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PubMed1997

Progesterone treatment increases Fos-immunoreactivity within some progestin receptor-containing neurons in localized regions of female rat forebrain.

In female rats, the sequential release of estradiol and progesterone from the ovaries is required for the expression of sexual behavior during the estrous cycle. Many of the neuronal effects of estradiol and progesterone involve estrogen and progestin receptors. Treatment with a behaviorally-effective dose of estradiol increases Fos expression, suggestive of neuronal response, and subsequent treatment with a behaviorally-effective dose of progesterone further increases Fos expression within a few hours in female rat brain. In order to determine if neurons that respond to progesterone with increase Fos expression also contain progestin receptors, we used a double-label immunofluorescent technique to label both progestin receptors and Fos protein following progesterone or vehicle treatment of estradiol-primed female rats. As shown previously, progesterone treatment increased Fos expression in progestin receptor-containing regions, such as the ventromedial nucleus of the hypothalamus and the medial preoptic area. In addition, progesterone treatment induced a statistically-significant increase in Fos-immunoreactivity within progestin receptor-containing cells in the medial preoptic area and the ventromedial nucleus of the hypothalamus, but not in the arcuate nucleus. Therefore, many but not all of the neurons that respond to progesterone with increased Fos expression also contain progestin receptor-immunoreactivity. The progesterone-induced Fos expression within progestin receptor-containing neurons may or may not be associated with the effects of progesterone on sexual or other reproductive behaviors, as it remains to be tested. However, the Fos expression provides a useful marker to aid in identification of neurons that respond to a behaviorally-relevant dose of progesterone.

Animals↗
PubMed1997

Effect of unilateral tympanotomy on auditory induced c-fos expression in cochlear nuclei.

The immediate early gene, c-fos, signals expression of target genes. Three natural occurring physiological entities: (1) learning, (2) plasticity, and (3) stress are proposed to use c-fos gene expression to signal molecular changes in neurons. The objective of this study was to determine whether c-fos expression is predominately activated by stress or by novel events associated with learning and plasticity. The approach was to quantitate the number of neurons in cochlear nuclei which express Fos protein following short-term novel sound stimuli together with either uni- or bilateral tympanotomy so as to differentiate novel sound stimuli from stress activation. The results show that routinely experienced sounds do not elicit c-fos expression in medullary cochlear nuclei, but novel sounds produced a 25-fold increase in the number of active cells. Following unilateral tympanotomy with novel sound stimulation, only a small number of cells were activated, ipsilaterally, (partially deafened side) while contralaterally, there was a 30-fold increase. After normalization of the data for control values, the data clearly indicate that novelty of sound stimuli induce c-fos gene expression. Furthermore, bilateral tympanotomy (bilateral partial deafening) with sound stimulation activated both sides by 20-fold, indicating that the c-fos response followed the sound stimulation. The data allow us to conclude that stress generates only a small contribution to c-fos gene expression while novel stimuli are potent signals, strongly implicating c-fos in novelty induced adaptation processes involved in learning and plasticity.

Acoustic Stimulation↗
PubMed1997

Nerve growth factor induces Fos-like immunoreactivity within identified cholinergic neurons in the adult rat basal forebrain.

Immunocytochemical techniques were used to examine and compare the effects of intracerebroventricular administration of nerve growth factor (NGF) on Fos expression within identified cholinergic and non-cholinergic neurons located in different regions of the adult rat basal forebrain. Animals were killed 1, 3, 6, and 12 h after receiving NGF (0.5 or 5.0 microg) or vehicle into the left lateral ventricle and sections through the medial septum, diagonal band of Broca, nucleus basalis magnocellularis, and striatum were processed for the combined immunocytochemical detection of Fos and choline acetyltransferase (a marker for cholinergic neurons), or Fos and parvalbumin (a marker for gamma aminobutyric acid (GABA)-containing neurons). NGF produced a significant increase in the percentage of cholinergic neurons containing Fos-like immunoreactivity within all four regions examined. The largest increases were detected in the medial septum (47.8%) and the horizontal limb of the diagonal band of Broca (67.7%). In these areas, NGF-mediated induction of Fos-like immunoreactivity was detected as early as 3 h, peaked at 6 h, and was reduced by 12 h, postinfusion. Small but significant increases in the percentage of cholinergic neurons containing Fos-like immunoreactivity were also detected in the striatum (4.2%) and in the nucleus basalis magnocellularis (19.2%) 3-12 h following administration of the higher dose of NGF. No evidence for an NGF-mediated induction of Fos within parvalbumin-containing neurons was detected in any of the four regions at any of the time-points examined; however, evidence for an NGF-mediated induction of Fos within epithelial cells lining the lateral ventricle was observed. These data demonstrate that NGF induces Fos expression within cholinergic, and not parvalbumin-containing (GABAergic), neurons in the basal forebrain, and furthermore that intracerebroventricular administration of NGF influences the different subgroups of basal forebrain cholinergic neurons to different degrees.

