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At least 775 records · Page 43Linked to original sources
PubMed1997

Morphological correlates of neural regeneration in the feeding system of Aplysia californica after central nervous system lesions.

Morphological techniques were used to study regeneration of central neural pathways involved in feeding behavior following bilateral crushes of the cerebral-buccal connectives (CBCs). Electron microscopic analysis revealed that CBC crushes completely transect axons within the nerve core while leaving a remnant of the nerve sheath intact. Changes in the ultrastructure of the CBCs at the crush site were determined for 1, 7, 14, 21, and 50 days postlesion. At 1 day postlesion, the crush site was no longer compressed, and the nerve core had assumed a circular shape. In addition, several small axon profiles were evident, and large areas of tissue debris and prominent microglial cells were observed. Membranous debris and hemocytes were also present in sinuses that appeared in the sheath adjacent to the crush site. From 7 to 50 days postlesion, the core of the nerve at the crush site increased in size due to the addition of small diameter axons. Initially, the sheath surrounding the crush site exhibited hyperplasia and contained a few small bundles of processes, apparently due to newly sprouted axons that had strayed from the nerve core. By 50 days postlesion, the crush site appeared nearly normal; the nerve core was reacquiring the normal radial pattern of axon profiles with some medium-sized axon profiles covered with glial sheath and exhibiting invaginations typical of the intact CBC. However, there was still a distinct lack of large diameter axons. Cobalt backfills across the crush site revealed neurons in the cerebral ganglion by postlesion day 9. Positions of stained cell bodies were consistent with those observed in controls, although the numbers of stained neurons did not recover to control levels even by postlesion day 63. The changes in the crush site and return of cell body staining with time postlesion are correlated with the recovery of consummatory feeding.

Animals↗
PubMed2004

Septopreoptic mu opioid receptor mediation of hindbrain glucoprivic inhibition of reproductive neuroendocrine function in the female rat.

Central glucostasis is a critical monitored variable in neuroendocrine regulation of pituitary LH secretion. Glucoprivic signals originating within the caudal hindbrain suppress LH. Septopreoptic mu opioid receptors (mu-R) function within neural pathways maintaining basal LH levels and mediate the effects of diverse physiological stimuli on hormone release. To identify potential sites in the septopreoptic area where ligand neuromodulatory actions may occur in response to hindbrain glucoprivic signaling, the present studies evaluated the distribution of mu-R-immunoreactive (-ir) neurons in the septopreoptic area that are genomically activated in response to caudal fourth ventricular (CV4) delivery of the glucose antimetabolite, 5-thioglucose (5TG). The effects of lateral ventricular pretreatment with the selective mu-R antagonist, d-Phe-Cys-Tyr-d-Trp-Orn-Thr-Pen-Thr-NH(2) (CTOP), on LH secretory and GnRH neuronal transcriptional responses to hindbrain glucoprivation were also evaluated. Estradiol benzoate- and progesterone-primed, ovariectomized female rats were treated by CV4 administration of 5TG or the vehicle, saline, at the onset of the afternoon LH surge. The inhibitory effects of hindbrain glucoprivation on mean plasma LH levels as well as colabeling of rostral preoptic GnRH neurons for Fos-ir were attenuated in animals pretreated by lateral ventricular delivery of CTOP. Dual immunocytochemical labeling for septopreoptic mu-R-ir and Fos-ir demonstrated a robust induction of Fos expression by receptor-positive neurons within discrete septopreoptic sites in response to CV4 5TG, a genomic response that was diminished by CTOP pretreatment. The current studies provide novel evidence for the transcriptional activation of neuroanatomically characterized, mu-R-expressing neurons by decreased hindbrain glucose utilization and show that the functional status of mu-R is critical for maximal induction of the Fos stimulus-transcription cascade in these cells by central glucoprivic signaling. The finding that receptor antagonist-mediated suppression of this genomic response is correlated with increased reproductive neuroendocrine output supports a role for these discrete mu-R-expressing neuron populations as substrates for ligand regulatory effects on the GnRH-pituitary LH axis during neuroglucopenia.

