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PubMed2006

Cortical responses to invisible faces: dissociating subsystems for facial-information processing.

Perceiving faces is critical for social interaction. Evidence suggests that different neural pathways may be responsible for processing face identity and expression information. By using functional magnetic resonance imaging (fMRI), we measured brain responses when observers viewed neutral, fearful, and scrambled faces, either visible or rendered invisible through interocular suppression. The right fusiform face area (FFA), the right superior temporal sulcus (STS), and the amygdala responded strongly to visible faces. However, when face images became invisible, activity in FFA to both neutral and fearful faces was much reduced, although still measurable; activity in the STS was robust only to invisible fearful faces but not to neutral faces. Activity in the amygdala was equally strong in both the visible and invisible conditions to fearful faces but much weaker in the invisible condition for the neutral faces. In the invisible condition, amygdala activity was highly correlated with that of the STS but not with FFA. The results in the invisible condition support the existence of dissociable neural systems specialized for processing facial identity and expression information. When images are invisible, cortical responses may reflect primarily feed-forward visual-information processing and thus allow us to reveal the distinct functions of FFA and STS.

Amygdala↗

PubMed1994

Effect of diabetes associated increases in lens optical density on colour discrimination in insulin dependent diabetes.

Optical density (OD) of the crystalline lens has been shown in non-diabetics to increase linearly with age over the first five decades and at an increased rate thereafter; in insulin dependent diabetic (IDDM) patients, lens OD increases with age and with duration of diabetes at a rate similar to that in non-diabetics over the age of 60 years. Recently, it has been established that colour discrimination is abnormal in a majority of young patients with uncomplicated IDDM and angiographically normal retinas. Colour discrimination loss was attributed to functional abnormalities in the retina or neural pathways; yet the possibility exists that increases in lens OD may account for part or all of the colour discrimination loss in IDDM. In the present study, colour discrimination was compared in aretinopathic IDDM patients and age-matched controls, and then in a group of aretinopathic IDDM patients individually matched to controls with respect to lens OD. Colour discrimination was significantly worse in diabetic patients than in age-matched controls, and was significantly worse when diabetic patients were compared with controls matched for OD. The magnitude of the difference in 100 hue error score between diabetic patients and OD matched controls was, however, considerably less than the difference between diabetic patients and age-matched controls. These data suggest that colour discrimination loss in aretinopathic IDDM patients cannot be explained solely on the basis of diabetes induced increases in lens OD, but must involve abnormalities of the retina or its neural connections.

Adolescent↗

PubMed2000

Vision and cognition in Alzheimer's disease.

Alzheimer's disease (AD) is known to affect visual pathways, but potential concomitant effects on vision and cognitive performance are not well understood. We studied 43 individuals with AD of mild severity and 22 individuals without dementia on a battery of tests designed to measure multiple aspects of basic and higher-order visual perception and cognition. All subjects performed on the same visual and cognitive test batteries. The results showed no differences between groups on tests of static visual acuity, stereoacuity, dynamic visual acuity or motion direction discrimination. However, individuals with AD performed significantly worse on tests of static spatial contrast sensitivity, visual attention, shape-from-motion, color, visuospatial construction and visual memory. Correlation analyses showed strong relationships between visual and cognitive scores. The findings show that AD affects several aspects of vision and are compatible with the hypothesis that visual dysfunction in AD may contribute to performance decrements in other cognitive domains. The pattern of involvement indicates that AD affects multiple visual neural pathways and regions. It is possible that better understanding of vision-related dysfunction could aid diagnosis and interventions to improve functional capacity in patients with dementia.

Aged↗

PubMedDate not supplied

Space vestibulo-neuroscience in the new century: why proceed in semi-darkness?

