Locating Photography

The specter of global dissemination haunted photography from its very beginning. This chapter explains two aspects of photography's “globalization”: its use as a “western” technique to document an increasingly colonized world and its dissemination around the world and its adoption by local practitioners. In rural and small‐town central India, the studio retains a central place in most people's encounters with photography. Martín Chambi would retain a lifelong adherence to the purity of the photographic image but other indigenista photographers, such as Juan Manuel Figueroa Aznar, would increasingly use paint alongside photography. A World System Photography, seen in networks that fold locally articulated practices into trajectories that fuse technics, history, and culture, can help people think in new ways about the “location” of photography. Locations have to be re‐imagined as “Terra Infirma”, unstable and complex positions which may have more of the quality of linking sections of a network than of territories

Synaptic Transmission from Horizontal Cells to Cones Is Impaired by Loss of Connexin Hemichannels

In the vertebrate retina, horizontal cells generate the inhibitory surround of bipolar cells, an essential step in contrast enhancement. For the last decades, the mechanism involved in this inhibitory synaptic pathway has been a major controversy in retinal research. One hypothesis suggests that connexin hemichannels mediate this negative feedback signal; another suggests that feedback is mediated by protons. Mutant zebrafish were generated that lack connexin 55.5 hemichannels in horizontal cells. Whole cell voltage clamp recordings were made from isolated horizontal cells and cones in flat mount retinas. Light-induced feedback from horizontal cells to cones was reduced in mutants. A reduction of feedback was also found when horizontal cells were pharmacologically hyperpolarized but was absent when they were pharmacologically depolarized. Hemichannel currents in isolated horizontal cells showed a similar behavior. The hyperpolarization-induced hemichannel current was strongly reduced in the mutants while the depolarization-induced hemichannel current was not. Intracellular recordings were made from horizontal cells. Consistent with impaired feedback in the mutant, spectral opponent responses in horizontal cells were diminished in these animals. A behavioral assay revealed a lower contrast-sensitivity, illustrating the role of the horizontal cell to cone feedback pathway in contrast enhancement. Model simulations showed that the observed modifications of feedback can be accounted for by an ephaptic mechanism. A model for feedback, in which the number of connexin hemichannels is reduced to about 40%, fully predicts the specific asymmetric modification of feedback. To our knowledge, this is the first successful genetic interference in the feedback pathway from horizontal cells to cones. It provides direct evidence for an unconventional role of connexin hemichannels in the inhibitory synapse between horizontal cells and cones. This is an important step in resolving a long-standing debate about the unusual form of (ephaptic) synaptic transmission between horizontal cells and cones in the vertebrate retina

A Positive Feedback Synapse from Retinal Horizontal Cells to Cone Photoreceptors

Cone photoreceptors and horizontal cells (HCs) have a reciprocal synapse that underlies lateral inhibition and establishes the antagonistic center-surround organization of the visual system. Cones transmit to HCs through an excitatory synapse and HCs feed back to cones through an inhibitory synapse. Here we report that HCs also transmit to cone terminals a positive feedback signal that elevates intracellular Ca2+ and accelerates neurotransmitter release. Positive and negative feedback are both initiated by AMPA receptors on HCs, but positive feedback appears to be mediated by a change in HC Ca2+, whereas negative feedback is mediated by a change in HC membrane potential. Local uncaging of AMPA receptor agonists suggests that positive feedback is spatially constrained to active HC-cone synapses, whereas the negative feedback signal spreads through HCs to affect release from surrounding cones. By locally offsetting the effects of negative feedback, positive feedback may amplify photoreceptor synaptic release without sacrificing HC-mediated contrast enhancement