Animals↗
PubMed1993

Thoracic epidural anesthesia increases diaphragmatic shortening after thoracotomy in the awake lamb.

BACKGROUND: Prolonged inhibition of diaphragmatic function occurs after thoracic and upper abdominal surgery. It was hypothesized that thoracic epidural anesthesia on the day after a thoracotomy could block inhibitory neural pathways and increase the shortening of costal and crural diaphragmatic segments. METHODS: Pairs of sonomicrometer crystals were implanted into the costal and crural regions of the diaphragm through a right lateral thoracotomy in 14 30-kg, 4-5-month-old lambs. One day after surgery, a thoracic epidural catheter was placed at the T8-T9 level. Regional diaphragmatic shortening normalized to end-expiratory length (%LFRC), was measured by sonomicrometry in these awake lambs. Changes in gastric (delta Pgas), esophageal (delta Pes), and transdiaphragmatic (delta Pdi) pressures were measured with transnasal balloon catheters. End-tidal carbon dioxide (FETCO2), costal and crural electromyogram (Edi), and tidal volume (VT) were measured. Inductance plethysmography was used in four lambs to assess relative contributions of the rib cage and abdomen to VT. Control values were obtained during quiet breathing and while rebreathing at up to 10% FETCO2. To block thoracic dermatomes, 1% or 2% lidocaine was injected through the epidural catheter. Measurements were repeated after each lidocaine injection. RESULTS: There was no change of resting length with 1% lidocaine; costal resting length increased by 22% with 2% lidocaine. After 2% lidocaine, costal %LFRC increased from control both during quiet breathing (8.7 +/- 0.7 to 18.1 +/- 1, mean +/- SEM%) and at FETCO2 10% (22.1 +/- 2 to 33.7 +/- 3%). VT during quiet breathing was unchanged after 1% lidocaine but increased from 235 +/- 16 to 283 +/- 28 ml after 2% lidocaine. At 10% FETCO2, delta Pdi was unchanged after 1% lidocaine and decreased from 36.5 +/- 4.3 to 26.3 +/- 4.9 cmH2O after 2% lidocaine. Regional delta Edi was unchanged with both 1% and 2% lidocaine at rest and during carbon dioxide rebreathing. Plethysmography in three lambs showed a reduction in rib cage contribution to tidal volume with 2% lidocaine during quiet breathing. CONCLUSIONS: Improved postoperative tidal volume and diaphragmatic shortening after thoracic epidural blockade may be due to changes of chest wall conformation and resting length and a shift of the workload of breathing from the rib cage to the diaphragm caused by intercostal muscle paralysis.

Anesthesia, Epidural↗
PubMed2001

PrP(CWD) in the myenteric plexus, vagosympathetic trunk and endocrine glands of deer with chronic wasting disease.

Accumulated evidence in experimental and natural prion disease systems supports a neural route of infectious prion spread from peripheral sites of entry to the central nervous system. However, little is known about prion trafficking routes in cervids with a naturally occurring prion disease known as chronic wasting disease (CWD). In the brain, the pathogenic isoform of the prion protein (PrP(CWD)) accumulates initially in the dorsal motor nucleus of the vagus nerve. To assess whether alimentary-associated neural pathways may play a role in prion trafficking, neural and endocrine tissues from mule deer naturally infected with CWD (n=6) were examined by immunohistochemistry. PrP(CWD) was detected in the myenteric plexus, vagosympathetic trunk, nodose ganglion, pituitary, adrenal medulla and pancreatic islets. No to scant PrP(CWD) staining was detected in other nerves or ganglia (brachial plexus, sciatic nerve, gasserian ganglion, coeliac ganglion, cranial cervical ganglion, spinal nerve roots) of CWD-positive deer and no PrP(CWD) was detected in nerves or endocrine tissues from 11 control deer. These findings suggest that: (i) transit of PrP(CWD) in nerves, either centrifugally or centripetally, is one route of prion trafficking and organ invasion and (ii) endocrine organs may also be targets for cervid pathogenic prion accumulation.