With advancing technology, neuroscientists have explored vestibular transducer microstructure and molecular processes, neural pathways of interaction between vestibular visual and proprioceptor systems and neurochemical processes of adaptive change. Progress in space vestibulo-neuroscience will be fostered by focus on interactions among the systems involved in whole-body movement relative to the earth. Description of perceptual and sensorimotor reactions to complex accelerative stimuli during goal-directed and passive movement is crucial to conceptualizing the functional significance of various interactions and viable theory. The vestibulo-ocular reflex is now quantifiable in three dimensions, but description of the dynamics of spatial orientation perception has progressed very little in the 20th century. Much is known about perception of static body tilt, but the dynamics of tilt and movement perception (beyond rotation about an earth-vertical axis) remains relatively unexplored. Innovative procedures and departure from accepted psychophysics are needed. Models developed to predict the dynamics of spatial orientation under complex conditions must be consistent with information at all levels (neural, sensorimotor, and perceptual). To close our eyes to any one aspect of the spatial orientation reaction is to proceed in semi-darkness unnecessarily.

Animals↗

PubMed1995

Descending peristaltic reflex in the opossum esophagus.

To test the hypothesis that the distension-induced esophageal peristaltic reflex involves a polysynaptic pathway, a triple-chamber organ bath was used to chemically isolate different regions of the opossum smooth muscle esophagus while leaving in continuity the intramural neuromuscular apparatus. Balloon distension in the oral chamber evoked membrane hyperpolarization in the aboral chamber, which was followed, on balloon deflation, by depolarization, spike burst, and circular smooth muscle contraction. This reflex was abolished by adding tetrodotoxin to any of the chambers. Addition of Ca(2+)-free 20 mM Mg2+ Krebs solution (to block synaptic transmission) to the intermediate chamber did not affect the descending peristaltic reflex. However, Ca(2+)-free 20 mM Mg2+ Krebs solution markedly attenuated the reflex when placed in either the oral or the aboral chamber. Furthermore, the nitric oxide synthase inhibitor N omega-nitro-L-arginine methyl ester, when placed in the aboral chamber, abolished the reflex. Other putative neurotransmitter antagonists were without effect when placed in any chamber. These studies suggest that the intramural neural pathway that mediates the descending peristaltic reflex in the opossum esophagus is not polysynaptic, but rather involves long descending neurons that depend on nitric oxide as a final mediator.

Animals↗

PubMed1998

Prepulse inhibition following lesions of the inferior colliculus: prepulse intensity functions.

The magnitude of the acoustic startle response can be reduced by a relatively weak sound presented immediately before the startle-eliciting sound; this phenomenon has been termed prepulse inhibition (PPI). Previous studies reported that PPI was present in the decerebrate rat, indicating that the primary neural pathways mediating PPI are located in the brainstem. The present study investigated the effects of focal excitotoxic lesions of the inferior colliculus (IC) on acoustic PPI in rats. In the first part, startle magnitudes were measured in six normal rats as the interstimulus interval (ISI) between the prepulse and startle-eliciting sounds varied between 10 and 100 ms. Prepulse-inhibited startle changed in an ISI-dependent manner with the most effective ISI at 50 ms. In the second part, 21 rats were assigned to three groups: normal unoperated, cortical lesion, and IC lesion. With the ISI fixed at 50 ms, as the prepulse sound level increased from 29 to 49 dB SPL, startle responses decreased quickly in both normal and cortical lesion rats. However, rats with unilateral IC lesions made with ibotenic acid had significantly lower PPI but did not display any increase in startle magnitude. These data suggest that the IC is an important structure in the neural circuit mediating acoustic PPI.

Acoustic Stimulation↗

PubMed1996

5-Hydroxytryptamine induces forestomach hypomotility in sheep through 5-HT4 receptors.

The effects evoked by 5-hydroxytryptamine (5-HT; serotonin) on forestomach myoelectric activity were investigated in conscious sheep. Myoelectric signals were recorded with electrodes chronically implanted in the reticulum, rumen (dorsal sac) and omasal body, and were analysed by a computer-based method. The 5-HT receptors and the neuronal pathways involved in these actions were studied. The intravenous (i.v.) infusion of 5-HT (8 micrograms kg-1 min-1 for 5 min) evoked an inhibition of activity of the whole forestomach. Methiothepin, injected i.v. at 0.1 mg kg-1, inhibited rumen secondary contractions and omasum activity. However, forestomach activity remained unchanged after the administration of 0.2 mg kg-1 of ketanserin, ondansetron, tropisetron, GR-113808, phentolamine, propranolol, domperidone and naloxone. Atropine (0.2 mg kg-1), hexamethonium (2 mg kg-1) or haloperidol (0.1 mg kg-1) abolished rumen secondary cycles and inhibited omasum activity. In addition, atropine also suppressed primary cycles. GR-113808 blocked all 5-HT-induced effects. Furthermore, atropine or hexamethonium prevented the 5-HT-evoked inhibition of reticulorumen primary cycles. In contrast, the remaining antagonists did not alter the 5-HT-evoked forestomach hypomotility. In conclusion, 5-HT induces inhibition of forestomach myoelectric activity through 5-HT4 receptors, these actions being mediated by cholinergic neural pathways involving muscarinic and nicotinic receptors. However, adrenergic, dopaminergic or opiate pathways are not implicated.

