Three rules for identifying abnormal child sexual behaviours

Addiction is a chronic, relapsing disorder involving changes in brain reward, motivation, learning, stress and executive control systems. While different substances (and behaviours) act through distinct primary mechanisms, they converge on common neurobiological pathways — particularly the mesocorticolimbic dopamine system.

Below is an overview in Australian English of the core mechanisms and then substance-specific and behavioural addiction processes.

Core Neurobiological Pathways in Addiction

1. The Mesocorticolimbic Dopamine System

The central pathway implicated in addiction is the mesocorticolimbic circuit, involving:

• Ventral tegmental area (VTA)
• Nucleus accumbens (NAc)
• Prefrontal cortex (PFC)
• Amygdala
• Hippocampus

All addictive drugs increase dopamine transmission in the nucleus accumbens, either directly or indirectly. Dopamine does not simply produce pleasure — it encodes reward prediction, salience and learning. With repeated exposure:

• Drug-related cues gain exaggerated salience
• Natural rewards become less reinforcing
• Behaviour becomes increasingly habitual and compulsive

2. Neuroadaptation and Allostasis

Repeated substance exposure produces:

Tolerance — Reduced response due to receptor downregulation or neurotransmitter depletion.

Dependence — Neuroadaptations that produce withdrawal when the substance is removed.

Allostatic shift — The brain’s reward set point shifts downward, mediated by stress systems (e.g. corticotropin-releasing factor), resulting in dysphoria during abstinence.

3. Habit Formation and Loss of Control

With repeated use:

• Control shifts from ventral striatum (goal-directed) to dorsal striatum (habit-based)
• Prefrontal cortex regulation weakens
• Impulsivity and compulsivity increase

Substance-Specific Mechanisms

Alcohol

Alcohol acts on multiple neurotransmitter systems:

• Enhances GABA-A receptor function (inhibitory)
• Inhibits NMDA glutamate receptors (excitatory)
• Increases dopamine release in nucleus accumbens
• Affects endogenous opioid systems

Chronic exposure leads to:

• GABA downregulation
• NMDA upregulation
• Hyperexcitable state during withdrawal (risk of seizures, delirium tremens)

Alcohol dependence also involves stress system activation and impaired frontal cortical control.

Methamphetamine

Methamphetamine is a potent psychostimulant that:

• Enters presynaptic terminals
• Reverses the dopamine transporter (DAT), causing carrier-mediated dopamine efflux
• Inhibits vesicular monoamine transporter 2 (VMAT2), releasing dopamine from synaptic vesicles into the cytoplasm
• Causes massive dopamine release into the synapse

It also increases noradrenaline and serotonin.

Chronic use causes:

• Dopamine neurotoxicity (particularly to dopaminergic terminals)
• Reduced dopamine transporter availability
• Structural changes in striatum and PFC
• Persistent cognitive deficits

Methamphetamine produces particularly strong sensitisation of cue-driven craving.

Cocaine

Cocaine:

• Blocks the dopamine transporter (DAT), preventing reuptake
• Increases synaptic dopamine concentration

Unlike methamphetamine, cocaine acts by blocking DAT rather than reversing it, and does not cause large presynaptic vesicular release — the elevation in synaptic dopamine arises from impaired clearance.

Repeated use leads to:

• Dopamine receptor downregulation
• Enhanced cue reactivity
• Rapid cycling between intoxication and crash
• Strong psychological dependence

Opioids (e.g. heroin, morphine, oxycodone)

Opioids act primarily at mu-opioid receptors (MORs), which are expressed throughout the brain, including in the VTA. Their dopaminergic effects arise through multiple mechanisms:

• MORs on GABAergic interneurons in the VTA suppress inhibitory tone, thereby disinhibiting dopamine neurons (the classical disinhibition mechanism)
• MORs are also expressed on VTA dopamine neurons and projection targets directly, contributing additional excitatory drive beyond the disinhibition pathway

They also act in brainstem respiratory centres, which underlies the risk of respiratory depression in overdose.

