The dopaminergic mind hypothesis seeks to explain the differences between modern humans and their hominid relatives by focusing on changes in dopamine.[59] It theorizes that increased levels of dopamine were part of a general physiological adaptation due to an increased consumption of meat around two million years ago in Homo habilis, and later enhanced by changes in diet and other environmental and social factors beginning approximately 80,000 years ago. Under this theory, the “high-dopamine” personality is characterized by high intelligence, a sense of personal destiny, a religious/cosmic preoccupation, an obsession with achieving goals and conquests, an emotional detachment that in many cases leads to ruthlessness, and a risk-taking mentality. High levels of dopamine are proposed to underlie increased psychological disorders in industrialized societies. According to this hypothesis, a “dopaminergic society” is an extremely goal-oriented, fast-paced, and even manic society, “given that dopamine is known to increase activity levels, speed up our internal clocks and create a preference for novel over unchanging environments.”[59] In the same way that high-dopamine individuals lack empathy and exhibit a more masculine behavioral style, dopaminergic societies are “typified by more conquest, competition, and aggression than nurturance and communality.”[59] Although behavioral evidence and some indirect anatomical evidence (e.g., enlargement of the dopamine-rich striatum in humans)[60] support a dopaminergic expansion in humans, there is still no direct evidence that dopamine levels are markedly higher in humans relative to other apes.[61] However, recent discoveries about the sea-side settlements of early man may provide evidence of dietary changes consistent with this hypothesis.[62]

Fruit browning
Polyphenol oxidases (PPOs) are a family of enzymes responsible for the browning of fresh fruits and vegetables when they are cut or bruised. These enzymes use molecular oxygen (O2) to oxidise various 1,2-diphenols to their corresponding quinones. The natural substrate for PPOs in bananas is dopamine. The product of their oxidation, dopamine quinone, spontaneously oxidises to other quinones. The quinones then polymerise and condense with amino acids and proteins to form brown pigments known as melanins. The quinones and melanins derived from dopamine may help protect damaged fruit and vegetables against growth of bacteria and fungi.[8

Neurons can generate rhythmic patterns of action potentials or spikes. Some types of neurons have the tendency to fire at particular frequencies, so-called resonators

Neural oscillation can also arise from interactions between different brain areas. Time delays play an important role here. Because all brain areas are bidirectionally coupled, these connections between brain areas form feedback loops. Positive feedback loops tends to cause oscillatory activity which frequency is inversely related to the delay time. An example of such a feedback loop is the connections between the thalamus and cortex. This thalamocortical network is able to generate oscillatory activity known as recurrent thalamo-cortical resonance.[16] The thalamocortical network plays an important role in the generation of alpha activity.[17][18]


Though most antidepressants selectively inhibit REM sleep due to their action on monoamines, this effect decreases after long-term use. It is interesting to note that REM sleep deprivation stimulates hippocampal neurogenesis much the same as antidepressants

A newborn baby spends more than 80% of total sleep time in REM.[5] During REM, the activity of the brain’s neurons is quite similar to that during waking hours; for this reason, the REM-sleep stage may be called paradoxical sleep.[6]
REM sleep is physiologically different from the other phases of sleep, which are collectively referred to as non-REM sleep (NREM sleep). Subjects’ vividly recalled dreams mostly occur during REM sleep
Heart rate and breathing rate are irregular during REM sleep, again similar to the waking hours. Body temperature is not well regulated during REM. Erections of the penis (nocturnal penile tumescence or NPT) normally accompany REM sleep

Intimately related to views on REM function in memory consolidation, Mitchison and Crick[13] have proposed that by virtue of its inherent spontaneous activity, the function of REM sleep “is to remove certain undesirable modes of interaction in networks of cells in the cerebral cortex”, which process they characterize as “unlearning”. As a result, those memories which are relevant (whose underlying neuronal substrate is strong enough to withstand such spontaneous, chaotic activation), are further strengthened, whilst weaker, transient, “noise” memory traces disintegrate.

Sex differences
Females have been shown to have more delta wave activity, and this is true across most mammal species. This discrepancy does not become apparent until early adulthood (in the 30’s or 40’s, in humans), with men showing greater age-related reductions in delta wave activity than their female counterparts.[5] It has been suggested[citation needed] that this discrepancy may be due to larger skull size in males, but this theory has been refuted[citation needed] by intracranial data from female cats, which still show more delta activity.