Animals↗

PubMed1995

Habituation of an invertebrate escape reflex due to modulation by higher centers rather than local events.

Learning is widely thought to result from altered potency of synapses within the neural pathways that mediate the learned behavior. Support for this belief, which pervades current physiological and computational thinking, comes especially from the analysis of cases of simple learning in invertebrates. Here, evidence is presented that in one such case, habituation of crayfish escape, the learning is more due to onset of tonic descending inhibition than to the intrinsic depression of circuit synapses to which it was previously attributed. Thus, the altered performance seems to depend at least as much on events in higher centers as on local plasticity.

Animals↗

PubMed2002

Different sensitivity to the motor-stimulating effect of amphetamine in Sardinian alcohol-preferring and non-preferring rats.

The selective breeding of rodents on the basis of ethanol intake and preference has led to the development of lines of alcohol-preferring and non-preferring animals. The divergent degree of alcohol preference and consumption displayed by these lines of animals appears to be related, among other factors, to the genetic differences in dopaminergic neurotransmission. Moreover, in genetically unselected rats, a positive correlation has been found between alcohol preference and several amphetamine effects, including the stimulation of motor hyperactivity, thus suggesting the hypothesis that a common neural pathway might underlie some aspects in both of the amphetamine-induced hypermotility and alcohol preference. In the present study, we compared the motor-stimulating effect of amphetamine, which is mediated by the release of dopamine in the nucleus accumbens and in the corpus striatum in two lines of rats selectively bred for high and low ethanol preference, the Sardinian alcohol-preferring (sP) and the Sardinian alcohol-non-preferring (sNP) rats, respectively. The results show that sP rats are less sensitive to the motor-stimulant effect of amphetamine with respect to sNP rats, thus suggesting a negative correlation between this behavioural response and alcohol preference. The present results might be explained by the previously reported reduced density of dopamine receptors in the nucleus accumbens of sP rats and are consistent with the view that alcohol preference is associated with a deficient dopaminergic transmission. Moreover, they are consistent with the hypothesis that alcohol preference and amphetamine motor effect share a common neural substrate and that hereditary factors determine individual variations in its sensitivity.

Alcohol Drinking↗

PubMed1995

Thyroid hormone control of thermogenesis and energy balance.

The mechanisms whereby thyroid hormone increases heat production have been analyzed with emphasis in more recent developments. Thyroid hormone increases obligatory thermogenesis as a result of the stimulation of numerous metabolic pathways involved in development, remodeling, and delivery of energy to the tissues. In addition, thyroid hormone may specifically stimulate some thermogenic mechanisms selected during evolution of homeotherms (e.g., Na/K-ATPase, Ca2+ cycling in muscle). Thyroid hormone also plays an essential role in facultative thermogenesis interacting with the sympathetic nervous system (SNS) at various levels. Peripherally, thyroid hormone potentiates the effects of the SNS at the level of the adrenergic receptor and adenylyl cyclase complex as well as distal from this point. Synergistic interactions between T3 and cAMP on the regulation of gene expression have been described. Brown adipose tissue (BAT) T4-5'-deiodinase plays a central role in controlling heat production. When this enzyme is stimulated by norepinephrine in the euthyroid and hypothyroid condition, it provides high concentrations of T3 to BAT; inhibition by T4 in hyperthyroidism may limit brown fat thermogenic responses. Also, thyrotoxicosis uniquely reduces the expression of beta 3-adrenergic receptors in brown adipose tissue, and the increased obligatory thermogenesis of this condition, via afferent neural pathways, may reduce the hypothalamic stimulation of brown fat, providing additional mechanisms to limit brown adipose tissue thermogenesis in hyperthyroidism.