Channelopathies in Cav1.1, Cav1.3, and Cav1.4 voltage-gated L-type Ca2+ channels

Voltage-gated Ca2+ channels couple membrane depolarization to Ca2+-dependent intracellular signaling events. This is achieved by mediating Ca2+ ion influx or by direct conformational coupling to intracellular Ca2+ release channels. The family of Cav1 channels, also termed L-type Ca2+ channels (LTCCs), is uniquely sensitive to organic Ca2+ channel blockers and expressed in many electrically excitable tissues. In this review, we summarize the role of LTCCs for human diseases caused by genetic Ca2+ channel defects (channelopathies). LTCC dysfunction can result from structural aberrations within their pore-forming α1 subunits causing hypokalemic periodic paralysis and malignant hyperthermia sensitivity (Cav1.1 α1), incomplete congenital stationary night blindness (CSNB2; Cav1.4 α1), and Timothy syndrome (Cav1.2 α1; reviewed separately in this issue). Cav1.3 α1 mutations have not been reported yet in humans, but channel loss of function would likely affect sinoatrial node function and hearing. Studies in mice revealed that LTCCs indirectly also contribute to neurological symptoms in Ca2+ channelopathies affecting non-LTCCs, such as Cav2.1 α1 in tottering mice. Ca2+ channelopathies provide exciting disease-related molecular detail that led to important novel insight not only into disease pathophysiology but also to mechanisms of channel function

γ Oscillations are involved in the sensorimotor transformation of pain

Pain signals threat and initiates motor responses to avoid harm. The transformation of pain into a motor response is thus an essential part of pain. Here, we investigated the neural mechanisms subserving the sensorimotor transformation of pain at the cortical level by using electroencephalography. In a simple reaction time experiment, brief painful stimuli were delivered to the left hand of healthy human subjects who responded with button presses of the right hand. The results show that the simple reaction time task was associated with neuronal responses at delta/theta, alpha/beta, and gamma frequencies. The analysis of the relationship between neuronal activity and response speed revealed that gamma oscillations, which were temporally coupled to the painful stimuli, but not temporally coupled to the motor response, predicted reaction times. Lateralization of gamma oscillations indicates that they originate from motor areas rather than from sensory areas. We conclude that gamma oscillations are involved in the sensorimotor transformation of pain whose efficiency they reflect. We hypothesize that the relationship between stimulus-locked gamma oscillations and reaction times reflects a direct thalamo-motor route of nociceptive information that is central to the biological function of pain

γ Oscillations are involved in the sensorimotor transformation of pain

Pain signals threat and initiates motor responses to avoid harm. The transformation of pain into a motor response is thus an essential part of pain. Here, we investigated the neural mechanisms subserving the sensorimotor transformation of pain at the cortical level by using electroencephalography. In a simple reaction time experiment, brief painful stimuli were delivered to the left hand of healthy human subjects who responded with button presses of the right hand. The results show that the simple reaction time task was associated with neuronal responses at delta/theta, alpha/beta, and gamma frequencies. The analysis of the relationship between neuronal activity and response speed revealed that gamma oscillations, which were temporally coupled to the painful stimuli, but not temporally coupled to the motor response, predicted reaction times. Lateralization of gamma oscillations indicates that they originate from motor areas rather than from sensory areas. We conclude that gamma oscillations are involved in the sensorimotor transformation of pain whose efficiency they reflect. We hypothesize that the relationship between stimulus-locked gamma oscillations and reaction times reflects a direct thalamo-motor route of nociceptive information that is central to the biological function of pain

Prefrontal Gamma Oscillations Encode Tonic Pain in Humans

Under physiological conditions, momentary pain serves vital protective functions. Ongoing pain in chronic pain states, on the other hand, is a pathological condition that causes widespread suffering and whose treatment remains unsatisfactory. The brain mechanisms of ongoing pain are largely unknown. In this study, we applied tonic painful heat stimuli of varying degree to healthy human subjects, obtained continuous pain ratings, and recorded electroencephalograms to relate ongoing pain to brain activity. Our results reveal that the subjective perception of tonic pain is selectively encoded by gamma oscillations in the medial prefrontal cortex. We further observed that the encoding of subjective pain intensity experienced by the participants differs fundamentally from that of objective stimulus intensity and from that of brief pain stimuli. These observations point to a role for gamma oscillations in the medial prefrontal cortex in ongoing, tonic pain and thereby extend current concepts of the brain mechanisms of pain to the clinically relevant state of ongoing pain. Furthermore, our approach might help to identify a brain marker of ongoing pain, which may prove useful for the diagnosis and therapy of chronic pain