Animals↗
PubMed1997

Fos-like immunoreactivity in the circadian timing system of calorie-restricted rats fed at dawn: daily rhythms and light pulse-induced changes.

Daily rhythms of pineal melatonin, body temperature, and locomotor activity are synchronized to the light-dark cycle (LD) via a circadian clock located in the suprachiasmatic nuclei (SCN). A timed caloric restriction in rats fed at dawn induces phase-advances and further phase-stabilization of these rhythms, suggesting that the circadian clock can integrate conflicting daily photic and non-photic cues. The present study investigated the daily expression of Fos-like immunoreactivity (Fos-ir) and light pulse-induced Fos-ir in the SCN, the intergeniculate leaflet (IGL) and the paraventricular thalamic nucleus (PVT) in calorie-restricted rats fed 2 h after the onset of light and in controls fed ad libitum. A daily rhythm of Fos-ir in the SCN was confirmed in control rats, with a peak approximately 2 h after lights on. At this time point (i.e. just prior to the feeding time), the level of SCN Fos-ir was lowered in calorie-restricted rats. Concomitantly, IGL Fos-ir was higher in calorie-restricted vs. control rats. In response to a light pulse during darkness, Fos-ir induction was found to be specifically (i.e. phase-dependently) lowered in the SCN and IGL of calorie-restricted rats. Observed changes of Fos-ir in the PVT were possibly related to the wake state of the animals. This study shows that repetitive non-photic cues presented in addition to a LD cycle affect the Fos expression in the circadian timing system.

Animals↗
PubMed1997

Peripheral administration of cholecystokinin activates c-fos expression in the locus coeruleus/subcoeruleus nucleus, dorsal vagal complex and paraventricular nucleus via capsaicin-sensitive vagal afferents and CCK-A receptors in the rat.

Intraperitoneal (i.p.) administration of sulfated CCK octapeptide (CCK-8S) has been shown to induce changes in neuronal activity in the nucleus of the solitary tract (NTS) and area postrema (AP), sensory parts of the dorsal vagal complex (DVC), and in the paraventricular nucleus of the hypothalamus (PVN), as determined by activation of c-fos expression. Whether peripheral CCK influences neuronal activity in the locus coeruleus (LC)/subcoeruleus nucleus (SC) was investigated in awake rats at intraperitoneal (i.p.) injection of CCK-8S by c-Fos immunohistochemistry. CCK-8S i.p. (25, 50, and 100 micrograms/kg, respectively) dose-dependently increased the average number of c-Fos-LI-positive cells/section in the LC/SC by the factor 5.9, 8.2, and 11.7, respectively. Pretreatment with the CCK-A receptor antagonist MK-329 (devazepide; 1 mg/kg and 2 mg/kg i.p.) reduced the CCK-induced increase in c-fos expression in the LC/SC by 54% and 75%, respectively; the CCK-B receptor antagonist L-365,260 had no effect. Perivagal capsaicin pretreatment diminished the CCK-induced increase in the number of c-Fos-LI-positive cells in the LC/SC by 65%. In comparison, the CCK-A antagonist devazepide (1 mg/kg and 2 mg/kg i.p.) reduced the increase in c-fos expression by 76% and 88% in the PVN, 69% and 88% in the NTS, 86% and 83%, respectively, in the AP. Capsaicin diminished the CCK-induced increase in c-Fos-LI-positive cells in the PVN by 64%, in the NTS by 60%, but in the AP only by 25%. Immunostaining against the nuclear antigen c-Fos and the cytoplasmatic antigen tyrosine hydroxylase (TH) showed that 40% of all c-Fos-LI-positive cells in the LC/SC were TH-LI positive at 25 micrograms CCK/kg. The data indicate that CCK-8S i.p. induces modulation of neuronal activity in the LC/SC, DVC and PVN predominantly by peripheral action of CCK-A receptors and capsaicin-sensitive vagal afferents. These findings suggest that the LC/SC is involved in CNS-mediated regulatory influences of peripheral CCK.