During delta wave sleep, neurons are globally inhibited by gamma-aminobutyric acid (GABA).[10]
Delta activity stimulates the release of several hormones, including growth hormone releasing hormone GHRH and prolactin (PRL). GHRH is released from the hypothalamus, which in turn stimulates release of growth hormone from the pituitary. Like growth hormone, the secretion of prolactin - which is closely related to growth hormone (GH) - is also regulated by the pituitary. Thyroid stimulating hormone (TSH) activity is decreased in response to delta-wave signaling.[11]

Sleep deprivation
Total sleep deprivation has been shown to increase delta wave activity during sleep recovery,[19] and has also been shown to increase hypersynchronous delta activity (HSD).[18]

Parkinson’s disease
Sleep disturbances, as well as dementia, are common features of Parkinson’s disease, and patients with PD show disrupted brain wave activity. The drug rotigotine, developed for PD, has been shown to increase delta power and slow-wave sleep in those with Parkinson’s disease. Interestingly, delta-wave inducing peptide injected into the substantia nigra of the rat model has been shown to increase parkinsonian symptoms.[20]

Schizophrenia
People suffering schizophrenia have shown disrupted EEG patterns, and there is a close association of reduced delta waves during deep sleep and negative symptoms associated with schizophrenia. During slow wave sleep (stages 3 and 4), schizophrenics have been shown to have reduced delta wave activity, although delta waves have also been shown to be increased during waking hours in more severe forms of schizophrenia.[21] A recent study has shown that the right frontal and central delta wave dominance, seen in healthy individuals, is absent in patients with schizophrenia. In addition, the negative correlation between delta wave activity and age is also not observed in those with schizophrenia.[22]

Diabetes and insulin resistance
Disruptions in slow wave (delta) sleep have been shown to increase risk for development of Type II diabetes, potentially due to disruptions in the growth hormone secreted by the pituitary. In addition, hypoglycemia occurring during sleep may also disrupt delta-wave activity.[23] Low-voltage irregular delta waves (TLID) have also been found in the left temporal lobe of diabetic patients, at a rate of 56% (compared to 14% in healthy controls).[24][25]

Fibromyalgia
Patients suffering from fibromyalgia often report unrefreshing sleep. A study conducted in 1975 by Moldovsky et al. showed that the delta wave activity of these patients in stages 3 and 4 sleep were often interrupted by alpha waves. They later showed that depriving the body of delta wave sleep activity also induced musculoskeletal pain and fatigue.[26]

Alcoholism
Alcohol has been shown to decrease slow wave sleep and delta power, while increasing stage 1 and REM incidence in both men and women. In long-term alcohol abuse, the influences of alcohol on sleep architecture and reductions in delta activity have been shown to persist even after long periods of abstinence.[27]

Consciousness and dreaming
Initially, dreaming was thought to only occur in rapid eye movement sleep, though it is now known that dreaming may also occur during slow-wave sleep. Delta waves and delta wave activity are marked by an unconscious state, and the loss of physical awareness as well as the “iteration of information”. Delta wave activity has also been purported to aid in the formation of declarative and explicit memory formation

Difference between Indica and Sativa

Indica has a higher CBD:THC ratio than Sativa. Cannabis with relatively high ratios of CBD:THC is less likely to induce anxiety than cannabis with low CBD:THC ratios.[11]

Natural occurence
A Cannabis sativa plant may have a THC:CBD ratio 4-5 times that of Cannabis Indica. Cannabis with relatively high ratios of CBD:THC is less likely to induce anxiety than vice versa. This may be due to CBD’s antagonist effects at the cannabinoid receptor, compared to THC’s partial agonist effect.[74] The relatively large amount of THC versus CBD contained in Cannabis sativa, means, compared to an indica, the effects are modulated significantly. The effects of Sativa are well known for its cerebral high, hence used daytime as medical cannabis, while Indica are well known for its sedative effects and preferred night time as medical cannabis.

