- 15th August
- 14th May
Cannabis is easily the most widely used illegal substance in the world. Although it still illegal at federal level, Washington and Colorado have legalized recreational cannabis use. Studies examining the relationship between marijuana use and neuropsychological function should be taken into consideration when making/reforming laws and health policies. I have received multiple questions regarding the effects of marijuana on memory and health and recently found a longitudinal study on this matter.
Prior evidence suggests that long-term, heavy cannabis use may cause enduring neuropsychological impairment beyond the period of acute intoxication (i.e. being high). Moreover, the magnitude and persistence of impairment depends on several factors including: quantity, frequency, duration and age of onset. Greater quantities, more frequent and earlier onset of use are associated with a poorer neuropsychological outcome. However, studies that compare pre-initiation neuropsychological functioning with longitudinal data on post-initiation functioning are scarce.
Meier et. al investigated the association between persistent cannabis use and neuropsychological functioning (assessed over a 20 year period) in over 1,000 individuals. Subjects received neuropsychological testing prior to onset of use (childhood; 1985-1986) and after some had developed a persistent pattern of use (~38 years old; 2010-2012).
Important findings included:
- Subjects with more persistence cannabis dependence showed greater IQ decline. Those who never experienced cannabis experienced a slight increase in IQ.
- Subjects with more persistent cannabis dependence generally showed greater neuropsychological impairment across different areas of mental function: executive function, memory, processing speed, perceptual reasoning and verbal comprehension. The greatest impairments were in the domains of executive function and processing speed.
- Neuropsychological deficits induced by cannabis use were still significant even when the researchers controlled for: past 24 hour cannabis use, past-week cannabis use, persistent tobacco, alcohol and/or hard drug dependence, and schizophrenia (all of which alternative explanations for poorer neuropsychological function).
- The effect of cannabis dependence on cognitive decline remained significant even after controlling for years of education. Persistent cannabis users with a high school education or less experienced greater IQ decline.
- Subjects who had an adolescent onset of use and were diagnosed with dependence prior to 18 years of age tended to become more persistent users. Importantly, adult-onset cannabis users did not appear to experience IQ decline as a function of cannabis use.
- Within-person IQ decline was apparent regardless of whether cannabis was used frequently or infrequently a year before testing. Thus, cessation of cannabis use did not restore neuropsychological functioning among adolescent-onset former persistent cannabis users.
So it looks like persistent use of cannabis is particularly detrimental with adolescent onset. Some have speculated that this may be due to puberty, a critical period of brain development in which circuits related to decision-making, executive-function, and reward are undergoing reorganization/rewiring. Neurotransmitter systems like dopamine are also vulnerable during this period as they have not fully matured yet. Thus, the authors suggest that cannabis use exerts neurotoxic effects during this developmental period.
However, one must remember that although the authors show compelling data, their data correlational and is not sufficient to establish causation. Furthermore, there is no mechanism underlying the negative impact of cannabis use on neuropsychological function- merely speculations (see above). It is also possible that there is another variable related to cannabis use and neuropsychological decline that the authors did not rule out. Another limitation of the study was the heavy reliance on self-reporting measures like self-reported frequency of use. Finally, it is hard to estimate dosages due to the variety of strains and potency of cannabis.
I would personally suggest taking this information for what it’s worth. Neuroimaging studies in adolescents (humans) reveal structural and functional brain differences associated with cannabis use so we know that cannabis use changes the brain. I personally believe that cannabis use has negative effects on memory and general health, but I do not think that it’s as simple as the “Weed will make you stupid.” notion that some adults try to instill in adolescents. After all, we already KNOW about the dangers and costs of alcohol/tobacco use and people still use them. For me, the key is to delay onset of use (if you must use) and to prevent adolescent use of cannabis. If you are a teenager with cannabis dependence, it is never to late to quit and try to remedy the effects.
Source: (Click on the link for abstract)
- 26th January
Asked by: aebl-deactivated20130619
Serotonin and prefrontal cortex function: neurons, networks, and circuits.
The Picower Institute for Learning and Memory and Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. email@example.com
Higher-order executive tasks such as learning, working memory, and behavioral flexibility depend on the prefrontal cortex (PFC), the brain region most elaborated in primates. The prominent innervation by serotonin neurons and the dense expression of serotonergic receptors in the PFC suggest that serotonin is a major modulator of its function. The most abundant serotonin receptors in the PFC, 5-HT1A, 5-HT2A and 5-HT3A receptors, are selectively expressed in distinct populations of pyramidal neurons and inhibitory interneurons, and play a critical role in modulating cortical activity and neural oscillations (brain waves). Serotonergic signaling is altered in many psychiatric disorders such as schizophrenia and depression, where parallel changes in receptor expression and brain waves have been observed. Furthermore, many psychiatric drug treatments target serotonergic receptors in the PFC. Thus, understanding the role of serotonergic neurotransmission in PFC function is of major clinical importance. Here, we review recent findings concerning the powerful influences of serotonin on single neurons, neural networks, and cortical circuits in the PFC of the rat, where the effects of serotonin have been most thoroughly studied.
Emotional enhancement of memory: how norepinephrine enables synaptic plasticity.