Animals↗
PubMed1998

The expression of Fos within the suprachiasmatic nucleus of the diurnal rodent Arvicanthis niloticus.

Rhythms in the expression of the nuclear phosphoprotein Fos, have been demonstrated in the suprachiasmatic nucleus (SCN) of nocturnal rodents. When rats are housed in a 12:12-h light/dark (LD) cycle the number of Fos-immunoreactive (-IR) cells within the SCN is higher during the day than at night [9,23]. In the two experiments reported here, Fos-IR was examined in the SCN of a diurnal murid rodent, Arvicanthis niloticus. First, thirty-six adult male A. niloticus housed in a 12:12-h LD cycle were perfused at six equally spaced time points beginning 1 h after lights on (n=6 per time point). Brains were sectioned and treated with immunohistochemical procedures for the identification of Fos. The number of Fos-IR cells in the SCN varied significantly as a function of time, and was highest 1 h after lights on and decreased thereafter. The distribution of Fos-IR within the SCN overlapped with that of arginine-vasopressin-IR (AVP-IR) and vasoactive intestinal peptide-IR (VIP-IR), but not with that of gastrin-releasing peptide-IR (GRP-IR). In the second study, double-labeling techniques revealed extensive Fos expression within SCN neurons containing AVP-IR, but not neurons containing GRP-IR. In conclusion, although the overall rhythm of Fos-IR in the SCN is similar in diurnal and nocturnal rodents, differences may exist with respect to the relative distribution of Fos-immunoreacte cells within different SCN cell populations.

Animals↗
PubMed1998

Water-deprived white-footed mice express c-fos on a day/night cycle graded according to the duration of deprivation.

Mammals respond to electrolyte and water imbalance by a variety of neural and endocrine mechanisms that regulate water and salt intake and loss. We used the expression of c-fos and Fos-related antigens to indicate neuronal activation in hypothalamic neurons of members of an outbred laboratory population of white-footed mice (Peromyscus leucopus) deprived of water for biologically reasonable periods of time (6-18 h). We examined Fos-like immunoreactivity (Fos-LIR) in the supraoptic nucleus (SON) and paraventricular nucleus (PVN). During the dark period, when these animals are normally active, 6 h of water deprivation produced near-maximal increases in the number of cells positive for Fos-LIR in the SON and PVN. In contrast, during the light period, when these mice are normally inactive and do not have access to water, 6 h of water deprivation only slightly affected Fos-LIR. During the day, it required as much as 12 h of water deprivation to produce increases in Fos-LIR cells approaching those achieved at night. Plasma osmolarity was directly related to the number of Fos-LIR cells. In addition, mice lost weight more rapidly at night than during the day when water-deprived, and also recovered that lost weight more rapidly when access to water was returned. Our results show (1) that biologically reasonable levels of water restriction (and resulting changes in blood osmolarity) induce changes in Fos-LIR in this wild mouse species, and (2) that these mice have a daily cycle of sensitivity to water deprivation that is demonstrated by both behavioral, psychological and immunohistological assessment of reactions to water deprivation.

Analysis of Variance↗
PubMed1998

Fos expression in the brain induced by peripheral injection of CCK or leptin plus CCK in fasted lean mice.

