Biomedical subjects

H Ferreyra-Moyano

Publications and source records attributed to H Ferreyra-Moyano.

8 recordsLinked to original sources

PubMed1995

Ventrostriopallidal functional interconnections with cortical and quasi-cortical regions.

A total of 287 neurons were antidromically driven in quasi-cortical regions, i.e., anterior olfactory nucleus (24%), basolateral amygdala (13%), main olfactory bulb (4%), prefrontal cortex (37%), and in the hippocampal formation (22%) following macro- and microstimulation of the rat's ventrostriopallidal region (VSPR). In addition, a substantial number of units (n = 175) were also transynaptically affected in all these structures by shocks delivered to the VSPR. Excitatory effects were detected in 50 neurons (56.1% of responsive cells), 36 cells (40.4%) responding with inhibition of spontaneous discharges. Conversely, stimulation of cortical and quasi-cortical regions antidromically discharged (n = 37) or transynaptically affected (n = 151) units in the VSPR; 168 neurons were not responsive to VSPR stimulation. Axon collateralization (branching) of 14 neurons in anterior olfactory nucleus, basolateral amygdala, and hippocampal formation was revealed with the use of the reciprocal collision test. Conduction properties of 35 neurons, evaluated by paired-pulse stimulation, indicated that only 26% showed a significant increase in conduction velocity and a decrease in threshold during the supernormal phase. The present findings confirm and extend previous neuroanatomical studies that have, first, described strong interconnections between the neocortex and striatal structures, and second, that the VSPR as suggested by previous structural, hodological, and histochemical studies, seems to maintain a more close relationship with olfactory related structures than hitherto suspected.

Animals↗

PubMed1989

The olfactory system and Alzheimer's disease.

Alzheimer's disease (AD) is considered to be the number one health problem and seems to be reaching epidemic proportion in the USA. The cause of AD is not known, a reliable animal model of the disease has not been found and appropriate treatment of this dementia is wanting. The present review focuses on the possibility that a virus or exogenous toxic materials may gain access to the CNS using the olfactory mucosa as a portal of entry. Anterograde and retrograde transport of the virus/zeolites to olfactory forebrain regions, which receive primary and secondary projections from the main olfactory bulb (MOB) and which, in turn, project centrifugal axons to the MOB, may initiate cell degeneration at such loci. Pathological changes may, thus, be initially confined to projecting and intrinsic neurons localized in cortical and subcortical olfactory structures; arguments are advanced which favor the view that excitotoxic phenomena could be mainly responsible for the overall degenerative picture. Neurotoxic activity may follow infection by the virus itself, be facilitated by loss of GABAergic terminals in olfactory cortex, develop following repeated episodes of physiological long term potentiation (which unmasks NMDA receptors) or be due to excessive release, faculty re-uptake or altered glutamate receptor sensitivity. Furthermore, a reduction in central inhibitory inputs to the MOB might then result in disinhibition of mitral/tufted neurons and enhance the excitotoxic phenomena in the MOB projecting field. Within this context, and in line with recent studies, it is believed that pathology begins at cortical (mainly olfactory) regions, basal forebrain neurons being secondarily affected due to retrograde degeneration. In addition, failure to produce a critical level of neurotrophic factors by a damaged MOB and olfactory cortex, could adversely affect survival of basal cholinergic neurons which innervate both regions. Support for these hypothesis is provided, first, by recent reports on pathological findings in AD brains which seem to involve preferentially the olfactory and entorhinal cortices, the olfactory amygdala and the hippocampus, all of which receive primary or secondary projections from the MOB; secondly, by the presence of severe olfactory deficits in the early stages of the disease, mainly of a discriminatory nature, which points to a malfunction of central olfactory structures.

Alzheimer Disease↗

PubMed1988

Electrophysiological connections of neurons in ventral pallidal regions of the olfactory tubercle with the main olfactory bulb and piriform cortex.