Animals↗

PubMed2001

Intact osmoregulatory centers in the preterm ovine fetus: Fos induction after an osmotic challenge.

We previously demonstrated a functional systemic dipsogenic response in the near-term fetal sheep (128-130 days; 145 days = full-term) with swallowing activity stimulated in response to central and systemic hypertonic saline. Preterm fetal sheep (110-115 days) do not consistently demonstrate swallowing in response to hypertonic stimuli, and it is unclear whether this is due to immaturity of osmoreceptor mechanisms or neuronal pathways activating swallowing motor neurons. To determine whether osmoreceptive regions in the preterm fetus are activated by changes in plasma tonicity, we examined Fos expression with immunostaining in these neurons in response to an osmotic challenge. Nine preterm fetal sheep [five hypertonic saline-treated fetuses (Hyp) and four isotonic saline-treated fetuses (Iso)] were prepared with vascular and intraperitoneal catheters. Seventy-five minutes before tissue collection, hypertonic (1.5 M) or isotonic saline was infused (12 ml/kg) via an intraperitoneal catheter to fetuses. Brains were examined for patterns of neuronal activation (demonstrated by Fos protein expression). Hyp demonstrated increases in plasma osmolality (~10 mosmol/kg H(2)O) and Na concentrations (5 meq/l). Increased Fos expression was detected in Hyp in the organum vasculosum of the lamina terminalis (OVLT), subfornical organ (SFO), median preoptic nucleus (MnPO), supraoptic (SON), and paraventricular nuclei (PVN) compared with Iso animals. Neuronal activation within the OVLT, SFO, and MnPO indicates intact osmoregulatory mechanisms, whereas activation of the SON and PVN suggests intact fetal neural pathways to arginine vasopressin neurons. These results suggest that preterm fetal swallowing insensitivity to osmotic stimuli may be due to immaturity of integrated motor neuron pathways.

Animals↗

PubMed2026

The Genetic Architecture of Chronic Cough: From Sensory Hypersensitivity to Treatable Trait.

Chronic cough is a prevalent global clinical disorder with substantial quality-of-life impairment, and refractory cases remain a major unmet medical need. Cough hypersensitivity syndrome is the core pathological mechanism of chronic cough, and growing genetic evidence has confirmed that inherited susceptibility shapes cough hypersensitivity, clinical heterogeneity and therapeutic responsiveness, redefining chronic cough as a biologically mediated sensory-neural disorder rather than a non-specific secondary symptom of airway diseases. This review summarises genetic evidence for chronic cough from family-based studies, pharmacogenomics and genome-wide association studies (GWAS), revealing distinct genetic architectures of chronic dry cough and sputum production, with enrichment of sensory-neural pathway variants and key genetic loci such as replication factor C subunit 1 (RFC1) functional genomic analyses link genetic variation to vagal afferent excitability, and rare genetic neurological disorders further illuminate the neurogenic basis of cough hypersensitivity. Moreover, genetic insights identify tractable treatable traits and rationalise antitussive drug development, supporting genotype-guided patient stratification. We conclude that integrating genetic architecture into clinical phenotyping and translational research provides a critical framework for precision management of chronic cough, and future progress relies on harmonised deep phenotyping and multi-ancestry genetic studies.

RFC1 gene↗

PubMed2002

Evidence for cortical encoding specificity in episodic memory: memory-induced re-activation of picture processing areas.