Animals↗
PubMed1994

Autonomic pathways in development of neural stimulation-induced gastric mucosal damage.

Gastric mucosal erosions can be induced by electrical stimulation of either vagus nerves (5 Hz, 5 V, 1 ms) or the paraventricular nucleus (PVN) of the hypothalamus (200 microA, 60 Hz, 100-microseconds pulse width). We have utilized various pharmacological and surgical interventions to determine the contributions of different components of the autonomic nervous system to the development of this neurally induced gastric damage in urethan-anesthetized Sprague-Dawley rats. In all experiments damage was assessed macroscopically and scored blindly on a 0 (normal) to 3 (severe) scale with samples sectioned for subsequent histological assessment of damage at the light microscopic level. Animals pretreated with either hexamethonium (30 mg/kg iv) or atropine (2 mg/kg iv) demonstrated reduced gastric damage scores after vagal stimulation compared with untreated control animals (P < 0.05). In contrast animals that underwent cervical cord transection exhibited gastric damage after both vagal and PVN stimulation that was not significantly different compared with animals with an intact cord undergoing similar stimulation (P > 0.05). Such cord transection itself did not cause any significant change to the gastric mucosa in the time period studied. These data emphasize the importance of the autonomic nervous system, in particular the parasympathetic component in the development of vagal stimulation-induced gastric damage. In addition, the present studies suggest that neither vagal nor PVN stimulation-induced gastric damage is dependent on neural projections to sympathetic preganglionic neurons of the intermediolateral cell column of the spinal cord.

Animals↗
PubMed1990

Physiatric therapeutics. 5. Pain.

This self-directed learning module highlights advances in the management of pain. It is part of the chapter on physiatric therapeutics for the Self-Directed Medical Knowledge Program Study Guide for practitioners and trainees in physical medicine and rehabilitation. This section discusses neuroanatomy and neurophysiology pertaining to pain, gating theories, therapeutic measures, transcutaneous electrical nerve stimulation, acupuncture, and behavioral methods. Advances that are covered in this section include various neural pathways involved in pain transmission, descending "pain control" neural networks, pain-modulating neurotransmitters, and the therapeutic use of pharmacologic agents and nonpharmacologic measures for pain management.

Acupuncture Analgesia↗
PubMed1986

Tensor tympani reflex pathways studied with retrograde horseradish peroxidase and transneuronal viral tracing techniques.

The neural pathway involved in activation of the tensor tympani (TT) muscle was studied in the rat using retrograde HRP and transneuronal viral tracing techniques. The pool of TT motoneurons labeled with HRP was located ipsilaterally under the anterior third of the trigeminal motor nucleus and extended rostrally towards the lateral lemniscus. The origin of the inputs to these motoneurons was then determined using transneuronal viral transport: presumably transneuronally infected neurons appeared bilaterally in the vicinity of the superior olivary complex, mainly in between the two nuclei of the trapezoid body. The present data are consistent with previous conclusions based on lesion experiments that the TT reflex loop is made up of a chain of 4 neurons.

Animals↗
PubMed1968

Factors affecting the conductivity of pathways in the cerebral cortex.

