Friday, December 18, 2015

Do you Have HPPD?

To those of you reading this blog, and also suffer Hallucinogen Persisting Perception Disorder, you can participate in an online survey to helps aid the awareness of HPPD. The researcher of this project, Doreen Lewis, PhD, is currently working on a book titled, "When The Party Is Over", which is being backed b Dr. Henry David Abraham as well.

Click the link below to visit the webpage.

http://www.facesofhppd.com/

Manipulating Consciousness In Rats


Thalamus Linked To HPPD

Scientists showed that they could alter brain activity of rats and either wake them up or put them in an unconscious state by changing the firing rates of neurons in the central thalamus, a region known to regulate arousal. The studyis published in the journal eLIFE.

“Our results suggest the central thalamus works like a radio dial that tunes the brain to different states of activity and arousal,” said Jin Hyung Lee, PhD, assistant professor of neurology, neurosurgery and bioengineering at Stanford University, and a senior author of the study.

Located deep inside the brain the thalamus acts as a relay station sending neural signals from the body to the cortex. Damage to neurons in the central part of the thalamus may lead to problems with sleep, attention, and memory. Previous studies suggested that stimulation of thalamic neurons may awaken patients who have suffered a traumatic brain injury from minimally conscious states.

Lee’s team flashed laser pulses onto light sensitive central thalamic neurons of sleeping rats, which caused the cells to fire. High frequency stimulation of 40 or 100 pulses per second woke the rats. In contrast, low frequency stimulation of 10 pulses per second sent the rats into a state reminiscent of absence seizures that caused them to stiffen and stare before returning to sleep.

“This study takes a big step towards understanding the brain circuitry that controls sleep and arousal,” Yejun (Janet) He, PhD, program director at the U.S. National Institute of Health (NIH)’s National Institute of Neurological Disorders and Stroke (NINDS).

When the scientists used functional magnetic resonance imaging (fMRI) to scan brain activity, they saw that high and low frequency stimulation put the rats in completely different states of activity. Cortical brain areas where activity was elevated during high frequency stimulation became inhibited with low frequency stimulation. Electrical recordings confirmed the results. Neurons in the somatosensory cortex fired more during high frequency stimulation of the central thalamus and less during low frequency stimulation.

“Dr. Lee’s innovative work demonstrates the power of using imaging technologies to study the brain at work,” said Guoying Liu, PhD, a program director at the NIH’s National Institute of Biomedical Imaging and Bioengineering (NIBIB).

How can changing the firing rate of the same neurons in one region lead to different effects on the rest of the brain?

Further experiments suggested the different effects may be due to a unique firing pattern by inhibitory neurons in a neighboring brain region, the zona incerta, during low frequency stimulation. Cells in this brain region have been shown to send inhibitory signals to cells in the sensory cortex.

Electrical recordings showed that during low frequency stimulation of the central thalamus, zona incerta neurons fired in a spindle pattern that often occurs during sleep. In contrast, sleep spindles did not occur during high frequency stimulation. Moreover, when the scientists blocked the firing of the zona incerta neurons during low frequency stimulation of the central thalamus, the average activity of sensory cortex cells increased.

Although deep brain stimulation of the thalamus has shown promise as a treatment for traumatic brain injury, patients who have decreased levels of consciousness show slow progress through these treatments.

“We showed how the circuits of the brain can regulate arousal states,” said Dr. Lee. “We hope to use this knowledge to develop better treatments for brain injuries and other neurological disorders.”

Article Link

Tuesday, December 15, 2015

Dr.Gerard Alderliefste

Recently I was emailed by Dr. Abraham about a researcher, Dr. Gerard Alderliefste in Amsterdam who has an HPPD Research Clinic currently established. My team and I will be working on a draft email to send to him about our approach into getting more awareness spread about these disorders and perhaps get him on board for a team research project.

