Dopamine and Glutamate signaling cascades in the prefrontal cortex (PFC) may be a potential therapeutic target for preventing the progression of drug abuse.
Most CPP studies occur during abstinence, so the learned memories during conditioning sessions would have to have been solidified and maintained for the animals to remember the association when reintroduced to the CPP chamber. On test day, the memory is recalled and destabilized, enabling the memory to be modified with new information. After this, the memory is again stabilized in a procedure known as reconsolidation Rossa & Taylor, 2013, 2016). Therefore, it is plausible that opiate-conditioning-based CPP relies on three stages of memory: Consolidate, Retrieve, and Reconsoldatedate.
The central amygdala, yet another brain area involved in learning and memory (Ciocchi, 2010; Goode & Maren, 2019), additionally impacts the acquisition of opiates CPP in this instance, via NMDAR and Dopamine-D1R activation (Zarranz et al., 2003; Resdayoff et al., 2007). In addition, inhibition of MEK and NMDAR in the central amygdala blocks opiates-based CPP (Li et al.,2011).
Humans have likewise been demonstrated to create CPP; for example, individuals who consume therapeutic amounts of amphetamines create a CPP for where he or they took the medication (Li et al., 2014).
For example, in studies testing drugs of abuse, when an experimental subject receives the substance and immediately feels its positive effects, they may experience a form of "conditioning" called "Conditioning by Contiguity." If the subject is exposed to the substance again after a certain period has passed, however, they may feel the negative side effects instead.
Neurotransmitters are small molecules that travel across synaptic gaps between neurons. Neuropeptide transmitters are larger molecules that are stored in larger vesicles. They're usually co-secreted along with other neurotransmitter substances, and their release isn't limited to the synapses.
The current review focuses on some of the major neuropeptide populations within the PFC—notably neuropeptide Y (NPY), corticotrophin-releasing factor (CRF), somatostatin (SST), dynorphin opioids (DYN), and the endorphin/enkephalin opioid systems.
Neuropeptide Y (NPY)
Neuropeptide Y Signaling and Overall Peptide Actions
Neuropeptide y (NPY) is an endogenous ligand for the Y1 and Y2 receptors. These two receptor subtypes belong to the family of G protein-coupled receptors (GPCRs) and share high-sequence homology. Both receptors are widely distributed throughout the brain and spinal cord. They mediate various biological actions, including feeding behavior, anxiety, depression, memory, learning, cardiovascular regulation, pain perception, and modulation of immune responses. In addition, they play important roles in regulating energy balance and body weight.
NPY in the CNS on alcohol consumption indicates that a lack of NPY can promote alcohol consumption.
Moreover, other drugs of abuse, such as cocaine, lead to reductions in NPY in the PFC (Wahlestedt et al., 1991). These findings indicate that NPY and its receptors play an important role in alcohol consumption; NPY and its corresponding receptors in the PFC are hypothesized to regulate behaviors associated with substance use disorder in humans. In animal models, NPY is downregulated by multiple forms of substance use (both binge alcohol and cocaine).
NPY in the PFC is region-specific even within the PFC, and its effect may depend largely on the injection site. The pre-clinical work supports the hypothesis that NPY plays a role in regulating a specific subset of behaviors associated with depression.
Male rats treated with Lithium exhibited increased NPY-like immunoreactivity in the frontal cortex, suggesting that NPY may be involved in response to lithium medications.
CRF Neuropeptide Signaling and Overall Actions
Corticotropin-releasing hormone (CRF) is a 41 amino acid peptide that stimulates the secretion of ACTH from the pituitary gland. It is produced mainly in the hypothalamus, amygdala, hippocampus, thalamus, and brainstem.
Substance Use Disorders
Somatostatin (SST)
This suggests that decreased binge-like ethanol drinking resulting from inhibition of CRF-R1 may result from increased activation of the CRF-R2, providing strong evidence in support of the important role of both CRF-R1 and CRF-R2 in the PFC in regulating substance abuse. However, in separate work, blocking CRF-R2 in the PFC partially inhibited cocaine-primed reinstatement of cocaine-conditioned place preference.
SST Neuropeptide Signaling and Overall Actions
SOM, also called somatotropin-releasing inhibiting factor (SRIF) has been identified for decades as a hypothalamic extract that inhibits the release of growth hormones from the rat anterior pituitary in vitro. Somatostatin was originally described as a 14 (SST-14) amino acid peptide (Brazeau et al., 1973).
SST exhibits diverse physiological effects, such as regulation of visceral functions and inhibition of a variety of biological processes, including anterior pituitary hormone secretion, insulin secretion, glucagon secretion, immune responses, DNA synthesis, and cell division (Brown and Taché, 1981; Kumar and Grant, 2010; Eigler and Ben-Shlomo, 2014; Morisset, 2017).
