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PubMed2004

Neuronal and glial cell populations in the piriform cortex distinguished by using an approximation of q-space imaging after status epilepticus.

BACKGROUND AND PURPOSE: Temporal lobe epilepsy produces an injury cascade that includes neuronal loss and gliosis. The pilocarpine model reliably reproduces the symptoms of temporal lobe epilepsy and the resulting neuronal glial changes can be accurately depicted on diffusion-weighted images. The judicious choice of diffusion-encoding gradients can isolate multiple apparently isochromatic diffusing populations, but the assignment of these populations to specific tissue characteristics has been difficult. We sought to distinguish neuronal tissue from glial cell-infiltrated tissue by using signatures from unique spin populations obtained from an approximation of q-space imaging. METHODS: Ten male Sprague-Dawley rats received pilocarpine injections to induce seizures. All animals underwent diffusion-weighted imaging at 12 hours, 24 hours, and 7 days. At least two animals were selected for histologic analysis at each imaging time point. RESULTS: The results indicated that seizure-induced neurologic dysfunction may have been reflected in the emergence of new spin populations. In the piriform cortex-amygdala region of interest, the mean free diffusion path increased from 12 to 20 microm within 12 hours of seizure onset and persisted for at least 7 days. These results were temporally correlated with histologic evidence of necrotic changes. CONCLUSION: Our results suggest that even incomplete sampling of q space can provide useful physiologic information.

Amygdala↗
PubMed1998

Localization of pontine PGO wave generation sites and their anatomical projections in the rat.

A number of experimental and theoretical reports have suggested that the ponto-geniculo-occipital (PGO) wave-generating cells are involved in the generation of rapid eye movement (REM) sleep and REM sleep dependent cognitive functions. No studies to date have examined anatomical projections from PGO-generating cells to those brain structures involved in REM sleep generation and cognitive functions. In the present study, pontine PGO wave-generating sites were mapped by microinjecting carbachol in 74 sites of the rat brainstem. Those microinjections elicited PGO waves only when made in the dorsal part of the nucleus subcoeruleus of the pons. In six rats, the anterograde tracer biotinylated dextran amine (BDA) was microinjected into the physiologically identified cholinoceptive pontine PGO-generating site to identify brain structures receiving efferent projections from those PGO-generating sites. In all cases, small volume injections of BDA in the cholinoceptive pontine PGO-generating sites resulted in anterograde labeling of fibers and terminals in many regions of the brain. The most important output structures of those PGO-generating cells were the occipital cortex, entorhinal cortex, piriform cortex, amygdala, hippocampus, and many other thalamic, hypothalamic, and brainstem nuclei that participate in the generation of REM sleep. These findings provide anatomical evidence for the hypothesis that the PGO-generating cells in the pons could be involved in the generation of REM sleep. Since PGO-generating cells project to the entorhinal cortex, piriform cortex, amygdala, and hippocampus, these PGO-generating cells could also be involved in the modulation of cognitive functions.

Action Potentials↗
PubMed1990

Transection of the rat olfactory nerve increases glial fibrillary acidic protein immunoreactivity from the olfactory bulb to the piriform cortex.

Astrocytic glial fibrillary acidic protein (GFAP) immunoreactivity in response to retrograde changes of motoneurons after axotomy has been the subject of a number of reports. In contrast, this study examined the astrocytic GFAP immunoreactivity in response to axotomy in a sensory system, the adult rat olfactory system. The purpose of this study was to determine, by immunolabeling GFAP, the extent and transience of astrocytic reactivity in the olfactory system. Unilateral transection of the olfactory nerve fascicles was performed intracranially at the level of the cribriform plate. Rats were allowed to survive from 24 hours to 1 month after axotomy. GFAP immunolabeling was examined throughout the rat olfactory system using the peroxidase-anti-peroxidase method. After axotomy, a transient increase occurred in the astrocytic GFAP immunoreactivity in the ipsilateral olfactory system. The greatest enhancement of GFAP immunoreactivity in the olfactory system occurred at 48 hours post-axotomy. Increased GFAP immunoreactivity occurred not only along the axons and synaptic endings of the injured primary olfactory neurons, but also along the dendrites, cell bodies, axons, and synaptic endings of the secondary sensory neurons. The increased GFAP immunoreactivity was specifically associated with the anatomical distribution pathways of the primary and secondary olfactory neurons. Increased GFAP immunoreactivity was not altered until 14 days post-axotomy. At 1 month post-axotomy, GFAP immunoreactivity returned to control levels. The time course and transience of increased GFAP immunoreactivity closely correlates with the time course of rat primary olfactory neuronal degeneration and regeneration after axotomy.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1998

Differential induction of immediate early gene mRNAs following cryogenic and impact trauma with/without craniotomy in rats.

Expression of immediate early gene (IEG) mRNAs following traumatic brain injury in 3 different models-cryogenic injury, impact injury with craniotomy and impact injury without craniotomy-was investigated using in situ hybridization. Cryogenic brain injury resulted in c-fos and c-jun mRNA expression throughout the ipsilateral cortex, piriform cortex and dentate gyrus on the injured side, with peak at 30 min to 1 h post-injury. Impact injury with craniotomy was associated with hybridization signals in the same areas and also in the subcortical white matter or ependyma underlying the impact site at 30 min post-injury. The expression was rather more prolonged than with cryogenic injury. Impact injury without craniotomy induced the expression of both mRNAs throughout the ipsilateral cortex, piriform cortex and dentate gyrus at 30 min post-injury, but this was promptly attenuated by 1 h post-injury, except for bilateral elevation in the dentate gyrus. The present study, thus, demonstrated that regional and temporal expression of IEG mRNAs is influenced by the intensity, quality and manner of application of the insult. Differences in the expression of IEGs may alter the late response gene expression and affect the succeeding events.

