Transmission Of Sensory Signals Research Articles

Synaptic motility and functional stability in the whisker cortex

The high motility of synaptic weights raises the question of how the brain can retain its functionality in the face of constant synaptic remodeling. Here we used the whisker system of rats and mice to study the interplay between synaptic plasticity (motility) and the transmission of sensory signals downstream. Rats and mice probe their surroundings by rhythmically moving their whiskers back and forth. The azimuthal position of a whisker can be estimated from the activity of whisking neurons that respond selectively to a preferred phase along the whisking cycle. These preferred phases are widely distributed on the ring. However, simple models for the transmission of the whisking signal downstream predict a distribution of preferred phases that is an order of magnitude narrower than empirically observed. Here, we suggest that synaptic plasticity in the form of spike-timing-dependent plasticity (STDP) may provide a solution to this conundrum. This hypothesis is addressed in the framework of a modeling study that investigated the STDP dynamics in a population of synapses that propagates the whisking signal downstream. The findings showed that, for a wide range of parameters, STDP dynamics do not relax to a fixed point. As a result, the preferred phases of downstream neurons drift in time at a nonuniform velocity, which in turn induces a nonuniform distribution of the preferred phases of the downstream population. This demonstrates how functionality, in terms of the distribution of preferred phases, can be retained not simply despite, but because of constant synaptic motility. Our analysis leads to several key empirical predictions to test this hypothesis. Published by the American Physical Society 2025

A distributed auditory network mediated by pontine central gray underlies ultra-fast awakening in response to alerting sounds

Sleeping animals can be woken up rapidly by external threat signals, which is an essential defense mechanism for survival. However, neuronal circuits underlying the fast transmission of sensory signals for this process remain unclear. Here, we report in mice that alerting sound can induce rapid awakening within hundreds of milliseconds and that glutamatergic neurons in the pontine central gray (PCG) play an important role in this process. These neurons exhibit higher sensitivity to auditory stimuli in sleep than wakefulness. Suppressing these neurons results in reduced sound-induced awakening and increased sleep in intrinsic sleep/wake cycles, whereas their activation induces ultra-fast awakening from sleep and accelerates awakening from anesthesia. Additionally, the sound-induced awakening can be attributed to the propagation of auditory signals from the PCG to multiple arousal-related regions, including the mediodorsal thalamus, lateral hypothalamus, and ventral tegmental area. Thus, the PCG serves as an essential distribution center to orchestrate a global auditory network to promote rapid awakening.

Spiking networks that efficiently process dynamic sensory features explain receptor information mixing in somatosensory cortex.

How do biological neural systems efficiently encode, transform and propagate information between the sensory periphery and the sensory cortex about sensory features evolving at different time scales? Are these computations efficient in normative information processing terms? While previous work has suggested that biologically plausible models of of such neural information processing may be implemented efficiently within a single processing layer, how such computations extend across several processing layers is less clear. Here, we model propagation of multiple time-varying sensory features across a sensory pathway, by extending the theory of efficient coding with spikes to efficient encoding, transformation and transmission of sensory signals. These computations are optimally realized by a multilayer spiking network with feedforward networks of spiking neurons (receptor layer) and recurrent excitatory-inhibitory networks of generalized leaky integrate-and-fire neurons (recurrent layers). Our model efficiently realizes a broad class of feature transformations, including positive and negative interaction across features, through specific and biologically plausible structures of feedforward connectivity. We find that mixing of sensory features in the activity of single neurons is beneficial because it lowers the metabolic cost at the network level. We apply the model to the somatosensory pathway by constraining it with parameters measured empirically and include in its last node, analogous to the primary somatosensory cortex (S1), two types of inhibitory neurons: parvalbumin-positive neurons realizing lateral inhibition, and somatostatin-positive neurons realizing winner-take-all inhibition. By implementing a negative interaction across stimulus features, this model captures several intriguing empirical observations from the somatosensory system of the mouse, including a decrease of sustained responses from subcortical networks to S1, a non-linear effect of the knock-out of receptor neuron types on the activity in S1, and amplification of weak signals from sensory neurons across the pathway.

The Design and Ground Test Verification of an Energy-Efficient Wireless System for the Fatigue Monitoring of Wind Turbine Blades Based on Bistable Piezoelectric Energy Harvesting.

