrates include the medial and the lateral olfactory tracts, the fornix, the medial and the lateral forebrain bundles, the stria medullaris pathways and the stria terminalis. In spite of the lack of lateral telencephalic ventricles in this form, nuclear areas were defined which, on the basis of topography, cellular morphology and fiber pathways, were homologized with the six basic regions found in the forebrain of higher vertebrates. The basic pattern of the fiber pathways present in the sea catfish corresponds to that found in the other submammalian vertebrates.

Amygdala↗