Yesterday 06:37 PM
Infant memories: Lost but not gone?
https://www.thetransmitter.org/memory/in...-not-gone/
EXCERPTS: More contemporary psychological accounts have linked infantile amnesia to the immaturity of the hippocampus, a brain structure critical for forming episodic memories in older children and adults. According to these accounts, hippocampal circuits are not sufficiently developed in infancy to form enduring traces of life events. That is, infantile amnesia reflects a failure to encode experiences.
Here, we argue for a different view. Early-life experiences are encoded by the hippocampus and may persist over time. What changes is how easily they can be accessed. Infantile amnesia, therefore, reflects not a failure to encode memories but a failure to naturally retrieve them.
[...] The advent of activity-dependent engram labeling and optogenetic tools has enabled researchers to directly address the encoding versus retrieval debate. ... Importantly, it is not just optogenetically activating any population of cells that produces the freezing response, only those that were active during infant learning. Together, these findings indicate that early-life memories are successfully encoded and may persist over time but cannot be accessed through natural sensory retrieval cues—pointing to a failure of retrieval rather than encoding.
[...] Research on human infants reveals that memory systems are active far earlier than once assumed; behavioral studies show that infants learn and remember from birth. But the tasks these studies employ involve motor actions, repeated training and reward or feedback. These requirements contribute to forms of memory, such as operant conditioning and priming, that can be dissociated from episodic memory and that engage brain regions other than the hippocampus, including the striatum, cerebellum and sensory systems.
[...] Why can’t early-life memories be accessed? Scientists have proposed several explanations, ranging from psychological theories emphasizing the development of consciousness, language and a sense of self to neurobiological accounts focused on circuit maturation, plasticity and neurogenesis.
[...] During development, the brain changes how it interprets the world. We learn language, become experts at recognizing objects and faces, organize experiences into concepts and begin to understand other people’s intentions. As a result, the same sights and sounds that once triggered a memory in infancy no longer produce the same pattern of brain activity. The hippocampal engram is still there, but the cues needed to reactivate it may no longer match, preventing the memory from being naturally expressed. In this view, cognitive and brain development gradually reduce access to early memories rather than erase them... (MORE - missing details)
A blind retina isn't silent & its noise may be getting in the way of restoring sight
https://www.eurekalert.org/news-releases/1143797
EXCERPTS: When retinitis pigmentosa takes a person's sight, the standard clinical test goes flat: no response, no signal, nothing. Yet the retina behind that flat line is anything but quiet. Researchers at the Jules-Gonin Eye Hospital, part of the Faculty of Biology and Medicine of the University of Lausanne, have recorded the spontaneous electrical activity of the retina -in darkness, with no light stimulation -and found it producing abnormal rhythms never before measured in a living person.
The findings are published in Nature Communications. Retinitis pigmentosa is a group of genetic diseases that progressively destroy the photoreceptors, the cells that capture light. At an advanced stage, the electroretinogram -the reference test for retinal function - detects nothing. The trace is flat.
But a flat trace is not a dead retina. Behind the lost photoreceptors, several layers of neurons survive and rewire, a process called retinal remodelling that has been documented for some twenty years in donor tissue examined after death. What no one had done was measure the activity of those rewired circuits in a living eye.
[...] A pilot study then enrolled five patients at an advanced stage of the disease and eight sighted volunteers. Recordings lasted forty minutes, eyes closed, in darkness, using thread electrodes already common in routine clinical care. The patients' retinas showed markedly stronger oscillatory activity than the sighted participants', in a frequency range close to the one seen in mice -the first evidence that degenerating human retinas are functionally, not just anatomically, remodelled.
In animals, the team went a step further. A drug that boosts the retina's own inhibitory signalling quieted the abnormal rhythm. And with the noise reduced, transcorneal electrical stimulation reached the visual cortex more effectively, at lower current and the retina became easier to drive.