A wireless monitoring system based on piezoelectric energy harvesting (PEH) is presented to provide fatigue data of wind turbine blades in operation. The system comprises three subsystems, each respectively providing the following functions: (i) the conversion of mechanical to electric energy by exploiting the bistable vibration of a composite beam with piezoelectric patches in post-buckling, (ii) harvesting the converted energy by means of a modified, commercial, off-the-shelf (COTS) circuit to feed a LiPo battery and (iii) the battery-powered acquisition and wireless transmission of sensory signals to the cloud to be elaborated upon by the end-user. The system was verified with ground tests under representative operation conditions, which demonstrated the fulfillment of the design requirements. The measurements indicated that the system provided 23% of the required power for fully autonomous operation when subjected to white noise base excitation of 1 g acceleration in the range of 1-20 Hz.

Cochlear inflammaging: cellular and molecular players of the innate and adaptive immune system in age-related hearing loss

Age-related hearing loss is the most common sensory disorder worldwide that contributes to numerous health conditions in the aging population. Despite its prevalence, current treatments, including hearing aids, are unsatisfactory in improving hearing deficits or slowing or reversing its pathophysiology. Immunosenescence is a key driver of neurodegenerative disease, and a similar mechanism has recently come to attention in age-related hearing loss. Imbalanced levels of cytokines and chemokines contribute to aberrant immune cell activity and a chronic pro-inflammatory microenvironment that may lead to degradation of inner ear structure and function. Macrophages, typically guardians of organ homeostasis, are found to develop dysregulated activity with aging due to unidentified factors, and they interact with other components of the innate immune system to damage sensory hair cells, synapses, neurons, and other structures of the inner ear critical to sensory signal transmission. They also increasingly trigger the inflammasome, a protein complex involved in inflammatory cell death, and the complement cascade, to perpetuate a cycle of inflammation and cellular damage in the cochlea, resulting in hearing loss. Senescence in certain T cell populations have indicated a role of adaptive immunity in age-related hearing loss as well. Deciphering the mechanisms of immune dysregulation is a critical first step in producing targeted therapies for hearing loss. This brief review describes the current and emerging research surrounding the dysregulation of the innate and adaptive immune systems in age-related hearing loss and its parallels with other neurodegenerative diseases.

Peripheral Sacral Magnetic Stimulation in Patients with Idiopathic Overactive Bladder: a Single Blind Prospective Randomized Comparative Clinical Study

INTRODUCTION. Overactive bladder (OAB) is a symptom complex that includes urgency, frequent urination, imperative urinary incontinence and nocturia. The idiopathic form of OAB is associated with dysfunction of sensory signal transmission at the level of the peripheral and central nervous system, which leads to bladder hypersensitivity. The low level of patients’ compliance to OAB drug therapy and the high level of refusal to take drugs emphasize the urgency of finding new effective methods of influencing the lower urinary tract. Magnetic stimulation (MS) is a non-drug treatment for lower urinary tract dysfunction. AIM. To study the efficacy and safety of the sacral MS method in women with idiopathic detrusor overactivity (DO) and OAB symptoms. MATERIALS AND METHODS. A single blind prospective randomized comparative study included 55 female patients with urodynamically confirmed idiopathic DO. The patients were divided by simple randomization into the main group (n = 29), which received MS 3 times a week for 5 weeks with a frequency of 5 Hz per sacral root area (S2–S4), and the placebo group (n = 26), in which sham stimulation was performed. RESULTS AND DISCUSSION. The study revealed that sacral MS is reliably effective against the clinical symptoms of OAB in idiopathic DO. The dynamics of clinical symptoms is confirmed by changes in urodynamic parameters. The effect of sacral MS significantly exceeds placebo. MS is a safe procedure and is well tolerated by patients. CONCLUSION. The sacral MS method, the effectiveness of which has been proven in comparison with placebo, is recommended to be included in the treatment regimen of patients with idiopathic OAB. The mechanism of action of sacral MS is associated with the activation of sympathetic and inhibition of parasympathetic influences, as well as changes in supraspinal control and cerebral activity.