Animals↗
PubMed1978

Exploration and avoidance in rats with lesions in amygdala and piriform cortex.

Lesions localized to specific areas of the amygdala and overlying cortex in rats produced differential effects in several behavioral tasks. Three different types of lesions were tested: central, basolateral, and cortex lateral to the amygdala. Lesions restricted to the central nucleus produced increased activity on all parameters studied in an open-field test, but the other two groups were not changed. In one-way active avoidance all three groups with lesions showed deficits. The most pronounced change was observed in the central group. All groups showed the same degree of retention loss, but in forced extinction of one-way active avoidance after retraining, the cortical and basolateral groups were most defective. A fear-reduction hypothesis is proposed for the central lesion. The basolateral and cortical areas may be more specifically involved in passive avoidance behavior.

Amygdala↗
PubMed1992

Expression of c-fos protein in rat brain elicited by electrical stimulation of the pontine parabrachial nucleus.

The expression of Fos, the protein product of the primary response gene c-fos, was used metabolically to map the short-term (1 hr) effects of urethane and sodium pentobarbital anesthesia in rat. Subsequently, urethane-anesthetized rats were used to study the integrated response to electrical stimulation (1-1.5 hr) of the pontine parabrachial nucleus (PBN), an important center for relay of autonomic information in the brain. Immunohistochemistry was used to localize Fos-like immunoreactivity (FLI) in the brain. To approximate amounts of FLI in the conscious animal, rats were killed immediately after attaining surgical anesthesia with sodium pentobarbital (50 mg/kg) or urethane (1.2-1.7 gm/kg). No FLI was found in the brains of these rats. In rats killed 1 hr after anesthesia with sodium pentobarbital, FLI was found only in the habenulae. After 1 h of urethane anesthesia, low levels of FLI were found in the following areas: nucleus of the tractus solitarius (NTS); caudal and rostral ventrolateral medulla (VLM); lateral PBN; ventromedial, paraventricular, and supraoptic nuclei (SON) of the hypothalamus; medial preoptic area; central nucleus of the amygdala (ACE); endopiriform cortex; insular cortex; piriform cortex; and islands of Calleja. Electrical stimulation of the PBN (10 sec on, 10 sec off; 15-50 microA at 20 Hz for 60-90 min) in rats anesthetized with urethane led to increases in mean arterial pressure (10-30 mm Hg) and to ipsilateral increases of FLI in the lateral PBN, dorsal division of SON, ACE, endopiriform nucleus, insular cortex, piriform cortex, and islands of Calleja. In two animals, ipsilateral increases were found in the ventromedial hypothalamus and medial amygdaloid nucleus.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1989

Bursting induces persistent all-or-none EPSPs by an NMDA-dependent process in piriform cortex.

Burst responses to stimulation of excitatory fiber tracts in olfactory cortex slices after removal of extracellular Mg2+ or decreases in extracellular Cl-, resulted in long-lasting changes in response properties of neurons following a return to normal bathing medium. After bursting activity, the response of pyramidal cells to stimulation of afferent or associational fiber systems consisted of the normal graded depolarizing postsynaptic potential and a new, high-amplitude depolarizing potential that followed the graded potential at a variable latency. The new late potential had a waveform that resembled the initial graded response, but it occurred in an all-or-none fashion with a discrete threshold and persisted for many hours. Threshold for the late potential was similar for different cells in the same slice and was not affected by intracellular current injection, indicating that a synchronized interaction among a large number of cells is involved in its generation. Properties of the late potential indicate that it is an EPSP. NMDA receptor antagonists (APV and ketamine) had little effect on the late potential but prevented its development if present during bursting activity. The possible relevance of these findings to the study of the neuronal substrate for long-term memory and epilepsy is discussed.

2-Amino-5-phosphonovalerate↗
PubMed1994

Neuronal injury produced by NMDA antagonists can be detected using heat shock proteins and can be blocked with antipsychotics.

Noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonists, including ketamine, MK-801, and phencyclidine (PCP), induce the HSP70 heat shock or stress gene in pyramidal neurons in rat posterior cingulate and retrosplenial cortex. PCP also induces HSP70 in many other pyramidal neurons in brain including neocortex, insular cortex, piriform cortex, hippocampus, and basal nuclei of the amygdala. Several neurotransmitter antagonists, including haloperidol, clozapine, SCH-22390, diazepam, and muscimol, inhibited induction of HSP70 produced by PCP. Baclofen had no effect. Nifedipine blocked induction of HSP70 by PCP in cingulate, neocortex, and insular cortex but only partially blocked HSP70 in piriform cortex and amygdala. These data suggest that phencyclidine injures pyramidal neurons via dopamine D1, D2, D4, sigma, and other receptors. Gamma-aminobutyric acid (GABA) agonists ameliorate the injury. A model is proposed whereby NMDA receptor blockade on GABA neurons decreases inhibitory inputs onto cortical pyramidal neurons and makes them more vulnerable to injury from a variety of excitatory inputs. It is possible that psychosis produced by PCP and other NMDA antagonists correlates with overactivity and eventual injury to cingulate pyramidal neurons.

Animals↗