Field potential and single unit recordings were used to assess the connections of the olfactory tubercle (OT) with the main olfactory bulb (MOB) and the piriform cortex (PC) in urethane-anesthetized rats. Current generators of depth profiles evoked in OT following MOB stimulation were localized 300 microns superficial to those elicited by PC shocks, suggesting that afferents from the MOB and PC end in different regions of the OT. Following MOB and PC stimulation antidromically invaded neurons were recorded in the ventral pallidal regions of the OT and in the vicinity of the islands of Calleja, respectively. These results demonstrate that the OT, which receives a monosynaptic input from the MOB, projects back to the bulb and that the PC seems to be also reciprocally linked with differentiated structures in the OT.

Animals↗

PubMed1988

Current generators and properties of late components evoked in rat olfactory cortex.

Following main olfactory bulb (MOB) stimulation at frequencies of 0.1-0.3 Hz, in addition to early field potentials, a frequency-sensitive, surface negative late N2 wave (latency range: 63-96 msec) followed occasionally by a late N3 transient, was evoked in the piriform cortex and endopiriform nucleus of the rat. The N2 wave inverted polarity at the Ib-II cortical layer interface (P2 wave) and was associated with late unit discharges 200 to 1200 microns deep to the turnover point. Response probability, peak latency, recovery curve and frequency-sensitivity of the P2 wave were not significantly different in animals under urethane or pentobarbital. Current-source-density (CSD) analysis revealed that the N2 wave generators were localized to the Ib-II layer interface. Since inhibitory activity does not contribute substantially to the second derivative curve, CSD analysis strengthens the assumption that late components (LCs) are excitatory events (compound EPSPs) presumably generated on the proximal apical dendritic segments of pyramidal cells by association axons. The early "b" wave in a test response was facilitated, rather than occluded, when a LC was present in the conditioning response, or when the priming volley was delivered to the mediodorsal thalamic nucleus. Clustering of unit and field activity in two distinct periods of the evoked response separated by a prolonged interval of cell silence suggests that cortical coding of olfactory cues might be more efficiently achieved by temporal modulation of the neuronal response rather than by spatial distribution of firing patterns.

Animals↗

PubMed1988

A computer program for automatic plotting of isopotential contours in CNS.

A computer program was developed in a Basic (Applesoft) version for generating up to five isopotential curves from field potentials recorded in nervous structures. Voltages are fed according to a cartesian coordinate system, and an area is delineated each four points in which a certain number of intermediate voltage points are calculated, according to the required resolution. The calculated values are compared to those prefixed for each curve and, if similar, their coordinates are stored in corresponding bidimensional matrixes. A special subroutine was designed for constructing an isometric tridimensional perspective of the isopotential curve ensemble. The reliability of this program was tested in the localization of sensory representation areas on the neocortex of the South American armadillo (Chaetophractus vellerosus) studied by evoked potential mapping following visual, auditory and somatosensory stimuli. The isopotential curves traced permitted a quantitative evaluation of the cortical activated areas, and from their topographical distribution, relative unresponsive zones could be inferred where only inconspicuous responses were obtained. It is concluded that the present program provides a reliable and fast method for studying the evoked potential's spatial distribution over the entire neocortex. In addition, it can be extended to the study of curves or contours which connect equivalent values pertaining to biophysical magnitudes other than voltage data.

Animals↗

PubMed1987

Reciprocal functional connections of the olfactory bulbs and other olfactory related areas with the prefrontal cortex.