Thalamic bursting and the role of timing and synchrony in thalamocortical signaling in the awake mouse

The thalamus controls transmission of sensory signals from periphery to cortex, ultimately shaping perception. Despite this significant role, dynamic thalamic gating and the consequences for downstream cortical sensory representations have not been well studied in the awake brain. We optogenetically modulated the ventro-posterior-medial thalamus in the vibrissa pathway of the awake mouse and measured spiking activity in the thalamus and activity in primary somatosensory cortex (S1) using extracellular electrophysiology and genetically encoded voltage imaging. Thalamic hyperpolarization significantly enhanced thalamic sensory-evoked bursting; however, surprisingly, the S1 cortical response was not amplified, but instead, timing precisionwas significantly increased, spatial activation more focused, and there was an increased synchronization of cortical inhibitory neurons. A thalamocortical network model implicates the modulation of precise timing of feedforward thalamic population spiking, presenting a highly sensitive, timing-based gating of sensory signaling to the cortex.

Role of GluA4 in the acoustic and tactile startle responses

The primary startle response (SR) is an innate reaction evoked by sudden and intense acoustic, tactile or visual stimuli. In rodents and humans the SR involves reflexive contractions of the face, neck and limb muscles. The acoustic startle response (ASR) pathway consists of auditory nerve fibers (AN), cochlear root neurons (CRNs) and giant neurons of the caudal pontine reticular nucleus (PnC), which synapse on cranial and spinal motor neurons. The tactile startle response (TSR) is transmitted by primary sensory neurons to the principal sensory (Pr5) and spinal (Sp5) trigeminal nuclei. The ventral part of Pr5 projects directly to the PnC neurons. The SR requires rapid transmission of sensory information to initiate a fast motor response. Alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPAR) are necessary to transmit auditory information to the PnC neurons and elicit the SR. AMPARs containing the glutamate AMPAR subunit 4 (GluA4) have fast kinetics, which makes them ideal candidates to transmit the SR signal. This study examined the role of GluA4 within the primary SR pathway by using GluA4 knockout (GluA4-KO) mice. Deletion of GluA4 considerably decreased the amplitude and probability of successful ASR and TSR, indicating that the presence of this subunit is critical at a common station within the startle pathway. We conclude that deletion of GluA4 affects the transmission of sensory signals from acoustic and tactile pathways to the motor component of the startle reflex. Therefore, GluA4 is required for the full response and for reliable elicitation of the startle response.

Особливості перерозподілу НМДА- та АМПА-рецеп- торів у синасах між гангліозними клітинами сітківки та нейронами superficial superior colliculus

We investigated the changes in distribution of the NMDA- and AMPA-receptors in the synapses in the in vitro model of the retinocollicular pathway. The model was a primary coculture of the retinal cells and superficial superior colliculus (SSC) neurons. Evoked postsynaptic currents (ePSCs) were recorded in SSC neurons in response to local electrical extracellular stimulation of the afferent retinal ganglion cells’ (RGC) axons. We analyzed the changes in the kinetic characteristics of ePSCs at different holding potentials during cocultivation. The results obtained reflect that NMDA receptors play an essential role in the formation of the retinocollicular synapses. After the formation of retinocollicular connections, the main role in the sensory signal transmission belongs to AMPA receptors. Thus, the data obtained indicate the specific dynamic changes of the functional roles of NMDA- and AMPA-receptors in the forma- tion and development of the retinocollicular synaptic contacts.

Restoration of sensory information via bionic hands.

Individuals who have lost the use of their hands because of amputation or spinal cord injury can use prosthetic hands to restore their independence. A dexterous prosthesis requires the acquisition of control signals that drive the movements of the robotic hand, and the transmission of sensory signals to convey information to the user about the consequences of these movements. In this Review, we describe non-invasive and invasive technologies for conveying artificial sensory feedback through bionic hands, and evaluate the technologies' long-term prospects.

Elemental imaging shows mercury in cells of the human lateral and medial geniculate nuclei.