Chronic use produces:

• Receptor desensitisation and internalisation
• Reduced endogenous opioid production
• Severe physical withdrawal mediated by noradrenergic rebound in the locus coeruleus
• Strong negative reinforcement (use to avoid withdrawal)

Cannabis

Δ9-tetrahydrocannabinol (THC):

• Activates CB1 receptors (the primary psychoactive cannabinoid receptor)
• Modulates GABA and glutamate release at presynaptic terminals
• Indirectly increases dopamine in NAc via disinhibitory mechanisms

Cannabis produces:

• Altered endocannabinoid system function
• CB1 receptor downregulation with chronic use
• A mild to moderate withdrawal syndrome (irritability, sleep disturbance, appetite changes)
• Effects on hippocampal memory circuits

While addiction risk is generally considered lower than for opioids or stimulants, it remains clinically significant and may be underestimated, particularly given the widespread availability of high-potency THC products (e.g. concentrates and high-THC flower), which are associated with greater dependence risk and more severe withdrawal.

MDMA (Ecstasy)

MDMA:

• Reverses the serotonin transporter (SERT), causing massive serotonin efflux — this is its primary mechanism
• Also increases dopamine and noradrenaline

Neurobiological consequences include:

• Acute empathogenic and entactogenic effects driven by serotonin release
• Post-use serotonin depletion, which may contribute to dysphoria in the days following use
• Potential serotonergic neurotoxicity, though this evidence comes largely from high-dose or repeated animal studies; the clinical significance in typical human recreational use remains under debate and is not definitively established
• Moderate addictive potential relative to psychostimulants, partly because dopaminergic effects are less prominent than with cocaine or methamphetamine

Prescription Psychoactive Medications

Certain prescribed medications also have addictive potential:

Benzodiazepines — Enhance GABA-A receptor activity. Cause tolerance via receptor downregulation. Dependence is primarily a GABAergic adaptation. Withdrawal can be protracted and, in cases of high-dose or long-term use, may produce seizures.

Prescription stimulants — Act via similar mechanisms to amphetamine, increasing dopamine and noradrenaline. Risk of misuse exists in susceptible individuals, though therapeutic doses in appropriately diagnosed patients are associated with substantially lower addiction risk than recreational use.

Behavioural (Process) Addictions

Gambling Disorder

Gambling disorder is recognised in DSM-5-TR as a non-substance-related addictive disorder. Although no substance is ingested, similar neurobiological mechanisms are involved.

Dopamine and reward prediction error — Near misses activate the nucleus accumbens similarly to wins. Variable ratio reinforcement schedules (as in poker machines) generate strong, unpredictable dopamine prediction error signalling that powerfully drives continued behaviour.

Cue reactivity — Gambling-related cues activate the same mesocorticolimbic circuitry as drug cues, with increased striatal activation and reduced prefrontal inhibitory control.

Habit circuitry — A shift from ventral to dorsal striatal control contributes to compulsive betting despite continued losses.

Other Emerging Behavioural Addictions

Conditions such as internet gaming disorder, compulsive sexual behaviour disorder, and problematic social media use share overlapping neurobiological features including:

• Dopamine dysregulation and sensitisation to cue salience
• Reduced executive control
• Stress system activation

However, the evidence base for most of these conditions is still developing, and their classification as formal addictive disorders remains an area of active research and debate. Internet gaming disorder is currently listed in DSM-5-TR as a condition for further study.

Shared Neurobiological Themes Across Addictions

Across substances and behaviours, addiction involves:

• Dopamine sensitisation to cues
• Reduced sensitivity to natural rewards
• Impaired prefrontal inhibitory control
• Stress system overactivation (particularly corticotropin-releasing factor)
• Habit circuitry dominance (dorsal striatum)
• Neuroplastic changes in glutamatergic signalling

Why Some Substances Are More Addictive

Addictive potential is influenced by multiple interacting factors. The speed of dopamine rise is one of the most studied — faster onset of dopamine elevation (e.g. via smoking or intravenous administration) is associated with stronger reinforcement. This framework, developed largely through the work of Volkow and colleagues, has strong empirical support, though it represents a mechanistic model rather than an established universal law. Other important factors include:

• Intensity of dopamine release
• Pharmacokinetics (e.g. route of administration)
• Withdrawal severity (which drives negative reinforcement)
• Social and environmental context
• Genetic vulnerability (heritability of addiction is estimated at 40–60% across substances)

Conclusion

Addiction is not simply about pleasure seeking. It reflects maladaptive neuroplasticity in reward, stress, learning and executive control circuits. While alcohol, methamphetamine, cannabis, opioids, cocaine and MDMA each act through different primary molecular mechanisms, they converge on common neural pathways that drive craving, tolerance, withdrawal and compulsive use. Behavioural addictions such as gambling engage these same circuits despite the absence of an ingested substance.