As the chemical THC reaches parts of the brain, it attaches to cannabinoid receptors. Usually the receptors are blocked by anandamide produced at low rates by the body, but the large percent of THC increases the blocking of the receptors, and allows dopamine to flow freely. As dopamine reaches the receptors, the body experiences a heightened focus, and a greater level of perception, sometimes resulting in extremely elevated emotions and feelings. Some effects may include a general alteration of conscious perception, euphoria, feelings of well-being, relaxation or stress reduction, increased appreciation of humor, music or the arts, joviality, metacognition and introspection, enhanced recollection (episodic memory), increased sensuality, increased awareness of sensation, increased libido,[30] and creativity. Abstract or philosophical thinking, disruption of linear memory and paranoia or anxiety are also typical. Anxiety is the most commonly reported side effect of smoking marijuana[citation needed]. Between 20 and 30 percent of recreational users experience intense anxiety and/or panic attacks after smoking cannabis.[31]

Cannabis also produces many subjective and highly tangible effects, such as greater enjoyment of food taste and aroma (“the munchies”), an enhanced enjoyment of music and comedy, and marked distortions in the perception of time and space (where experiencing a “rush” of ideas from the bank of long-term memory can create the subjective impression of long elapsed time, while a clock reveals that only a short time has passed). At higher doses, effects can include altered body image, auditory and/or visual illusions, pseudo-hallucinatory or (rarely, at very high doses) fully hallucinatory experiences, and ataxia from selective impairment of polysynaptic reflexes. In some cases, cannabis can lead to dissociative states such as depersonalization[32][33] and derealization;[34] such effects are most often considered desirable, but have the potential to induce panic attack and paranoia in some unaccustomed users.[citation needed]

Dopamine (abbreviated as DA^[1]) is a simple organic chemical in the catecholamine family, is a monoamine neurotransmitter which plays a number of important physiological roles in the bodies of animals. In addition to being a catecholamine and a monoamine, dopamine may be classified as a substituted phenethylamine. Its name derives from its chemical structure, which consists of an amine group (NH₂) linked to a catechol structure called dihydroxyphenethylamine, the decarboxylated form of dihydroxyphenylalanine (acronym DOPA). In the brain, dopamine functions as a neurotransmitter—a chemical released by nerve cells to send signals to other nerve cells. The human brain uses five known types of dopamine receptors, labeled D₁, D₂, D₃, D₄, and D₅. Dopamine is produced in several areas of the brain, including the substantia nigra and the ventral tegmental area.

Dopamine plays a major role in the brain system that is responsible for reward-driven learning. Every type of reward that has been studied increases the level of dopamine transmission in the brain, and a variety of highly addictive drugs, including stimulants such as cocaine and methamphetamine, act directly on the dopamine system.^[2] There is evidence that people with extraverted (reward-seeking) personality types tend to show higher levels of dopamine activity than people with introverted personalities. Several important diseases of the nervous system are associated with dysfunctions of the dopamine system. Parkinson’s disease, an age-related degenerative condition causing tremor and motor impairment, is caused by loss of dopamine-secreting neurons in the substantia nigra. Schizophrenia has been shown to involve elevated levels of dopamine activity in the mesolimbic pathway and decreased levels of dopamine in the prefrontal cortex.^[3][4]Attention deficit hyperactivity disorder (ADHD) is also believed to be associated with decreased dopamine activity.^[5]

Dopamine is available as an intravenous medication acting on the sympathetic nervous system, producing effects such as increased heart rate and blood pressure. However, because dopamine cannot cross the blood–brain barrier, dopamine given as a drug does not directly affect the central nervous system. To increase the amount of dopamine in the brains of patients with diseases such as Parkinson’s disease and dopa-responsive dystonia, L-DOPA (the precursor of dopamine) is often given because it crosses the blood–brain barrier relatively easily.

Somatic effects
Some of the short-term physical effects of cannabis use include increased heart rate, dry mouth (“cotton mouth”), reddening of the eyes (congestion of the conjunctival blood vessels), a reduction in intra-ocular pressure, muscle relaxation and a sensation of cold or hot hands and feet.[35]

Electroencephalography or EEG shows somewhat more persistent alpha waves of slightly lower frequency than usual.[12] Cannabinoids produce a “marked depression of motor activity” via activation of neuronal cannabinoid receptors belonging to the CB1 subtype.