We previously reported a synergistic interaction between leptin and cholecystokinin (CCK) to reduce food intake through CCK-A receptors in lean mice fasted for 24 h. To identify the activated neuronal pathways, we investigated changes in Fos expression in brain nuclei 2 h after single or combined intraperitoneal (i.p.) injections of leptin (120 microg/kg) and sulfated CCK-8 (3.5 microg/kg) in male lean mice (C57BL/6) fasted for 24 h using immunohistochemistry for Fos, the protein product of the early gene, c-fos. Leptin did not increase Fos expression in the brain compared with vehicle-treated mice. CCK increased the numbers of Fos-positive neurons in the nucleus of the solitary tract (NTS)/area postrema (AP), central nucleus of the amygdala (CeA) and, to a smaller extent, in the paraventricular nucleus of the hypothalamus (PVN) (5.2-, 2.3- and 0. 3-fold respectively). Injections of leptin-CCK further enhanced Fos expression by 40% in the PVN compared with that induced by CCK alone, but not in the other nuclei. Devazepide (a CCK-A receptor antagonist, 1 mg/kg, i.p.) prevented the increase in Fos expression induced by leptin-CCK in the PVN and by CCK alone in the PVN, CeA and NTS/AP. These results indicate that in fasted mice, i.p. injection of CCK increases Fos expression in specific brain nuclei through CCK-A receptors while leptin alone had no effect. Leptin in conjunction with CCK selectively enhanced Fos expression in the PVN. The PVN may be an important site mediating the synergistic effect of leptin-CCK to regulate food intake.

Adipose Tissue↗
PubMed1998

Transient c-fos gene expression in cerebellar development and functional stimulation.

This study examined the temporal appearance of c-fos expression in rat cerebella from birth to postnatal day 21 (P21) and following systemic kainic acid administration in adults. During development, Fos positive granule cells appeared first at P3 in caudal lobules and extended to all folia by P9. These reactive cells occurred in clusters throughout the granular layer and reached their highest reactivity by P15. In addition, Fos positive basket and stellate cells were seen in the molecular layer at this time. A steep decline in Fos protein labeling of the cerebellum began by P18 and was barely detectable in adulthood. In adult rats, systemic injection of kainic acid induced c-fos expression in granule cells and stellate/basket interneurons within 1 h of treatment. Fos reactive granule cells appeared in clusters with some forming distinct parasagittal bands in caudal folia. One day after unilateral cerebellar lesioning, a limited number of reactive cells were found on the lesion margins. A combination of lesioning and systemic kainic acid produced a strong, c-fos expression throughout the ipsilateral granular layer as well as in Purkinje cell nuclei. Contralateral to the lesion, the pattern of granule cell reactivity appeared the same but slightly stronger than those with kainate alone. We conclude that c-fos gene expression occurs transiently in granule cells during postnatal development and can be rapidly re-induced in the adult following systemic injection of glutamate agonists. The c-fos expression patterns suggest that subpopulations of granule cells are clustered and related to the parasagittal compartments of Purkinje cells.

Age Factors↗
PubMed1998

Spatial and temporal expression of c-Fos protein in the spinal cord of anesthetized rat induced by subcutaneous bee venom injection.

In order to study central neuronal components involved in subcutaneous (s.c.) bee venom-induced persistent pain (a new tonic pain model), we use Fos immunostaining technique to study the spatial and temporal patterns of neuronal activity in the spinal cord of anesthetized rats. Following intraplantar bee venom injection, Fos-like immunoreactive (ir) neurons were only seen from L1 to S3 rostrocaudally with distinct distribution at L4-5 segments. At segments of L1-2 and S1-3, Fos-ir labelings were diffusely and symmetrically distributed on both sides of the gray matter; however, at L4-5 segments, Fos-ir neurons were densely localized in medial portion of laminae I-II, less densely in laminae V-VI and a few in laminae VII and X ipsilateral to the injection side. No Fos labeling was seen in ventral horn of the spinal cord at L4-5 segments. Fos protein began to express only within lamina I at 0.5 h, but increased over the whole dorsal horn at 1 h and reached peak labeling at 2 h after bee venom. Expression of c-Fos in laminae I-II decreased at 4 h, and completely disappeared at 24 h, however, labeling in laminae V-VI disappeared much slowly and existed even at 96 h after bee venom. Within laminae III-IV, Fos-ir neurons could not be seen at 0.5 h, but began to be seen at 1 h and appeared to exist even at 24 h after bee venom. Systemic morphine suppressed c-Fos expression dose-dependently in both superficial and deep layers of dorsal horn and the latter region was much more sensitive to morphine than the former one. The present results demonstrated that prolonged neuronal activities in superficial and deep layers of dorsal horn were essential to mediation of bee venom induced tonic pain and may have different roles in generation and/or modulation of spontaneous pain and hyperalgesia and allodynia.