In short, somatostatin inhibits various cellular processes, such as the secretion of hormones and other secretory proteins (Benali et al., 2000; Morisset, 2017). Somatostatin has been gaining attention for its role in the CNS as a neuromodulator and in regulating behaviors linked to stress, including substance abuse and affective disorders (Liguz-Lecznar et al., 2016; Robinson and Thiele, 2020).
Cortical neurons' response to SST depends on concentration and corresponding receptor activation (Delfs and Dichter, 1983). Delfs and Dichter (1983) found that in cultured rat cortical neurons, low concentrations of SST-14 (100 pM–1 μM) caused an excitatory response and depolarization in neurons, while at higher concentrations (10 μM–1 mM), SST-14 was more likely to have no effect or to produce an inhibitory response.
Schizophrenia
These studies support the hypothesis that BDNF underlies changes in SST in the PFC and may precede changes in SST.
Consistent with this hypothesis, strong positive correlations between BDNF protein levels and SST mRNA levels were observed in the PFC of human subjects (post-mortem tissue) with schizophrenia, suggesting that BDNF may function to regulate SST expression in the PFC.
Note: Improve BDNF using cerebrolysin/NASA followed by SST.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5701766/ (Cerebrolysin & BDNF)
Protocol study: Cerebrolysin (10 mL, 5 days/week during 4 weeks) was administered alone or associated with Donepezil (5 mg/die during 28 weeks). Brain-Derived Neurotrophic Factor (BDNF) serum levels were evaluated before treatment and at the end of each period. Cognitive functions were assessed at baseline and every four weeks.
Patients treated with Cerebrolysin showed increased serum BDNF levels compared to the placebo group. Moreover, the association of Cerebrolysin with Donepezil induced a further increment in BDNF levels. In addition, we found a positive correlation between BDNF and Free Insulin Growth Factor I (IGF-1) levels.
These data confirm the neuroprotective role of Cerebrolysin and the synergism between Cerebrolysin and Donepezil. Furthermore, our findings show that the improvement of cognitive function observed in patients treated with both drugs lasted until week 28. In contrast, patients treated with monotherapies lost part of their cognitive gains after 16 weeks.
Dynorphin
Dynorphin Signaling and Overall Peptide Actions
Dynorphin, an endogenous member of the opioid neuropeptide family (Goldstein et al., 1979), is thought to mediate negative emotional states associated with stress, depression, and drug use withdrawal.
Consistent with the human literature, pre-clinical animal studies also indicate altered dynorphin/KOR following the administration of substances of abuse other than alcohol. Acute (8 mg/kg, intraperitoneal) administration of 3,4-methylenedioxy-N-methylamphetamine (ecstasy) in male Sprague–Dawley rats raised levels of prodynorphin mRNA in the PFC and decreased levels of Dynorphin-A.
Note: MDMA can reduce Dynorphin-A
TAT-DATING
Sequence: TAT-DATNT (YGRKKRRQRRRMSKSKCSVGLMSSVV) was commercially obtained from GenScript USA Inc
Animals were then given an intracranial injection of 40 nmol TAT or TAT-DATNT,
Our results suggest that disrupting the D2R-DA transporter interaction may effectively treat ADHD.
https://molecularbrain.biomedcentral.com/articles/10.1186/s13041-018-0409-0
Oxytocin
Oxytocin administration regulated GABA cell signaling in this region [62]. The administration of oxytocin into the prelimbic cortex reduced anxiety and was associated with increased activation of GABA cells [63]. In addition, intracerebroventricular (icv) administration of oxytocin enhanced the level of GABA in the PFC, and significantly reduced methamphetamine-induced increases in glutamate and glutamate NMDAR1 expression in this brain region [64], [65], [66].
A study found that in cocaine-experienced rats, a reduction in drug-seeking behavior by oxytocin administration was also associated with recovery in glutamatergic neurotransmission in the prefrontal cortex (PFC). A recent mouse experiment found that intranasal application of oxytocin could reverse the cognitive deficits caused by long-term exposure to methamphetamines.
Given the recent findings showing reduced cell activity in the prelimbic cortex in acutely methamphetamine-exposed rats [54], we hypothesized that the direct administration of vasopressin into the prelimbic cortex would significantly decrease methamphetamine self-administration behavior. MDMA increases levels of oxytocin, which has both prosocial and anxioleptic effects.
These effects are mediated by the V1a receptor. V1a receptors, on the other hands, are involved in mediating
the stress response. V1b receptors (also known as vasopressin 1B receptors) are found in the anterior pituitaries, amygdalas, hippocampi, and paraventricular nuclei of rats, and mice, Vasopressin released by the paraventricular nucleus of the hypothalamus stimulates the secretion of ACTH from the anterior pituitary gland.