Therapies that aim to restore sight -retinal implants, optogenetics, regenerative approaches -all depend on the surviving retina being able to listen. If it is busy talking to itself, that is a problem... (MORE - missing details, no ads)
https://www.thetransmitter.org/memory/in...-not-gone/
EXCERPTS: More contemporary psychological accounts have linked infantile amnesia to the immaturity of the hippocampus, a brain structure critical for forming episodic memories in older children and adults. According to these accounts, hippocampal circuits are not sufficiently developed in infancy to form enduring traces of life events. That is, infantile amnesia reflects a failure to encode experiences.
Here, we argue for a different view. Early-life experiences are encoded by the hippocampus and may persist over time. What changes is how easily they can be accessed. Infantile amnesia, therefore, reflects not a failure to encode memories but a failure to naturally retrieve them.
[...] The advent of activity-dependent engram labeling and optogenetic tools has enabled researchers to directly address the encoding versus retrieval debate. ... Importantly, it is not just optogenetically activating any population of cells that produces the freezing response, only those that were active during infant learning. Together, these findings indicate that early-life memories are successfully encoded and may persist over time but cannot be accessed through natural sensory retrieval cues—pointing to a failure of retrieval rather than encoding.
[...] Research on human infants reveals that memory systems are active far earlier than once assumed; behavioral studies show that infants learn and remember from birth. But the tasks these studies employ involve motor actions, repeated training and reward or feedback. These requirements contribute to forms of memory, such as operant conditioning and priming, that can be dissociated from episodic memory and that engage brain regions other than the hippocampus, including the striatum, cerebellum and sensory systems.
[...] Why can’t early-life memories be accessed? Scientists have proposed several explanations, ranging from psychological theories emphasizing the development of consciousness, language and a sense of self to neurobiological accounts focused on circuit maturation, plasticity and neurogenesis.
[...] During development, the brain changes how it interprets the world. We learn language, become experts at recognizing objects and faces, organize experiences into concepts and begin to understand other people’s intentions. As a result, the same sights and sounds that once triggered a memory in infancy no longer produce the same pattern of brain activity. The hippocampal engram is still there, but the cues needed to reactivate it may no longer match, preventing the memory from being naturally expressed. In this view, cognitive and brain development gradually reduce access to early memories rather than erase them... (MORE - missing details)
A blind retina isn't silent & its noise may be getting in the way of restoring sight
https://www.eurekalert.org/news-releases/1143797
EXCERPTS: When retinitis pigmentosa takes a person's sight, the standard clinical test goes flat: no response, no signal, nothing. Yet the retina behind that flat line is anything but quiet. Researchers at the Jules-Gonin Eye Hospital, part of the Faculty of Biology and Medicine of the University of Lausanne, have recorded the spontaneous electrical activity of the retina -in darkness, with no light stimulation -and found it producing abnormal rhythms never before measured in a living person.
The findings are published in Nature Communications. Retinitis pigmentosa is a group of genetic diseases that progressively destroy the photoreceptors, the cells that capture light. At an advanced stage, the electroretinogram -the reference test for retinal function - detects nothing. The trace is flat.
But a flat trace is not a dead retina. Behind the lost photoreceptors, several layers of neurons survive and rewire, a process called retinal remodelling that has been documented for some twenty years in donor tissue examined after death. What no one had done was measure the activity of those rewired circuits in a living eye.
[...] A pilot study then enrolled five patients at an advanced stage of the disease and eight sighted volunteers. Recordings lasted forty minutes, eyes closed, in darkness, using thread electrodes already common in routine clinical care. The patients' retinas showed markedly stronger oscillatory activity than the sighted participants', in a frequency range close to the one seen in mice -the first evidence that degenerating human retinas are functionally, not just anatomically, remodelled.
In animals, the team went a step further. A drug that boosts the retina's own inhibitory signalling quieted the abnormal rhythm. And with the noise reduced, transcorneal electrical stimulation reached the visual cortex more effectively, at lower current and the retina became easier to drive.
Therapies that aim to restore sight -retinal implants, optogenetics, regenerative approaches -all depend on the surviving retina being able to listen. If it is busy talking to itself, that is a problem... (MORE - missing details, no ads)