ObjectiveInterference with the transmission of sensory signals along visual and auditory pathways has been implicated in the pathogenesis of hallucinations. The relay centres for vision (the lateral geniculate nucleus) and hearing (the medial geniculate nucleus) appear to be susceptible to the uptake of circulating mercury. We therefore investigated the distribution of mercury in cells of both these geniculate nuclei.Materials and methodsParaffin-embedded tissue sections containing the lateral geniculate nucleus were obtained from 50 adults (age range 20–104 years) who at autopsy had a variety of clinicopathological conditions, including neurological and psychiatric disorders. The medial geniculate nucleus was present in seven sections. Sections were stained for mercury using autometallography. Laser ablation-inductively coupled plasma-mass spectrometry was used to confirm the presence of mercury.ResultsTen people had mercury in cells of the lateral geniculate nucleus, and in the medial geniculate nucleus of three of these. Medical diagnoses in these individuals were: none (3), Parkinson disease (3), and one each of depression, bipolar disorder, multiple sclerosis, and mercury self-injection. Mercury was distributed in different groups of geniculate capillary endothelial cells, neurons, oligodendrocytes, and astrocytes. Mass spectrometry confirmed the presence of mercury.ConclusionMercury is present in different combinations of cell types in the lateral and medial geniculate nuclei in a proportion of people from varied backgrounds. This raises the possibility that mercury-induced impairment of the function of the geniculate nuclei could play a part in the genesis of visual and auditory hallucinations. Although these findings do not provide a direct link between mercury in geniculate cells and hallucinations, they suggest that further investigations into the possibility of toxicant-induced hallucinations are warranted.

Sensory Neurons Expressing Calcitonin Gene-Related Peptide Regulate Adaptive Thermogenesis and Diet-Induced Obesity

Sensory neurons arising from the dorsal root ganglia play a pivotal role in thermoregulation through the detection of cutaneous temperature and transmission of sensory signals to the brain. However, the functional significance of sensory perception in thermogenesis and weight loss has remained elusive. Here, we show that genetic ablation of heat sensing neurons containing Calcitonin Gene-Related Peptide (CGRPα) promotes resistance to weight gain upon high fat diet (HFD) feeding and drives a thermogenic program in brown and white adipose tissues. Remarkably, mice lacking CGRPα-expressing sensory neurons feel colder when challenged with cooling stimuli and their brown fat displays increased energy utilization during cold and HFD challenges. As these neurons are peptidergic, we also investigated the role of the CGRPα secreted peptide in this process. Depletion of CGRPα with a monoclonal antibody leads to a lesser weight loss than full neural depletion on HFD and partially recapitulates the increased energy expenditure and brown fat thermogenic profile observed with sensory ablation. Mechanistically, recombinant CGRPα impaired glycolysis and reduced fatty acid oxidation in cultured cells. Collectively, our results suggest that CGRPα-expressing sensory neurons are the first step to regulate adaptive thermogenesis in brown adipose tissue by detecting alterations in environmental temperatures. These neural processes have the dual ability to both influence central regulation of adrenergic stimulation of thermogenesis and to release peptidergic signals inhibiting fuel consumption in adipocytes.

Efferent Inputs Are Required for Normal Function of Vestibular Nerve Afferents

A group of vestibular afferent nerve fibers with irregular-firing resting discharges are thought to play a prominent role in responses to fast head movements and vestibular plasticity. We show that, in C57BL/6 mice (either sex, 4-5 weeks old), normal activity in the efferent vestibular pathway is required for function of these irregular afferents. Thermal inhibition of efferent fibers results in a profound inhibition of irregular afferents' resting discharges, rendering them inadequate for signaling head movements. In this way, efferent inputs adjust the contribution of the peripheral irregular afferent pathway that plays a critical role in peripheral vestibular signaling and plasticity.SIGNIFICANCE STATEMENT Vestibular end organs in the inner ear receive efferent inputs from the brainstem. Previously, electrical stimulation of efferents was linked to an increase in resting discharges of afferents and a decrease in their sensitivities. Here, we show that localized thermal inhibition of unmyelinated efferents results in a significant decrease in the activity of afferent nerve fibers, particularly those with irregular resting discharges implicated in responses to fast head movements and vestibular compensation. Thus, by upregulating and downregulating of afferent firing, particularly irregular afferents, efferents adjust neural activity sensitive to rapid head movements. These findings support the notion that peripheral vestibular end organs are not passive transducers of head movements and their sensory signal transmission is modulated by efferent inputs.

The Effects of NMDA Receptor Blockade on Sensory-Evoked Responses in Superficial Layers of the Rat Barrel Cortex.

Transmission of excitation from L4 to L2/3 is a part of a canonical circuit of cortical sensory signal processing. While synapses from L4 to L2/3 are mediated by both AMPA and NMDA glutamate receptors, previous studies suggested that sensory-evoked excitation of neurons in supragranular layers is almost entirely mediated by NMDA receptors. Here, we readdressed this question using extracellular recordings of sensory-evoked potentials (SEPs) and multiple unit activity (MUA) in the rat barrel cortex. We found that blockade of NMDA receptors using the selective antagonist dAPV profoundly inhibited the late part of L2/3 SEP, the associated sink, and MUA response but did not affect its initial part. Our results indicate that both non-NMDA and NMDA receptors are involved in sensory signal transmission from L4 to L2/3. While non-NMDA receptors mediate fast transmission of sensory signals, NMDA-Rs are importantly involved in the generation of the late phase of the sensory-evoked response in supragranular layers.

