Neurophysiological responses to stressful motion and anti-motion sickness drugs as mediated by the limbic system

Performance is characterized in terms of attention and memory, categorizing extrinsic mechanism mediated by ACTH, norepinephrine and dopamine, and intrinsic mechanisms as cholinergic. The cholinergic role in memory and performance was viewed from within the limbic system and related to volitional influences of frontal cortical afferents and behavioral responses of hypothalamic and reticular system efferents. The inhibitory influence of the hippocampus on the autonomic and hormonal responses mediated through the hypothalamus, pituitary, and brain stem are correlated with the actions of such anti-motion sickness drugs as scopolamine and amphetamine. These drugs appear to exert their effects on motion sickness symptomatology through diverse though synergistic neurochemical mechanisms involving the septohippocampal pathway and other limbic system structures. The particular impact of the limbic system on an animal's behavioral and hormonal responses to stress is influenced by ACTH, cortisol, scopolamine, and amphetamine

Acetylcholine neuromodulation in normal and abnormal learning and memory: vigilance control in waking, sleep, autism, amnesia, and Alzheimer's disease

This article provides a unified mechanistic neural explanation of how learning, recognition, and cognition break down during Alzheimer's disease, medial temporal amnesia, and autism. It also clarifies whey there are often sleep disturbances during these disorders. A key mechanism is how acetylcholine modules vigilance control in cortical layer

Parkinson's disease dementia: a neural networks perspective.

In the long-term, with progression of the illness, Parkinson's disease dementia affects up to 90% of patients with Parkinson's disease. With increasing life expectancy in western countries, Parkinson's disease dementia is set to become even more prevalent in the future. However, current treatments only give modest symptomatic benefit at best. New treatments are slow in development because unlike the pathological processes underlying the motor deficits of Parkinson's disease, the neural mechanisms underlying the dementing process and its associated cognitive deficits are still poorly understood. Recent insights from neuroscience research have begun to unravel the heterogeneous involvement of several distinct neural networks underlying the cognitive deficits in Parkinson's disease dementia, and their modulation by both dopaminergic and non-dopaminergic transmitter systems in the brain. In this review we collate emerging evidence regarding these distinct brain networks to give a novel perspective on the pathological mechanisms underlying Parkinson's disease dementia, and discuss how this may offer new therapeutic opportunities

Plasticity in the Olfactory System: Lessons for the Neurobiology of Memory

We are rapidly advancing toward an understanding of the molecular events underlying odor transduction, mechanisms of spatiotemporal central odor processing, and neural correlates of olfactory perception and cognition. A thread running through each of these broad components that define olfaction appears to be their dynamic nature. How odors are processed, at both the behavioral and neural level, is heavily dependent on past experience, current environmental context, and internal state. The neural plasticity that allows this dynamic processing is expressed nearly ubiquitously in the olfactory pathway, from olfactory receptor neurons to the higher-order cortex, and includes mechanisms ranging from changes in membrane excitability to changes in synaptic efficacy to neurogenesis and apoptosis. This review will describe recent findings regarding plasticity in the mammalian olfactory system that are believed to have general relevance for understanding the neurobiology of memory.Yeshttps://us.sagepub.com/en-us/nam/manuscript-submission-guideline

Anatomy and computational modeling of networks underlying cognitive-emotional interaction

The classical dichotomy between cognition and emotion equated the first with rationality or logic and the second with irrational behaviors. The idea that cognition and emotion are separable, antagonistic forces competing for dominance of mind has been hard to displace despite abundant evidence to the contrary. For instance, it is now known that a pathological absence of emotion leads to profound impairment of decision making. Behavioral observations of this kind are corroborated at the mechanistic level: neuroanatomical studies reveal that brain areas typically described as underlying either cognitive or emotional processes are linked in ways that imply complex interactions that do not resemble a simple mutual antagonism. Instead, physiological studies and network simulations suggest that top-down signals from prefrontal cortex realize "cognitive control" in part by either suppressing or promoting emotional responses controlled by the amygdala, in a way that facilitates adaptation to changing task demands. Behavioral, anatomical, and physiological data suggest that emotion and cognition are equal partners in enabling a continuum or matrix of flexible behaviors that are subserved by multiple brain regions acting in concert. Here we focus on neuroanatomical data that highlight circuitry that structures cognitive-emotional interactions by directly or indirectly linking prefrontal areas with the amygdala. We also present an initial computational circuit model, based on anatomical, physiological, and behavioral data to explicitly frame the learning and performance mechanisms by which cognition and emotion interact to achieve flexible behavior.R01 MH057414 - NIMH NIH HHS; R01 NS024760 - NINDS NIH HH

Prediction and memory: A predictive coding account

The hippocampus is crucial for episodic memory, but it is also involved in online prediction. Evidence suggests that a unitary hippocampal code underlies both episodic memory and predictive processing, yet within a predictive coding framework the hippocampal-neocortical interactions that accompany these two phenomena are distinct and opposing. Namely, during episodic recall, the hippocampus is thought to exert an excitatory influence on the neocortex, to reinstate activity patterns across cortical circuits. This contrasts with empirical and theoretical work on predictive processing, where descending predictions suppress prediction errors to ‘explain away’ ascending inputs via cortical inhibition. In this hypothesis piece, we attempt to dissolve this previously overlooked dialectic. We consider how the hippocampus may facilitate both prediction and memory, respectively, by inhibiting neocortical prediction errors or increasing their gain. We propose that these distinct processing modes depend upon the neuromodulatory gain (or precision) ascribed to prediction error units. Within this framework, memory recall is cast as arising from fictive prediction errors that furnish training signals to optimise generative models of the world, in the absence of sensory data

Top-down modulation by medial prefrontal cortex of basal forebrain activation of auditory cortex during learning

The experiment tested the hypothesis that the acetylcholine (ACh) release in the rat auditory cortex is greater in rats undergoing auditory classical conditioning compared to rats in a truly random control paradigm where no associative learning takes place and that this is mediated by prefrontal afferent projections influencing the nucleus basalis magnocellularis (NBM), which in turn modulates ACh release in neocortex. Rats with bilateral ibotenic acid lesions of medial prefrontal and agranular insular cortices were tested in an auditory classical conditioning task while ACh was collected from the primary auditory cortex. It was hypothesized that lesions of these prefrontal areas would prevent learning-related increases of ACh release in the primary auditory cortex. The hypothesized results were supported. Results from this experiment provide unique evidence that medial prefrontal cortex projections to the NBM are important for mediating cortical ACh release during associative learning