Reciprocal putative connections of the prefrontal cortex (PFC) (agranular insular, ventral and lateral orbital region) with the ipsi and contralateral main olfactory bulb (IOB; COB), the mediodorsal thalamic nucleus (MD), the basolateral amygdaloid nucleus (BLA) and the piriform cortex (PC) were investigated with electrophysiological techniques. Evoked field responses and orthodromic unit driving, generated in PFC following electrical stimulation of the above mentioned structures, were abolished following topical application of KCl, except for COB evoked mass potentials. Thus, locally generated activity was elicited in agranular insular cortex following IOB activation, the same region where recently, the taste cortex in the rat was localized. Since gustatory-visceral afferent information reaches insular cortex via 2-3 synaptic relays, autonomic, olfactory and gustatory inputs may interact at this level, and, as suggested previously for the mouse, play a key integrative role in flavor perception. Antidromically invaded neurons, 47% of which were identified by the collision-extinction technique, were also found in PFC areas which overlapped to a considerable extent with those from which orthodromic unit responses were obtained. In particular, closely spaced neurons in ventrolateral orbital (VLO) and lateral orbital (LO) regions were antidromically invaded following IOB and PC shocks; some neurons antidromically discharged by IOB were also transsynaptically activated following PC stimulation. These findings are in agreement with recent neuroanatomical studies which demonstrate axonal projections from PFC neurons to the IOB and COB in the rat and South American armadillo. In addition, stimulation of PFC regions dorsal to the rhinal fissure mostly inhibited spontaneous unit discharges recorded at the mitral cell layer of the IOB, suggesting that this effect may be partially mediated by excitatory inputs of prefrontal axons onto granule cells. The conduction properties, antidromic thresholds and activity-dependent variations in conduction velocity (CV) of bulbopetal neurons in prefrontal cortex were found to be similar to those exhibited by cells projecting to the IOB from olfactory peduncle regions, but not to those present in bulbopetal neurons of the horizontal limb of diagonal band, indicating that the OB may be subjected to centrifugal control by at least two cell groups differing in both histochemical and electrophysiological properties.

Afferent Pathways↗

PubMed1986

Axonal projections and conduction properties of olfactory peduncle neurons in the armadillo (Chaetophractus vellerosus).

Extracellular unit recording was employed to study the axonal properties and efferent projections of antidromically identified neurons in the olfactory peduncle (OP) region of a primitive eutherian macrosmatic mammal, the south american armadillo (Chaetophractus vellerosus). Of 72 cells which satisfied the criteria for antidromic invasion, 55 (76%) and 17 (24%) responded to ipsi- and contralateral olfactory bulb (IOB; COB) stimulation, respectively. The absolute refractory period (3.25 +/- 0.3 ms; mean +/- SE) and the conduction velocity (CV; 1.94 +/- 0.2 m/s; mean +/- SE) of IOB and COB driven neurons were negatively correlated (r = -0.52; p less than 0.001). In paired-shock tests (8-1950 ms interval), and early supernormal period (SPN) of increased CV and excitability was found following the relative refractory period in 82% of tested cells (N = 50); this period was followed by a late subnormal phase (SBN) of decreased CV and increased threshold in 58% of neurons (N = 50). Significant correlations were found to exist between: CV and absolute magnitude of latency variation (r = -0.55; p less than 0.001; n = 43), CV and duration of SPN and SBN periods (r = -0.60; p less than 0.002; n = 24 and r = 0.58; p less than 0.02; n = 19, respectively) and between duration of SPN and SBN phases (r = 0.79; p less than 0.001; n = 30). Maximum latency variation during the SPN and SBN periods was attained in a gradual, additive manner.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

An automatic device for determining threshold variations in antidromically activated neurons.

A device was designed and constructed with the purpose of evaluating threshold variations for antidromic invasion of extracellularly recorded neurons. Identification of a neuron is carried out by two procedures, an amplitude discriminator, which isolates the spike from the baseline noise, and by a latency window which is set accordingly to the neuron's antidromic latency. During threshold evaluation, the duration of an electric pulse applied to the neuron's axon is automatically varied depending on the presence or not of an action potential. For a given spike, the stimulus is progressively decreased (-delta i) up to a point where the neuron ceases to respond and thereafter, the stimulus amplitude is progressively increased (+delta i) until slightly suprathreshold values are obtained. The procedure guarantees a discharge probability of the neuron equivalent to 50% of all applied stimuli, and the simple monitoring of the stimulus amplitude is enough to obtain the threshold value for a predetermined intensity. The reliability of this device was checked in studies related to threshold variations in neurons antidromically driven in prefrontal cortex following stimulation of the ipsi and contralateral olfactory bulb. Variations in excitability were found during and following tetanic stimulation and throughout the axon's supernormal conduction period. This technique allows the assessment of threshold variations in antidromic driving, not only in the present experimental design, but also in other conditions induced by changes in extracellular ionic concentrations, drug applications or in those produced by excitatory or inhibitory synaptic activity on the neuron under study.

Animals↗