Top-Down Suppression of Sensory Cortex in an NMDAR Hypofunction Model of Psychosis.

Conceptual and computational models have been advanced that propose that perceptual disturbances in psychosis, such as hallucinations, may arise due to a disruption in the balance between bottom-up (ie sensory) and top-down (ie from higher brain areas) information streams in sensory cortex. However, the neural activity underlying this hypothesized alteration remains largely unexplored. Pharmacological N-methyl-d-aspartate receptor (NMDAR) antagonism presents an attractive model to examine potential changes as it acutely recapitulates many of the symptoms of schizophrenia including hallucinations, and NMDAR hypofunction is strongly implicated in the pathogenesis of schizophrenia as evidenced by large-scale genetic studies. Here we use in vivo 2-photon imaging to measure frontal top-down signals from the anterior cingulate cortex (ACC) and their influence on activity of the primary visual cortex (V1) in mice during pharmacologically induced NMDAR hypofunction. We find that global NMDAR hypofunction causes a significant increase in activation of top-down ACC axons, and that surprisingly this is associated with an ACC-dependent net suppression of spontaneous activity in V1 as well as a reduction in V1 sensory-evoked activity. These findings are consistent with a model in which perceptual disturbances in psychosis are caused in part by aberrant top-down frontal cortex activity that suppresses the transmission of sensory signals through early sensory areas.

Multiplicative noise is beneficial for the transmission of sensory signals in simple neuron models

We study simple integrate-and-fire type models with multiplicative noise and consider the transmission of a weak and slow signal, i.e. a signal that evokes a small modulation of the instantaneous firing rate on time scales that are much larger than the membrane time scale and the mean interspike interval. The specific question of interest is whether and how the state-dependence of the noise can be optimized with respect to information transmission. First, in a simple model in which the noise intensity varies linearly with the state variable, we show analytically that multiplicative fluctuations may benefit the signal transfer and we elucidate the mechanism for this improvement. In a conductance-based integrate-and-fire model with synaptically filtered shot-noise input, we show by means of extended numerical simulations that also in a biophysically more relevant situation, multiplicative noise can enhance the signal-to-noise ratio. Our results shed light on a so far unexplored aspect of stochastic signal transmission in neural systems.

Spinal Afferent Innervation of the Colon and Rectum.

Despite their seemingly elementary roles, the colon and rectum undertake a variety of key processes to ensure our overall wellbeing. Such processes are coordinated by the transmission of sensory signals from the periphery to the central nervous system, allowing communication from the gut to the brain via the “gut-brain axis”. These signals are transmitted from the peripheral terminals of extrinsic sensory nerve fibers, located within the wall of the colon or rectum, and via their axons within the spinal splanchnic and pelvic nerves to the spinal cord. Recent studies utilizing electrophysiological, anatomical and gene expression techniques indicate a surprisingly diverse set of distinct afferent subclasses, which innervate all layers of the colon and rectum. Combined these afferent sub-types allow the detection of luminal contents, low- and high-intensity stretch or contraction, in addition to the detection of inflammatory, immune, and microbial mediators. To add further complexity, the proportions of these afferents vary within splanchnic and pelvic pathways, whilst the density of the splanchnic and pelvic innervation also varies along the colon and rectum. In this review we traverse this complicated landscape to elucidate afferent function, structure, and nomenclature to provide insights into how the extrinsic sensory afferent innervation of the colon and rectum gives rise to physiological defecatory reflexes and sensations of discomfort, bloating, urgency, and pain.

Serotonergic paraneurones in the female mouse urethral epithelium and their potential role in peripheral sensory information processing.