Functional magnetic resonance imaging (fMRI) was used to examine whether neural pathways used to encode pictures into memory were re-activated during retrieval of those memories. At encoding, subjects semantically classified common objects presented as pictures or words. At retrieval, subjects performed yes/no recognition memory judgments on words that had been encoded as pictures or as words. The retrieval test probed memory for the encoded item, but not memory for the modality of the encoded item (picture/word). Results revealed that a subset of the brain regions involved specifically in encoding of pictures were also engaged during recognition memory for the encoded pictures. Specifically, encoding of pictures relative to words engaged bilateral extrastriate visual cortex, namely fusiform, lingual, middle occipital, and inferior temporal gyri (Broadman area (BA) 18/19/37). Recognition memory judgments about words that were encoded as pictures relative to those that were encoded as words activated fusiform and inferior temporal gyri primarily in the left hemisphere. Thus, cortical areas originally involved in perception of a visual experience become part of the long-term memory trace for that experience. These findings suggest a neural basis for encoding specificity and transfer appropriate processing in human memory.

Adult↗

PubMed2000

Habituation and desensitization of the Hering-Breuer reflex in rat.

1. Many processes in mammalian and invertebrate central nervous systems exhibit habituation and/or sensitization of their responses to repetitive stimuli. Here, we studied the adaptive behaviours of the respiratory pattern generator in rat on repetitive vagal-afferent stimulation and compared these behaviours obtained in vivo with the reported effects of such stimuli on synaptic transmission in the corresponding signal pathway in vitro. 2. Sustained (1 min) electrical pulsed stimulation of the vagus nerve elicited the classic Hering-Breuer (HB) reflex slowing of the respiratory rhythm followed by a bi-exponential recovery, and a post-stimulus rebound (PR). The recovery from the HB reflex satisfied the classic criteria of habituation. 3. The fast component of the recovery and the PR were abolished by systemic administration of an NMDA receptor antagonist or electrolytic lesioning of the pontine Kolliker-Fuse nucleus. The characteristics of the fast recovery and PR suggest a vagally induced desensitization of the NMDA receptor-dependent pontine input to the respiratory pattern generator. 4. The slow component of recovery persist after both experimental interventions and accounted for the habituation to the vagal input. The characteristics of the slow recovery in vivo were reminiscent of the reported synaptic accommodation in vitro in the medullary region where vagal afferents terminate. 5. The habituation of vagal input and desensitization of pontine input act in concert to offset the HB reflex. Such simultaneous habituation-desensitization in parallel neural pathways with differing sensitivities to NMDA receptor activation represent a hitherto unknown pairing of dual non-associative learning processes in the mammalian brain.

Animals↗

PubMed1990

Ileocecal sphincter contraction to colonic distension: a tachykinin-mediated spinal reflex.

The ileocecal sphincter in the cat demonstrates a reflex contraction to colonic distension. This study investigates the pathway mediating this reflex in the intact bowel using an in vivo model. The ileocecal sphincter (ICS) and distal ileal intraluminal pressures were recorded in fasted chloralose-anesthetized cats. Colonic balloon distension caused a slight, but significant, ileal inhibition with a maximum decrease from resting ileal pressure by 2.6 +/- 0.76 mmHg (P less than 0.005) to 3 ml distension. A volume-dependent contraction at the ICS was seen with a maximal contraction of 16.8 +/- 2.2 mmHg (P less than 0.005) with 4 ml distension. The reflex ICS contraction was inhibited by tetrodotoxin and phentolamine but not by bilateral cervical vagotomy, naloxone, atropine, or trimethaphan camsylate. The reflex contraction at the ICS was inhibited by substance P tachyphylaxis. Substance P tachyphylaxis did not inhibit ICS contraction to phenylephrine. The substance P antagonist, [DArg1,DTrp7,9,Leu11]substance P failed to antagonize substance P and failed to inhibit the ICS contractile response to colonic balloon distension. Spinal anesthesia inhibited this reflex. We have thus demonstrated that the ICS reflex contraction to colonic balloon distension in the intact bowel is mediated by an extrinsic spinal neural pathway involving both tachykinin and catecholamines as neurotransmitters.

Animals↗

PubMed2004

In search of the sky compass in the insect brain.