Analgesics, Opioid↗
PubMed1998

Temporospatial characteristics of light-induced fos immunoreactivity in suprachiasmatic nuclei are not modified in Syrian hamsters treated neonatally with monosodium glutamate.

Neonatal treatment of rodents by intraperitoneal injections of monosodium glutamate (MSG) destroys many retinal ganglion cells whose neurons belong to the circadian system; howertheless, adults always synchronize their locomotor activity rhythm (LAR) to the light/dark cycle. Recent studies have shown that light-induced phase shifts of LAR are associated with the c-fos induction in suprachiasmatic nuclei (SCN) of nocturnal rodents. In this study, the circadian system was analyzed in treated and control hamsters maintained in constant darkness and exposed to light at circadian times (CTs) 13 and 18 during subjective night, 1 and 6 h after the onset of LAR. The period of the LAR and delay (CT13) and advance (CT18) phase shifts of LAR were not significantly different between MSG-treated and control hamsters. Temporospatial variations of Fos induction after light exposure were similar in both MSG-treated and control hamsters although the total number of Fos immunoreactive (Fos-ir) nuclei in the SCN was always lower in treated hamsters. However, the decrease in Fos-ir was significant only for the caudal third of the SCN of treated hamsters, the part where retinal afferents are most dense. The effect of light exposure on Fos expression in SCN of MSG-treated and control hamsters was the same at CT13 and CT18: (1) Fos-ir nuclei were significantly more numerous at CT18 than at CT13 in the rostral SCN; (2) dorsal Fos-ir cells were observed in the SCN only at CT18; (3) a ventral subgroup expressed Fos protein in intermediate SCN only at CT13. This study demonstrates that MSG-treatment does not significantly modify the phase-shifting effects of light on either the LAR or the associated cellular activation.

Animals↗
PubMed1999

Correlation of Fos expression and circling asymmetry during gerbil vestibular compensation.

Vestibular compensation is a central nervous system process resulting in recovery of functional movement and control following a unilateral vestibular lesion. Small pressure injections of phosphorothioate 20mer oligonucleotides were used to probe the role of the Fos transcription protein during vestibular compensation in the gerbil brainstem. During isoflurane gas anesthesia, antisense probes against the c-fos mRNA sequence were injected into the medial vestibular and prepositus nuclei unilaterally prior to a unilateral surgical labyrinthectomy. Anionic dyes, which did not interact with the oligonucleotides, were used to mark the injection site and help determine the extent of diffusion. The antiFos oligonucleotide injections reduced Fos expression at the injection site in neurons which normally express Fos after the lesion, and also affected circling behavior induced by hemilabyrinthectomy. With both ipsilateral and contralateral medial vestibular and prepositus nuclei injections, less ipsilateral and more contralateral circling was noted in animals injected with antiFos injections as compared to non-injected controls. The degree of change in these behaviors was dependent upon the side of the injection. Histologically, antiFos injections reduced the number of Fos immunolabeled neurons around the injection site, and increased Fos expression contralaterally. The correlation of the number of neurons with Fos expression to turning behavior was stronger for contralateral versus ipsilateral turns, and for neurons in the caudal and ipsilateral sub-regions of the medial vestibular and prepositus nuclei. The results are discussed in terms of neuronal firing activity versus translational activity based on the asymmetrical expression of the Fos inducible transcription factor in the medial vestibular and prepositus nuclei. Although ubiquitous in the brain, transcription factors like Fos can serve localized and specific roles in sensory-specific adaptive stimuli. Antisense injections can be an effective procedure for localized intervention into complex physiological functions, e.g. vestibular compensation.

Adaptation, Physiological↗
PubMed1999

Effect of post-injury NMDA antagonist treatment on long-term Fos expression and hyperalgesia in a model of chronic neuropathic pain.