The mechanisms underlying detection and transmission of sensory signals arising from visceral organs, such as the urethra, are poorly understood. Recently, specialized ACh-expressing cells embedded in the urethral epithelium have been proposed as chemosensory sentinels for detection of bacterial infection. Here, we examined the morphology and potential role in sensory signalling of a different class of specialized cells that express serotonin (5-HT), termed paraneurones. Urethrae, dorsal root ganglia neurones and spinal cords were isolated from adult female mice and used for immunohistochemistry and calcium imaging. Visceromotor reflexes (VMRs) were recorded in vivo. We identified two morphologically distinct groups of 5-HT+ cells with distinct regional locations: bipolar-like cells predominant in the mid-urethra and multipolar-like cells predominant in the proximal and distal urethra. Sensory nerve fibres positive for calcitonin gene-related peptide, substance P, and TRPV1 were found in close proximity to 5-HT+ paraneurones. In vitro 5-HT (1 μm) stimulation of urethral primary afferent neurones, mimicking 5-HT release from paraneurones, elicited changes in the intracellular calcium concentration ([Ca2+ ]i ) mediated by 5-HT2 and 5-HT3 receptors. Approximately 50% of 5-HT responding cells also responded to capsaicin with changes in the [Ca2+ ]i . In vivo intra-urethral 5-HT application increased VMRs induced by urethral distention and activated pERK in lumbosacral spinal cord neurones. These morphological and functional findings provide insights into a putative paraneurone-neural network within the urethra that utilizes 5-HT signalling, presumably from paraneurones, to modulate primary sensory pathways carrying nociceptive and non-nociceptive (mechano-sensitive) information to the central nervous system.

Preparation of Horizontal Slices of Adult Mouse Retina for Electrophysiological Studies.

Vertical slice preparations are well established to study circuitry and signal transmission in the adult mammalian retina. The plane of sectioning in these preparations is perpendicular to the retinal surface, making it ideal for the study of radially oriented neurons like photoreceptors and bipolar cells. However, the large dendritic arbors of horizontal cells, wide-field amacrine cells, and ganglion cells are mostly truncated, leaving markedly reduced synaptic activity in these cells. Whereas ganglion cells and displaced amacrine cells can be studied in a whole-mounted preparation of the retina, horizontal cells and amacrine cells located in the inner nuclear layer are only poorly accessible for electrodes in whole retina tissue. To achieve maximum accessibility and synaptic integrity, we developed a horizontal slice preparation of the mouse retina, and studied signal transmission at the synapse between photoreceptors and horizontal cells. Horizontal sectioning allows(1) easy and unambiguous visual identification of horizontal cell bodies for electrode targeting, and (2) preservation of the extended horizontal cell dendritic fields, as a prerequisite for intact and functional cone synaptic input to horizontal cell dendrites. Horizontal cells from horizontal slices exhibited tonic synaptic activity in the dark, and they responded to brief flashes of light with a reduction of inward current and diminished synaptic activity. Immunocytochemical evidence indicates that almost all cones within the dendritic field of a horizontal cell establish synapses with its peripheral dendrites. The horizontal slice preparation is therefore well suited to study the physiological properties of horizontally extended retinal neurons as well as sensory signal transmission and integration across selected synapses.

Preparation of Horizontal Slices of Adult Mouse Retina for Electrophysiological Studies

Vertical slice preparations are well established to study circuitry and signal transmission in the adult mammalian retina. The plane of sectioning in these preparations is perpendicular to the retinal surface, making it ideal for the study of radially oriented neurons like photoreceptors and bipolar cells. However, the large dendritic arbors of horizontal cells, wide-field amacrine cells, and ganglion cells are mostly truncated, leaving markedly reduced synaptic activity in these cells. Whereas ganglion cells and displaced amacrine cells can be studied in a whole-mounted preparation of the retina, horizontal cells and amacrine cells located in the inner nuclear layer are only poorly accessible for electrodes in whole retina tissue. To achieve maximum accessibility and synaptic integrity, we developed a horizontal slice preparation of the mouse retina, and studied signal transmission at the synapse between photoreceptors and horizontal cells. Horizontal sectioning allows (1) easy and unambiguous visual identification of horizontal cell bodies for electrode targeting, and (2) preservation of the extended horizontal cell dendritic fields, as a prerequisite for intact and functional cone synaptic input to horizontal cell dendrites. Horizontal cells from horizontal slices exhibited tonic synaptic activity in the dark, and they responded to brief flashes of light with a reduction of inward current and diminished synaptic activity. Immunocytochemical evidence indicates that almost all cones within the dendritic field of a horizontal cell establish synapses with its peripheral dendrites. The horizontal slice preparation is therefore well suited to study the physiological properties of horizontally extended retinal neurons as well as sensory signal transmission and integration across selected synapses.