THC and cannabidiol are also neuroprotective antioxidants. Research in rats has indicated that THC prevented hydroperoxide-induced oxidative damage as well as or better than other antioxidants in a chemical (Fenton reaction) system and neuronal cultures. Cannabidiol was significantly more protective than either vitamin E or vitamin C.[14]

Neuroprotection is the effect of any chemical, biological molecule or medical practice which has a protective effect in the nervous system against neurodegenerative disease or brain injury. This effect may take the form of protection of neurons from apoptosis or degeneration.
Currently, there is a broad interest in applying neuroprotection in the prevention and treatment of a number of diseases of the central nervous system such as Alzheimer’s, Parkinson’s, schizophrenia, and stroke.[1]

Biochemical mechanisms in the brain
In 1990, the discovery of cannabinoid receptors located throughout the brain and body, along with endogenous cannabinoid neurotransmitters like anandamide (a lipid material derived ligand from arachidonic acid), suggested that the use of cannabis affects the brain in the same manner as a naturally occurring brain chemical. Cannabinoids usually contain a 1,1’-di-methyl-pyrane ring, a variedly derivatized aromatic ring and a variedly unsaturated cyclohexyl ring and their immediate chemical precursors, constituting a family of about 60 bi-cyclic and tri-cyclic compounds. Like most other neurological processes, the effects of cannabis on the brain follow the standard protocol of signal transduction, the electrochemical system of sending signals through neurons for a biological response. It is now understood that cannabinoid receptors appear in similar forms in most vertebrates and invertebrates and have a long evolutionary history of 500 million years. The binding of cannabinoids to cannabinoid receptors decrease adenylyl cyclase activity, inhibit calcium N channels, and disinhibit K+A channels. There are two types of cannabinoid receptors (CB1 and CB2).
The CB1 receptor is found primarily in the brain and mediates the psychological effects of THC. The CB2 receptor is most abundantly found on cells of the immune system. Cannabinoids act as immunomodulators at CB2 receptors, meaning they increase some immune responses and decrease others. For example, nonpsychotropic cannabinoids can be used as a very effective anti-inflammatory.[11] The affinity of cannabinoids to bind to either receptor is about the same, with only a slight increase observed with the plant-derived compound CBD binding to CB2 receptors more frequently. Cannabinoids likely have a role in the brain’s control of movement and memory, as well as natural pain modulation. It is clear that cannabinoids can affect pain transmission and, specifically, that cannabinoids interact with the brain’s endogenous opioid system and may affect dopamine transmission.[15] This is an important physiological pathway for the medical treatment of pain.

Toxicity

According to a 2006 United Kingdom government report, using cannabis is much less dangerous than tobacco, prescription drugs, and alcohol in social harms, physical harm, and addiction.[24] It was found in 2007 that while tobacco and cannabis smoke are quite similar, cannabis smoke contained higher amounts of ammonia, hydrogen cyanide, and nitrogen oxides, but lower levels of carcinogenic polycyclic aromatic hydrocarbons (PAHs).[25] This study found that directly inhaled cannabis smoke contained as much as 20 times as much ammonia and 5 times as much hydrogen cyanide as tobacco smoke and compared the properties of both mainstream and sidestream (smoke emitted from a smouldering ‘joint’ or ‘cone’) smoke.[25] Mainstream cannabis smoke was found to contain higher concentrations of selected polycyclic aromatic hydrocarbons (PAHs) than sidestream tobacco smoke.[25] However, other studies have found much lower disparities in ammonia and hydrogen cyanide between cannabis and tobacco, and that some other constituents (such as polonium-210, lead, arsenic, nicotine, and tobacco-specific nitrosamines) are either lower or non-existent in cannabis smoke

Several studies have suggested that THC also has an anticholinesterase action[15][16] which may implicate it as a potential treatment for Alzheimer’s and Myasthenia Gravis.


A 2008 study by the University of Melbourne of 15 heavy marijuana users (consuming at least 5 marijuana cigarettes daily for on average 20 years) and 16 controls found an average size difference for the smokers in the hippocampus (12 percent smaller) and the amygdala (7 percent smaller).[64] It has been suggested that such effects can be reversed with long term abstinence.[65] However, the study indicates that they are unsure that the problems were caused by marijuana alone.