Chronic constriction injury (CCI) of the sciatic nerve results in persistent mechanical hyperalgesia together with Fos protein expression in the lumbar spinal cord. We have examined the relationship between mechanical hyperalgesia and Fos expression within the lumbar spinal cord on days 14, 35 and 55 after either CCI or sham operation. To determine the role of NMDA receptor mechanisms in the maintenance of hyperalgesia and Fos expression, the NMDA antagonist MK-801 (0.3 mg kg-1 s.c.) was administered daily on days 28 to 34 after operation. CCI animals developed unilateral hind limb hyperalgesia that persisted unchanged from days 14 to 55 of the study. MK-801 treatment reduced hyperalgesia by 57% (p=0.02) on day 35 in CCI animals but did influence hyperalgesia at day 55. In the spinal cord, Fos positive cells were present bilaterally throughout laminae 3-10 at all time points examined in both CCI and sham group animals. Fos counts ipsilateral to the side of injury in laminae 3-10 correlated significantly with hyperalgesia scores in the CCI but not sham animals. MK-801 treatment resulted in a suppression of Fos expression in ipsilateral laminae 3-4 (p=0.0017) and laminae 5-10 (p=0.0026) of CCI animals on day 35. Fos expression in sham group animals was not inhibited by MK-801 treatment at day 35. These results indicate that Fos expression is maintained by differing mechanisms following nerve injury or sham operation. The functional consequences of Fos expression following nerve injury and sham operation are discussed.

Animals↗
PubMed2000

Nitric oxide synthase and glutamate receptor immunoreactivity in the rat spinal trigeminal neurons expressing Fos protein after formalin injection.

Although recent studies implicated glutamate receptors and nitric oxide in nociception, much still needs to be known about their localisation in neurons involved in nociceptive transmission from the orofacial region. In this study, c-fos expression indicated by Fos immunohistochemistry in the caudal spinal trigeminal nucleus induced by subcutaneous injection of formalin into the lateral face of the rat was used as a marker for nociceptive neurons. The study sought to determine whether Fos-positive neurons express nitric oxide synthase, glutamate N-methyl-D-aspartate type receptor subunit 1, and glutamate alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid type receptor subunit 2/3; and whether they project to the thalamus. After formalin injection, many Fos-positive nuclei appeared in the superficial laminae of the ipsilateral trigeminal nucleus. Confocal laser scanning microscope revealed that almost all neurons with Fos immunofluorescent nuclei were colocalised with N-methyl-D-aspartate receptor 1, 94% with glutamate receptor 2/3 and 14% with nitric oxide synthase. Some of them were closely related to neurons labelled by nitric oxide synthase. Lastly, some of the Fos-positive neurons were labelled by tetramethylrhodamine-dextran injected into the trigeminothalamic tract or the thalamic region. The results suggested that activation of N-methyl-D-aspartate receptor 1 and glutamate receptor 2/3 upon glutamate release in response to noxious stimulation to the orofacial region might mediate c-fos expression in neurons involved in nociception. The expression of Fos in the neurons could also be mediated by nitric oxide produced from the same, as well as neighbouring neurons, when nociceptive stimulation persisted. Fos-positive neurons in the spinal trigeminal nucleus may project to the thalamus, relaying orofacial nociception to the higher sensory centre.

Animals↗
PubMed1990

Photic regulation of c-fos expression in neural components governing the entrainment of circadian rhythms.

The rapid and transient induction of the proto-oncogene c-fos in mature neurons within the brain occurs in response to a variety of extracellular stimuli. To determine whether lighting conditions influence c-fos gene expression in the primary neural structures mediating the photoentrainment and generation of mammalian circadian rhythms, the expression of the c-fos protein (Fos) and related proteins in the retina and suprachiasmatic nuclei (SCN) of the anterior hypothalamus was examined immunohistochemically in rats exposed to a light-dark cycle of 12 h of light and 12 h of darkness (LD 12:12), constant light (LL), or constant dark (DD). The retina exhibited clear light-dark differences in the expression of Fos protein(s), such that immunopositive nuclei were readily evident during exposure to light (i.e., during the day of diurnal lighting or in LL), but were absent during exposure to darkness. In the SCN, the distribution of Fos immunoreactivity within specific subfields was differentially affected by photic conditions. Following exposure to light, a dense population of Fos-immunopositive cells was found in close association with the immunohistochemically distinct cell and fiber populations distinguishing the ventrolateral subfield of the SCN. In dark-exposed animals, Fos-immuno-reactive profiles were distributed throughout the SCN in areas coextensive with the immunohistochemical localization of peptidergic neural elements in both the ventrolateral and dorsomedial subfields. As a consequence of this light-dark difference in the distribution of Fos immunoreactivity, the density of labeled cells was increased within the ventrolateral SCN, but was decreased within the dorsomedial subfield, as a result of exposure to light versus darkness.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Induction of Fos-immunostaining by nicotine and nicotinic receptor antagonists in rat brain.