1. We have investigated the conductivity of neural pathways in slabs of unanaesthetized, isolated, cerebral cortex, cut from the isolated forebrains of twenty-five cats.2. Neurones within the isolated area were indirectly excited, either by a small electrode thrust into the subcortical white matter, or by remote stimulation of the pial surface. Sometimes a small electrode was employed for intracortical stimulation.3. The response of single neurones to these stimuli was recorded with extracellular micropipettes. Submaximal stimuli produced a stochastic response which was measured from the post-stimulus histogram (PSH) and provided an estimate of the probability of discharge at various times after the stimulus.4. The PSH often displayed several discrete humps of different latencies, indicating several pathways between stimulated and recording point. Conductivity measurements were usually restricted to the pathway of shortest latency.5. The conductivity of a pathway was defined as C = xy/x, averaged over 1 or 2 min, wherex = frequency of afferent test volleys,xy = frequency of response: i.e. of those action potentials contained within a well-defined hump of the PSH,(y = frequency of all discharges of the recorded neurone).6. The progress of conductivity was tested with some constant form of cortical stimulation, repeated at regular intervals of 1-5 sec. Reliable results were obtained for twenty-six pathways subjected to thirty-eight experiments.7. Temporary alteration of x, y or xy (conditioning with Deltax, Deltay or Deltaxy), for a period of 6-25 min, often caused a subsequent change in the conductivity (DeltaC) of a pathway which sometimes attenuated with a time constant of about 10 min, but which could persist without detectable attenuation for 20-30 min.8. Conditioning periods less than 6 min rarely produced changes in conductivity; alterations of conductivity were more likely to be caused by conditioning periods longer than 17 min, than by periods of 6-16 min.9. Changes in conductivity were usually correlatednegatively with temporary changes in xy,negatively with temporary changes in x,positively with temporary changes in y.10. Nineteen of twenty-six pathways tested showed properties consistent with the formula [Formula: see text], whereG(1) lies between -1.0 and -0.16, with mean value -0.50,G(2) lies between 0 and 0.42, with mean value +0.12,G(3) lies between -0.61 and 0 with mean value -0.38,K is a coefficient which is usually different for each experiment. Four out of twenty-six pathways so tested provided results which did not fit this formula; three out of twenty-six pathways did not give adequate information.

Animals↗
PubMed1992

Distribution and developmental change in [3H]MK-801 binding within zebra finch song nuclei.

In many songbirds, vocal learning depends upon appropriate auditory experience during a sensitive period that coincides with the formation and reorganization of song-related neural pathways. Because some effects of early sensory experience on neural organization and early learning have been linked to activation of N-methyl-D-aspartate (NMDA) receptors, we measured binding to this receptor within the neural system controlling song behavior in zebra finches. Quantitative autoradiography was used to measure binding of the noncompetitive antagonist [3H]MK-801 (dizocilpine) in the brains of both adult and juvenile male zebra finches, focusing on four telencephalic regions implicated in song learning and production. Overall, the pattern of MK-801 binding in zebra finches was similar to the pattern found in rats (Monaghan and Cotman, 1985, J. Neurosci. 5:2909-2919; Sakurai, Cha, Penney, and Young, 1991, Neuroscience 40:533-543). That is, binding was highest in the telencephalon, intermediate in thalamic regions, and virtually absent from the brain stem and cerebellum. The telencephalic song areas exhibited intermediate levels of binding, and binding in the juveniles was not significantly different from adult levels in most song nuclei. However, in the lateral magnocellular nucleus of the anterior neostriatum (IMAN), binding at 30 days of age was significantly higher than binding in adults. Given the established role of NMDA receptors in other developing neural systems, both their presence in song control nuclei and their developmental regulation within a region implicated in song learning suggest that NMDA receptors play a role in mediating effects of auditory experience on the development of song behavior.

Aging↗
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↗
PubMedDate not supplied

Dark-adaptive cone elongation in the blue acara retina is triggered by green-sensitive cones.

In a dichromatic teleost species, we determined the intensity of light of various wavelengths required to prevent cone elongation by exposing fish at the time of their normal "dusk" phase to monochromatic light (479, 623, and 660 nm) at eight to ten different intensities for 75 min. The positions of single and double cones were measured in tangential sections and expressed as cone indices. At all wavelengths, the spectral responses of both cone types were virtually identical. Furthermore, the sensitivity of the blocking effect was highest at shorter wavelengths. When comparing the relative quantal sensitivities of myoid elongation for the two cone types to the spectral sensitivities of the three types of Aequidens pulcher photoreceptor, we found the closest match between the action spectrum and the absorption spectrum of the green-sensitive single cones. This may indicate that this cone type is capable of reacting directly to decreasing levels of illumination. On the other hand, the identical sensitivity of both cone types argues for an indirect control mechanism of dark-adaptive cone elongation, possibly via a neural pathway involving the inner retinal layers, complementary to the neural control of light adaptation. Green-sensitive single cones are well suited to trigger this response, since (1) their sensitivity is inferior to that of double cones; (2) waters inhabited by the blue acara transmit best at long wavelengths; and (3) at dusk, long-wavelength radiation dominates over other parts of the spectrum. Therefore, green-sensitive cone threshold will be reached first at dusk.