The neurobiological understanding of addiction continues to evolve, and where evidence is still emerging — particularly regarding emerging behavioural addictions and the long-term neurotoxic effects of substances like MDMA — clinical interpretation should be appropriately cautious.

If you’ve ever found yourself thinking “Part of me wants to change… but part of me’s not sure”, you’re not alone. That back-and-forth, weighing things up—“Should I? Shouldn’t I?”—is a normal part of how people process big (and small) decisions. In counselling, this is called ambivalence, and rather than seeing it as a barrier, Motivational Interviewing (MI) treats it as a starting point for meaningful conversations.

What Is Motivational Interviewing?

Motivational Interviewing is a counselling approach that helps people explore their own reasons for change, without pressure or judgment. It’s a respectful, supportive way of helping you work through the push-pull that often comes with making decisions. You’re in the driver’s seat—we’re just here to help you navigate.

You might hear MI described in different ways:

In simple terms:
“MI is a collaborative conversation style that helps strengthen your own motivation and commitment to change.”

In practice:
“MI is about helping you make sense of mixed feelings and explore what’s right for you—based on your values, your goals, and your life.”

MI isn’t about telling you what to do. It’s about listening deeply, asking thoughtful questions, and helping you make sense of where you’re at—and where you might want to go.

Why It’s Not Just a Quick Fix

While MI can be used in short sessions, the research shows it works best when there’s time to really explore your thinking. In studies where people had just one 15-minute session, the outcomes were decent. But when they had more time—say, several sessions of an hour—the results were much stronger. That’s probably because real change often takes time, reflection, and a bit of back-and-forth.

MI originally started in the health world—helping people reduce alcohol use, manage weight, or improve their health. More recently, it’s been used to address things like vaccine hesitancy. But MI isn’t just for health issues. It can also help with things like relationship struggles, career decisions, or anything where you might feel stuck or unsure.

Ambivalence Is Normal

Let’s say you’re thinking about quitting smoking, leaving a relationship, or starting something new. You might feel torn—part of you is ready, and another part isn’t. That’s ambivalence.

MI offers tools to help with this, including something called the Decisional Balance, which simply helps you look at both sides: What are the good things about staying the same? What are the reasons you might want to change?

But here’s the thing—MI isn’t about pushing you toward a particular outcome. If you’re trying to make a decision where there’s no obvious “right” answer—like whether to stay in a relationship—the counsellor stays neutral. They don’t steer you in one direction. Instead, they help you explore what matters to you.

Talking Your Way Toward Change

One of the interesting things about MI is how it pays attention to the language you use when you talk about change.

Some of the things people say when they’re starting to think about change include:

• “I probably should cut down…”
• “I’d like to feel better about this…”
• “I don’t know if I can keep doing this…”

These kinds of statements are called change talk—and they’re actually signs that something inside you is shifting. MI aims to gently encourage and grow this kind of talk, because research shows that the more someone talks about change, the more likely they are to act on it.

There’s also sustain talk, which sounds like:

• “I don’t smoke that much…”
• “I know I should, but it helps me relax.”
• “Now’s not really the right time.”

Both are normal. In MI, there’s no need to rush. Instead, the focus is on listening to both sides of you—and helping you get clearer about what you want to do next.

Getting Skilled Support

Like any professional approach, MI works best when the counsellor is trained and skilled in using it. Some practitioners have their sessions reviewed (with consent) by independent experts to make sure the spirit and skills of MI are being used well.

If you ever hear a practitioner say they “do MI”, you can ask what that looks like. The most effective use of MI goes beyond just asking open-ended questions or offering summaries—it’s about how your counsellor supports you in finding your own reasons for change.

What a Session Might Involve

Motivational Interviewing tends to follow a flexible process with four key parts:

1. Engaging – Building trust and understanding
2. Focusing – Exploring what matters most to you
3. Evoking – Drawing out your own reasons for change
4. Planning – When you’re ready, looking at possible next steps

You don’t have to go through these in a straight line. Some days you might focus on one step, then circle back to another later. It’s all guided by you—your pace, your readiness, your goals.

In Summary

If you’re feeling uncertain about making a change—or you’ve been thinking about it for a while but haven’t quite landed on what to do—Motivational Interviewing could be a really helpful way to explore things.

It’s not about being told what to do, and it’s not about “fixing” you. It’s a respectful, evidence-based approach that helps people work through their own ambivalence, connect with what matters to them, and move toward change when they’re ready.

Change doesn’t have to be instant. And it doesn’t have to be perfect. But it can start with a conversation.