Using Fos protein immunohistochemistry, we have studied the effects of acute nicotine (0.5 mg/kg s.c.) and nicotinic acetylcholine receptor (nAChR) antagonists in eleven rat brain areas. Acute nicotine elevated Fos-like immunostaining (Fos IS) significantly in all studied areas except the medial prefrontal cortex. Nicotine increased the Fos IS in cortical, limbic and hypothalamic areas by 2-10-fold, and in the interpeduncular nucleus as well as in the visual areas the increases were 15-150-fold. When given alone, the nAChR antagonists mecamylamine (1.0 or 5.0 mg/kg i.p.) and dihydro-beta-erythroidine (DHE; 1.4 or 2.8 mg/kg i.p.) increased Fos IS in most brain areas maximally by 2-10-fold, but methyllycaconitine (MLA; 4.0 mg/kg i.p.) only in three areas and maximally by 4-fold. The efficacy of nAChR antagonists in blocking nicotine's effects on Fos IS varied noticeably with respect to region and antagonist, and the combined effect of nicotine+antagonist did not exceed that of either treatment alone. Mecamylamine and DHE significantly reduced nicotine-induced Fos IS in most of the studied areas, and MLA only in two areas. Thus, nAChRs seem to mediate the effects of nicotine on Fos IS, and the differences in the effects of the antagonists studied suggest that more than one subtype of nAChRs are involved. The present experiments also provide evidence that nAChR blockade itself may result in increased Fos protein expression in the brain. This could be due to blockade of presynaptic nAChRs modulating transmitter release or interruption of complex polysynaptic feedback pathways.

Animals↗
PubMed2000

Fos expression in female hamsters after various stimuli associated with mating.

Detection of the expression of c-fos mRNA or its protein product, Fos, has been used to indicate differences in neuronal response to exogenous stimuli. Factors contributing to differences in Fos expression as a result of various stimuli associated with mating have been extensively studied in the female rat. Less is known about the factors that contribute to Fos expression in female hamsters. Female hamsters differ from female rats in several aspects of sexual behavior; therefore, it seems likely that Fos expression may also differ. The purpose of this study was to determine which factors associated with mating selectively affect Fos expression in the female hamster. Animals were ovariectomized, hormone treated, and then exposed to several behavioral conditions. Fos expression in several brain areas was then assessed via immunocytochemistry (ICC). As has been found by others, mating increases Fos immunoreactivity in a number of brain regions. Specifically, vaginal-cervical stimulation (VCS) was determined to be the salient factor contributing to Fos expression in the preoptic area (POA) and bed nucleus of the stria terminalis (BNST) of ovariectomized hormone primed female hamsters that received a mating interaction.

Animals↗
PubMed2003

Cortical spreading depression affects Fos expression in the hypothalamic paraventricular nucleus and the cerebral cortex of both hemispheres.

The present experiments were performed to clarify the brain sites whose activity is affected exclusively by cortical spreading depression (CoSD). For this purpose, Fos protein, a product of an immediate early gene, was used as a marker of neuronal activation. Because Fos can be induced by many manipulations such as stress stimuli, we verified CoSD-induced Fos expression by excluding the influence of other factors such as anaesthesia and surgical manipulation. CoSD was induced by applying a KCl solution directly to the dura mater over the cerebral cortex, and Fos expression in the brain was assessed by immunohistochemistry using antibodies against Fos protein. We found that during CoSD, Fos expression was increased specifically in the magnocellular region of the hypothalamic paraventricular nucleus (PVN), as well as in the ipsilateral cortex, whereas reduced Fos expression was observed in both the parvocellular region of the PVN and the whole cortex contralateral to the CoSD site. Consistent with the reduced Fos expression, approximately 40% of neurons in the contralateral cortex revealed a suppression of electrical activity during CoSD. These results suggest that in addition to the ipsilateral cortex, CoSD affects Fos expression exclusively in the PVN and the contralateral cortex.

Animals↗