Animals↗
PubMed2003

A catheter based method to activate urethral sensory nerve fibers.

PURPOSE: The ability to control bladder activity would provide a valuable tool to assist individuals with neurological disorders or spinal cord injury (SCI). Recent studies in animal models have shown that bladder contractions can be evoked by electrical stimulation of urethral afferent nerves. We developed and validated in cats a minimally invasive method to stimulate electrically the sensory nerve fibers that innervate the urethra. MATERIALS AND METHODS: The urethra was stimulated electrically along its length via a catheter mounted circumferential electrode in 6 cats. The urethra was similarly stimulated in a male individual with complete SCI. RESULTS: Robust bladder contractions were generated via intraurethral electrical stimulation in all cat experiments. Peak responses were obtained in the proximal and prostatic urethra. In the individual with SCI bladder contractions were generated via intraurethral stimulation at a position 4 cm distal to the bladder. Responses in cats and the human depended on bladder volume. CONCLUSIONS: To our knowledge this study provides the first documentation of generating bladder contractions via intraurethral electrical stimulation in cats and humans. This method provides a research tool for future studies to investigate these pathways in humans. Preliminary human results suggest that urethral afferent mediated neural pathways demonstrated in animal models exist in humans and support the development of neural prostheses using electrical stimulation of these nerves to restore control of bladder function in individuals with neurological disorders or SCI.

Adult↗
PubMed1984

Contributions of the mesencephalic dopaminergic system and the trigeminal sensory pathway to the ventral tegmental aphagia syndrome in rats.

Four experiments examined the neural substrates for the aphagia and adipsia syndrome resulting from damage of the ventral tegmental region. Radiofrequency (RF) lesions at the level of the mesencephalon in rats showed that the most effective site for producing aphagia and adipsia was in an intermediate zone between the substantia nigra and the ventral tegmental area. Injection of the neurotoxin 6-hydroxydopamine (6-OHDA) into this intermediate zone led to a less severe feeding deficit, suggesting that both dopaminergic and non-dopaminergic neurons are involved in the mesencephalic aphagic syndrome. As the lemniscus trigeminalis was destroyed after the RF lesion of the intermediate zone, the hypothesis of trigeminal projection involvement was tested by lesioning (RF) the sensory trigeminal nucleus. These rats were aphagic but they recovered and their deficit was less severe than after RF lesion of the mesencephalic intermediate zone. In the last experiment, a combined 6-OHDA lesion of the mesencephalic intermediate zone and RF lesion of the trigeminal sensory nucleus led to a more severe deficit in feeding behavior than either lesion alone. These results further demonstrate that feeding behavior is under the control of a complex system involving several neural pathways.

Animals↗
PubMed1996

Ventromedial preoptic prostaglandin E2 activates fever-producing autonomic pathways.

Fever is thought to be initiated by pyrogenic cytokines inducing the production of prostaglandin E2 (PGE2) in the preoptic area (POA); PGE2 may act as a paracrine mediator that stimulates the neural pathways that raise body temperature. This essential role for prostaglandins in fever first was proposed 25 years ago, but the specific preoptic cell groups at which PGE2 acts and the pathways through which fever is produced remain poorly understood. To better define the role of preoptic PGE2 in fever, we developed a new method for combining acute brain injections with Fos immunohistochemistry. We microinjected a threshold dose of PGE2 to construct an anatomically detailed map of fever-producing preoptic sites. The most pyrogenic preoptic sites were clustered along the ventromedial aspect of the POA, surrounding and just anterior to the organum vasculosum of the lamina terminalis. We then used Fos immunohistochemistry to identify the pattern of neural activation induced by fever-producing preoptic injections of PGE2 and compared it with the Fos pattern seen after systemic immune stimulation. PGE2 fever was accompanied by Fos induction in the ventromedial POA and the parvicellular subnuclei of the paraventricular nucleus of the hypothalamus (PVH). In contrast to the Fos pattern seen after intravenous lipopolysaccharide administration, PGE2 injection did not induce Fos in the circumventricular organs or the magnocellular subnuclei of the PVH. These observations establish a potential site of PGE2 action during fever and help define candidate pathways through which fever occurs.