Dr. Alderliefste's website has some intriguing information, including a list of other specialists and and he also has a "Visual Snow Simulation" page that correctly portrays what the symptoms of HPPD/VS look like to an individual that suffers from these disorders. 



Sunday, December 13, 2015

Plant Compounds Increase Brain Connections

Brazilian researchers have demonstrated in laboratory that apigenin, a substance found in parsley, thyme, chamomile and red pepper, improves neuron formation and strengthens the connections between brain cells.
Previous experiments with animals had already shown that substances from the same chemical group as the apigenin, known as flavonoids, positively affect memory and learning. Many studies highlight the potential of flavonoids to preserve and enhance brain function. While the effectiveness of flavonoids for brain health is not an entirely new concept, this research is the first to show the positive effects of apigegin directly on human cells and the first to unraveling its mechanism.











Wednesday, December 9, 2015

Thalamus Linked To HPPD

The thalamus (from Greek θάλαμος, "chamber") is a midline symmetrical structure of two halves, within the vertebrate brain, situated between the cerebral cortex and the midbrain. Some of its functions are the relaying of sensory and motor signals to the cerebral cortex, and the regulation of consciousness, sleep, and alertness. The two parts of the thalamus surround the third ventricle. It is the main product of the embryonic diencephalon.

The role of the thalamus in the more anterior pallidal and nigral territories in the basal ganglia system disturbances is recognized but still poorly understood. The contribution of the thalamus to vestibular or to tectal functions is almost ignored. The thalamus has been thought of as a "relay" that simply forwards signals to the cerebral cortex. Newer research suggests that thalamic function is more selective. Many different functions are linked to various regions of the thalamus. This is the case for many of the sensory systems (except for the olfactory system), such as the auditory, somatic, visceral, gustatory and visual systems where localized lesions provoke specific sensory deficits. A major role of the thalamus is support of motor and language systems, and much of the circuitry implicated for these systems is shared. The thalamus is functionally connected to the hippocampus as part of the extended hippocampal system at the thalamic anterior nuclei with respect to spatial memory and spatial sensory datum they are crucial for human episodic memory and rodent event memory. There is support for the hypothesis that thalamic regions connection to particular parts of the mesio-temporal lobe provide differentiation of the functioning of recollective and familiarity memory.

The neuronal information processes necessary for motor control were proposed as a network involving the thalamus as a subcortical motor centre. Through investigations of the anatomy of the brains of primates the nature of the interconnected tissues of the cerebellum to the multiple motor cortices suggested that the thalamus fulfills a key function in providing the specific channels from the basal ganglia and cerebellum to the cortical motor areas. In an investigation of the saccade and antisaccade motor response in three monkeys, the thalamic regions were found to be involved in the generation of antisaccade eye-movement.



Thalamus Wikipedia Link





Brain Mechanisms of Hallucinogens and Entactogens

This review focuses on recent brain imaging and behavioral studies of sensory gating functions, which assess similarities between the effects of classic hallucinogens (eg, psilocybin), dissociative anesthetics (eg, ketamine), and entactogens (eg, 3,4-methylenedioxymethamphetamine [MDMA]) in humans. Serotonergic hallucinogens and psychotomimetic anesthetics produce overlapping psychotic syndromes associated with a marked activation of the prefrontal cortex (hyperfrontality) and other overlapping changes in temporoparietal, striatal, and thalamic regions, suggesting that both classes of drugs act upon a common final pathway. Together with the observation that both hallucinogens and N-methyl-oaspartate (NMDA) antagonists disrupt sensory gating in rats by acting on 5-hydroxytryptamine (serotonin) 5-HT2 receptors located in cortico-striato-thalamic circuitry these findings suggest that disruption of cortico-subcortical processing leading to sensory overload of the cortex is a communality of these psychoses. In contrast to hallucinogens, the entactogen MDMA produces an emotional state of positive mood, concomitant with an activation of prefrontolimbiclparalimbic structures and a deactivation of amygdala and thalamus.



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