Damage to the hippocampus does not affect some types of memory, such as the ability to learn new motor or cognitive skills (playing a musical instrument, or solving certain types of puzzles, for example). This fact suggests that such abilities depend on different types of memory (procedural memory) and different brain regions. Furthermore, amnesic patients frequently show “implicit” memory for experiences even in the absence of conscious knowledge. For example, a patient asked to guess which of two faces they have seen most recently may give the correct answer the majority of the time, in spite of stating that they have never seen either of the faces before. Some researchers distinguish between conscious recollection, which depends on the hippocampus, and familiarity, which depends on portions of the medial temporal cortex.[24]

Theta rhythm
Main article: Theta rhythm
Because of its densely packed neural layers, the hippocampus generates some of the largest EEG signals of any brain structure. In some situations the EEG is dominated by regular waves at 3–10 Hz, often continuing for many seconds. These reflect subthreshold membrane potentials and strongly modulate the spiking of hippocampal neurons and synchronise across the hippocampus in a travelling wave pattern.[47] This EEG pattern is known as a theta rhythm.[48] Theta rhythmicity is very obvious in rabbits and rodents, and also clearly present in cats and dogs. Whether theta can be seen in primates is a vexing question.[49] In rats (the animals that have been the most extensively studied), theta is seen mainly in two conditions: first, when an animal is walking or in some other way actively interacting with its surroundings; second, during REM sleep.[50] The function of theta has not yet been convincingly explained, although numerous theories have been proposed.[44] The most popular hypothesis has been to relate it to learning and memory. For example, the phase with which theta at the time of stimulation of a neuron shapes the effect of that stimulation upon its synapses and therefore may affect learning and memory dependent upon synaptic plasticity.[51] It is well-established that lesions of the medial septum—the central node of the theta system—cause severe disruptions of memory. However, the medium septum is more than just the controller of theta, it is also the main source of cholinergic projections to the hippocampus.[39] It has not been established that septal lesions exert their effects specifically by eliminating the theta rhythm.[52]

‪Theta rhythm‬
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“Thetawaves” redirects here. “Thetawaves” is also a song on Steal This Album!.


Example of an EEG theta wave
The theta rhythm is an oscillatory pattern in EEG signals recorded either from inside the brain or from electrodes glued to the scalp. Two types of theta rhythm have been described. The “hippocampal theta rhythm” is a strong oscillation that can be observed in the hippocampus and other brain structures in numerous species of mammals including rodents, rabbits, dogs, cats, bats, and marsupials. “Cortical theta rhythms” are low-frequency components of scalp EEG, usually recorded from humans.
In rats, the most frequently studied species, theta rhythmicity is easily observed in the hippocampus, but can also be detected in numerous other cortical and subcortical brain structures. Hippocampal theta, with a frequency range of 6–10 Hz, appears when a rat is engaged in active motor behavior such as walking or exploratory sniffing, and also during REM sleep. Theta waves with a lower frequency range, usually around 6–7 Hz, are sometimes observed when a rat is motionless but alert. When a rat is eating, grooming, or sleeping, the hippocampal EEG usually shows a non-rhythmic pattern known as Large Irregular Activity or LIA. The hippocampal theta rhythm depends critically on projections from the medial septal area, which in turn receives input from the hypothalamus and several brainstem areas. Hippocampal theta rhythms in other species differ in some respects from those in rats. In cats and rabbits, the frequency range is lower (around 4–6 Hz), and theta is less strongly associated with movement than in rats. In bats, theta appears in short bursts associated with echolocation. In humans and other primates, hippocampal theta is difficult to observe at all.
The function of the hippocampal theta rhythm is not clearly understood. Green and Arduini, in the first major study of this phenomenon, noted that hippocampal theta usually occurs together with desynchronized EEG in the neocortex, and proposed that it is related to arousal. Vanderwolf and his colleagues, noting the strong relationship between theta and motor behavior, have argued that it is related to sensorimotor processing. Another school, led by John O’Keefe, have suggested that theta is part of the mechanism animals use to keep track of their location within the environment. The most popular theories, however, link the theta rhythm to mechanisms of learning and memory (Hasselmo, 2005).
Cortical theta rhythms observed in human scalp EEG are a different phenomenon, with no clear relationship to the hippocampus. In human EEG studies, the term theta refers to frequency components in the 4–7 Hz range, regardless of their source. Cortical theta is observed frequently in young children. In older children and adults, it tends to appear during drowsy, meditative, or sleeping states, but not during the deepest stages of sleep. Several types of brain pathology can give rise to abnormally strong or persistent cortical theta waves.

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