Department of Psychiatry, McLean Hospital, Harvard Medical School, 115 Mill Street, Belmont, Massachusetts 02478, USA. firstname.lastname@example.org
Changes in synaptic strength are believed to underlie learning and memory. We explore the idea that norepinephrine is an essential modulator of memory through its ability to regulate synaptic mechanisms. Emotional arousal leads to activation of the locus coeruleus with the subsequent release of norepineprine in the brain, resulting in the enhancement of memory. Norepinephrine activates both pre- and post-synaptic adrenergic receptors at central synapses with different functional outcomes, depending on the expression pattern of these receptors in specific neural circuitries underlying distinct behavioral processes. We review the evidence for noradrenergic modulation of synaptic plasticity with consideration of how this may contribute to the mechanisms of learning and memory.
Neurotransmitter roles in synaptic modulation, plasticity and learning in the dorsal striatum.
Laboratory for Integrative Neuroscience, NIAAA/NIH, 5625 Fishers Lane, Rockville, MD 20852, USA. email@example.com
The dorsal striatum is a large forebrain region involved in action initiation, timing, control, learning and memory. Learning and remembering skilled movement sequences requires the dorsal striatum, and striatal subregions participate in both goal-directed (action-outcome) and habitual (stimulus-response) learning. Modulation of synaptic transmission plays a large part in controlling input to as well as the output from striatal medium spiny projection neurons (MSNs). Synapses in this brain region are subject to short-term modulation, including allosteric alterations in ion channel function and prominent presynaptic inhibition. Two forms of long-term synaptic plasticity have also been observed in striatum, long-term potentiation (LTP) and long-term depression (LTD). LTP at glutamatergic synapses onto MSNs involves activation of NMDA-type glutamate receptors and D1 dopamine or A2A adenosine receptors. Expression of LTP appears to involve postsynaptic mechanisms. LTD at glutamatergic synapses involves retrograde endocannabinoid signaling stimulated by activation of metabotropic glutamate receptors (mGluRs) and D2 dopamine receptors. While postsynaptic mechanisms participate in LTD induction, maintained expression involves presynaptic mechanisms. A similar form of LTD has also been observed at GABAergic synapses onto MSNs. Studies have just begun to examine the roles of synaptic plasticity in striatal-based learning. Findings to date indicate that molecules implicated in induction of plasticity participate in these forms of learning. Neurotransmitter receptors involved in LTP induction are necessary for proper skill and goal-directed instrumental learning. Interestingly, receptors involved in LTP and LTD at glutamatergic synapses onto MSNs of the “indirect pathway” appear to have important roles in habit learning. More work is needed to reveal if and when synaptic plasticity occurs during learning and if so what molecules and cellular processes, both short- and long-term, contribute to this plasticity.
(c) 2009. Published by Elsevier Ltd.
Neuro-transmitters in the central nervous system & their implication in learning and memory processes.
This review article gives an overview of a number of central neuro-transmitters, which are essential for integrating many functions in the central nervous system (CNS), such as learning, memory, sleep cycle, body movement, hormone regulation and many others. Neurons use neuro-transmitters to communicate, and a great variety of molecules are known to fit the criteria to be classified as such. A process shared by all neuro-transmitters is their release by excocytosis, and we give an outline of the molecular events and protein complexes involved in this mechanism. Synthesis, transport, inactivation, and cellular signaling can be very diverse when different neuro-transmitters are compared, and these processes are described separately for each neuro-transmitter system. Here we focus on the most well known neuro-transmitters: acetyl-choline, catechol-amines (dopamine and nor-adrenalin), indole-amine (serotonin), glutamate, and gamma-amino-butyric acid (GABA). Glutamate is the major excitatory neuro-transmitter in the brain and its actions are counter-balanced by GABA, which is the major inhibitory substance in the CNS. A balance of neuronal transmission between these two neuro-transmitters is essential to normal brain function. Acetyl-choline, serotonin and catechol-amines have a more modulatory function in the brain, being involved in many neuronal circuits. Apart from summarizing the current knowledge about the synthesis, release and receptor signaling of these transmitters, some disease states due to alteration of their normal neuro-transmission are also described.
Serotonin/dopamine interaction in learning.
Laboratorio de Neurofisiología Experimental, Centro de Investigación Biomédica de Michoacán, Instituto Mexicano del Seguro Social, Morelia, México. firstname.lastname@example.org
Dopamine (DA)-serotonin interactions dealing with learning and memory functions have been apparent from experimental approaches over the past decade. However, since the former evidence showing that these cerebral neurotransmitter systems are involved in the regulation of the same cognitive processes, few experimental studies have been done to further clarify the nature of DA-serotonin interactions for cognitive processes sharing common brain structures. Nevertheless, a regulatory role of 5-HT/DA interactions in cognition and the prefrontal cortex (PFC) and the striatum as a neuroanatomical substrate for these DA/5-HT interactions, are now recognized. Experimental evidence indicates that pharmacological disruption of serotonin neurotransmission results in a facilitative effect on the processing of mnemonic information by cerebral regions under strong, functional DA modulation, such as the striatum and the PFC; on the other hand, increased serotonin neurotransmission appears to have a detrimental effect on cognitive functions integrated in these structures. These effects seem to occur through the interaction of different pre- and postsynaptic DA and serotonin receptor subtypes acting as opposite systems underlying cognitive abilities. Some studies, focused on DA-serotonin interactions underlying the pathophysiology of neurological and psychiatric diseases, which evolve with cognitive dysfunctions in human beings, have shown that drugs that are able to modify DA or serotonin neurotransmission may exert beneficial effects on cognitive functions, even though improvement of motor, mood and behavioural disturbances are the main objectives of pharmacological treatment of these diseases. The complete significance of DA-serotonin interactions in cognitive functions could be addressed by future experimental and clinical studies.
- 31st August
- 15th July
- 6th March