Animals↗
PubMed1985

The neural circuit for touch sensitivity in Caenorhabditis elegans.

The neural pathways for touch-induced movement in Caenorhabditis elegans contain six touch receptors, five pairs of interneurons, and 69 motor neurons. The synaptic relationships among these cells have been deduced from reconstructions from serial section electron micrographs, and the roles of the cells were assessed by examining the behavior of animals after selective killing of precursors of the cells by laser microsurgery. This analysis revealed that there are two pathways for touch-mediated movement for anterior touch (through the AVD and AVB interneurons) and a single pathway for posterior touch (via the PVC interneurons). The anterior touch circuitry changes in two ways as the animal matures. First, there is the formation of a neural network of touch cells as the three anterior touch cells become coupled by gap junctions. Second, there is the addition of the AVB pathway to the pre-existing AVD pathway. The touch cells also synapse onto many cells that are probably not involved in the generation of movement. Such synapses suggest that stimulation of these receptors may modify a number of behaviors.

Animals↗
PubMed2001

A cerebral nitrergic pathway modulates endotoxin-induced changes in gastric motility.

1. This study analyses the neural pathway involved in the modulation of gastric motor function by stress. 2. Systemic administration of low doses of endotoxin (40 microg kg(-1), i.v.) prevents the increase in gastric tone induced by 2-deoxy-D-glucose (200 mg kg(-1), i.v., 2-DG) in urethane-anaesthetized rats. 3. Functional inhibition of afferent neurones by systemic administration of capsaicin (20+30+50 mg kg(-1), i.m.) in adult rats prevented the inhibitory effects of endotoxin. 4. Pre-treatment with the nitric oxide synthase (NOS) inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), both i.v. (10 mg kg(-1)) and i.c. (200 microg rat(-1)), prevented the inhibitory effects of endotoxin on gastric tone induced by 2-DG. 5. Immunohistochemical studies show Fos expression in the dorsal vagal complex (DVC) of the brainstem of 2-DG-treated animals. Peripheral administration of endotoxin (40 microg kg(-1), i.p.) increased the number of Fos-immunoreactive cells induced by 2-DG, both in the nucleus tractus solitarii (NTS) and in the dorsal motor nucleus (DMN) of the DVC. Pre-treatment with L-NAME prevented the increase in Fos expression induced by endotoxin in both nuclei. 6. Endotoxin (40 microg kg(-1), i.p.) increased Ca(2+)-dependent nitric oxide synthase (cNOS) activity in the brainstem. Addition of 7-nitroindazole (600 microM, 7-NI) to the assay significantly inhibited the increase in cNOS activity caused by endotoxin. No change in NOS activity of any isoform was observed in the stomach of animals treated with endotoxin. 7. The present study suggests that inhibition of gastric motor function by low doses of endotoxin involves activation of capsaicin-sensitive afferent neurones and neuronal NOS in the brainstem.

Animals↗
PubMed2001

Vergence dynamics predict fixation disparity.

The neural origin of the steady-state vergence eye movement error, called binocular fixation disparity, is not well understood. Further, there has been no study that quantitatively relates the dynamics of the vergence system to its steady-state behavior, a critical test for the understanding of any oculomotor system. We investigate whether fixation disparity can be related to the dynamics of opponent convergence and divergence neural pathways. Using binocular eye movement recordings, we first show that opponent vergence pathways exhibit asymmetric angle-dependent gains. We then present a neural model that combines physiological properties of disparity-tuned cells and vergence premotor cells with the asymmetric gain properties of the opponent pathways. Quantitative comparison of the model predictions with our experimental data suggests that fixation disparity can arise when asymmetric opponent vergence pathways are driven by a distributed disparity code.

Accommodation, Ocular↗