Oxytocin has also been shown to increase the secretion of adrenocorticotropic hormone (ACTH) from the anterior pituitary gland [87] and vasopressins levels are decreased in opiate dependent patients [88], during withdrawal from alcohol [89], and a decrease in immunoreactive-vasopressins-has been measured in post mortem alcohol addicts [90]. The effects of drug abuse on the vasopressinsystem appear to change across the stages of addiction and abstinence.
Likewise, rats that showed a preference for methamphetamine in a self-administration protocol (high takers) had increased OXR1 compared to low takers and saline controls when measured after 30 days of abstinence, however, this was not present in females [148]. There was a strong positive correlation between OXR1 mRNA expression and cue-induced lever presses after abstinence in male rats [148], while OXR2 expression was negatively correlated with lever pressing, in both male and female rats [148,149]. Similarly, in a binge drinking a protocol, mice classed as high drinkers showed greater OX1R receptor expression in the PFC than low drinkers [150].
Furthermore, astrocytes are greatly involved in synaptic transmission and plasticity, and importantly determine GABA and glutamate homeostasis, a key regulator of pyramidal cell function in driving relapse behaviour [173,174]. Recent research determined that GABA interneurons have an intimate relationship with regulating astrocytes in the co-ordination of executive function [175 and that astrocytes may be regulated by peptides, such as oxytocin [176], vasopressin (V1a receptors)[177], CRF [178] or orexin [179]. Together, these data highlight important avenues for therapeutic interactions and future treatment discoveries for SUD.
https://www.sciencedirect.com/science/article/pii/S277239252200013X
Glutamate and GABA Homeostasis and Neurometabolism in Major Depressive Disorder
Glutamate and γ-aminobutyric acid (GABA) are the major excitatory and inhibitory neurotransmitters, respectively, in the matured central nervous system. Imbalance in the levels of these neurotransmitters has been implicated in different neurological and psychiatric disorders including MDD.
Certain environmental factors such as prematernal stress, childhood abuse, physical and sexual abuse, continuous failures, substance abuse, sadness, and severe trauma increase the risk of depression (6, 7). Depression has been often seen to be associated with various neurodegenerative disorders (8) such as Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis, and systemic diseases like diabetes (9) and cancer (10).
Box 1. Symptoms of MDD: as per the diagnostic and statistical manual of mental disorder (DSM-V) at least five of the following symptoms must be present during entire 2-week period (5).
➢ Consistently feeling sad, empty, and hopeless
➢ Markedly diminished interest in pleasurable activities
➢ Significant weight loss or weight gain
➢ Increased or decreased appetite
➢ Insomnia or hypersomnia
➢ Fatigue or loss of energy
➢ Feeling of worthlessness, feeling excessive, or inappropriate guilt
➢ Diminished ability to think or concentrate, or indecisiveness
➢ Recurrent thoughts of death and suicidal ideation without a specific plan
➢ Psychomotor agitation or retardation
A new study found that IV ketamine treatment may help people who suffer from depression by increasing brain activity in an important part of the brain called the mPFC. GABA/water and glutamate/water levels increased significantly after ketamine infusion.
However, most of the studies reported no significant change in GABA and glutamate levels after ketamine administration. As mentioned above, ketamine may exert its antidepressant effect by impacting neurotransmitter cycling, oxidative metabolism, and neuronal–glial interactions.
We've found that a low-dosage injection of ketamine increases the levels of brain metabolites derived from both glucose and acetate. These findings suggest that ketamine may be able to normalize the metabolic activity of glutamate and gamma-aminobutyric acid (GABA) receptors in depressed patients. Furthermore, recent research has shown that ketamine increases the rate of glutamatergic neurotransmission without affecting mitochondrial respiration in neurons (182).
Scientists at the University of California San Francisco (UCSF) have created an experimental drug that could help prevent seizures following head injuries, strokes, and even Alzheimer’s disease. A single peptide calledbidentatee has been isolated and purified from the plant Achyranthes bBidensBlume. Bidentatides' amino acids sequence and disulfide bond connectivity was determined by Edman degradation and mass spectrometry.
We evaluated the neuroactive properties of bidentate by observing its effects on NMDAR-mediated neurotoxicity in vitro and discovered that preincubating cells with bibidentaterotected them against NMDA-mediated toxicity through several mechanisms including inhibition of calcium influx, reduction of NMDA currents, and up-regulating antiapoptotic proteins.
All of the above methods were dependent on the inhibitory modulation of NMDARsbidentatetide (BIM). Overall, this study could help develop promising new drugs for treating neurological diseases and promote the modernization of traditional Chinese medicines. Furthermore, an in-depth knowledge of the structural characteristics identitiesses would be helpful for the development of synthetic peptide-based drugs with neurotrophic/neuroprotective properties.
file:///Users/labme/Library/Mobile%20Documents/com~apple~CloudDocs/DripDok/Photos/journal.pone.0254493.pdf
https://www.frontiersin.org/articles/10.3389/fpsyt.2021.637863/full
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