Like many vertebrate species, insects rely on a sun compass for spatial orientation and long- range navigation. In addition to the sun, however, insects can also use the polarization pattern of the sky as a reference for estimating navigational directions. Recent analysis of polarization vision pathways in the brain of orthopteroid insects sheds some light onto brain areas that might act as internal navigation centers. Here I review the significance, peripheral mechanisms, and central processing stages for polarization vision in insects with special reference to the locust Schistocerca gregaria. As in other insect species, polarization vision in locusts relies on specialized photoreceptor cells in a small dorsal rim area of the compound eye. Stages in the brain involved in polarized light signaling include specific areas in the lamina, medulla and lobula of the optic lobe and, in the midbrain, the anterior optic tubercle, the lateral accessory lobe, and the central complex. Integration of polarized-light signals with information on solar position appears to start in the optic lobe. In the central complex, polarization-opponent interneurons form a network of interconnected neurons. The organization of the central complex, its connections to thoracic motor centers, and its involvement in the spatial control of locomotion strongly suggest that it serves as a spatial organizer within the insect brain, including the functions of compass orientation and path integration. Time compensation in compass orientation is possibly achieved through a neural pathway from the internal circadian clock in the accessory medulla to the protocerebral bridge of the central complex.

Animals↗

PubMed1995

Ciliary ganglion choline acetyltransferase activity in avian macrophthalmos.

While present evidence fails to support an etiologic mechanism for myopia based on accommodation or choroidal blood flow, atropine exhibits anti-myopia activity in many species. Accordingly, we studied choline acetyl transferase (ChAT) activity in the ciliary ganglion, uvea and retina of chicks with experimental macrophthalmos to identify a potential pathway for the moderation of eye growth by cholinergic neurons. Following unilateral lid suture or goggle, chicks were reared for 1 week under one of four lighting conditions known to induce macrophthalmos or myopia. Ocular tissues and ciliary ganglia were assayed for ChAT activity by measuring the conversion of 14C-acetyl CoA to 14C-acetylcholine. For some chicks, the goggles were removed at 1 week, and ChAT activity was measured 2 or 7 days later. Depending on the rearing condition, ciliary ganglion ChAT activity was depressed from 16 to 28% ipsilateral to the lid suture; enzyme activity also was reduced in the choroid of visually deprived eyes under most conditions. In contrast, lid suture resulted in no consistent trend in ChAT activity in either the anterior uvea or retina. For chicks wearing a unilateral goggle and reared under a 12:12 hr light/dark cycle, ChAT activity was depressed in the ciliary ganglion, anterior uvea and choroid on the visually deprived side. Following goggle removal to allow recovery from myopia. ChAT activity in the ciliary ganglion and uvea was returned toward that of the control side. The ciliary ganglion may participate in a neural pathway influencing the development of form-deprivation myopia.

Animals↗

PubMed2003

Interleukin-1beta activates specific populations of enteric neurons and enteric glia in the guinea pig ileum and colon.

Fos expression was used to assess whether the proinflammatory cytokine interleukin-1beta (IL-1beta) activated specific, chemically coded neuronal populations in isolated preparations of guinea pig ileum and colon. Whether the effects of IL-1beta were mediated through a prostaglandin pathway and whether IL-1beta induced the expression of cyclooxygenase (COX)-2 was also examined. Single- and double-labeling immunohistochemistry was used after treatment of isolated tissues with IL-1beta (0.1-10 ng/ml). IL-1beta induced Fos expression in enteric neurons and also in enteric glia in the ileum and colon. For enteric neurons, activation was concentration-dependent and sensitive to indomethacin, in both the myenteric and submucosal plexuses in both regions of the gut. The maximum proportion of activated neurons differed between the ileal (approximately 15%) and colonic (approximately 42%) myenteric and ileal (approximately 60%) and colonic (approximately 75%) submucosal plexuses. The majority of neurons activated in the myenteric plexus of the ileum expressed nitric oxide synthase (NOS) or enkephalin immunoreactivity. In the colon, activated myenteric neurons expressed NOS. In the submucosal plexus of both regions of the gut, the majority of activated neurons were vasoactive intestinal polypeptide (VIP) immunoreactive. After treatment with IL-1beta, COX-2 immunoreactivity was detected in the wall of the gut in both neurons and nonneuronal cells. In conclusion, we have found that the proinflammatory cytokine IL-1beta specifically activates certain neurochemically defined neural pathways and that these changes may lead to disturbances in motility observed in the inflamed bowel.

Animals↗