Table 1 |.
Effects associated with exposure to cannabis or cannabinoid agonists during gestation and/or lactation in humans and animal models in relation to behavioural and neurobiological outcomes during exposure and later in life
| Gestation (0–40 weeks for humans, GD0–GD22 for rodents) | Infancy and childhood (0–11 years for humans, PND1–PND25 for rodents) | Adolescence (12–18 years for humans, PND28–PND65 for rodents) | Adulthood (>18 years for humans, >PND70 for rodents) |
|---|---|---|---|
| Humans | |||
| ↓ D2R mRNA (NAc and amygdala)26 | ↑ Sleep disturbances146,147 | ↑ Delinquency148 | ↑ Drug use47 |
| ↓ SCG10 (also known as stathmin 2) mRNA (hippocampus and striatum)24 | ↓ Cognition (verbal reasoning, attention, memory)42 | ↑ Drug-seeking behaviours46 | ↓ Executive functions43 |
| ↓ CB1R mRNA (cerebrum)24 | ↑ Aggression and impulsivity149,150 | ↓ Visual memory and integration151 | ↑ Neuronal functioning in cortical regions during a visuospatial task43 |
| ↓ DAGL mRNA (cerebrum)24 | ↑ Depressive and anxious behaviours44,45 | - | - |
| ↑ MAGL mRNA (cerebrum)24 | - | - | - |
| Rodents | |||
| ↓ CB1R mRNA and function in cortical neurons11 | Change in social communication33*,61,66* | ↓ Memory retention36* | ↓ Social interaction39,41,60 |
| ↓ D2R mRNA in NAc26 | ↑ Locomotor activity66* | ↑ Social anxiety152 | ↑ Social discrimination60 |
| - | GABA switch delayed in PFC61 | ↑ Sensitivity to THC challenge35 | ↑ Opioid sensitivity29,57 |
| - | ↓ NMDAR functions33* | ↓ Glutamate levels in PFC and hippocampus31,36*,37*,55 | ↓ Memory33*,36*,40,55 |
| - | ↓ CB1R density in hippocampus40 | ↓ NMDA-mediated LTP in hippocampus36* | Change in motor functions11,36* |
| - | - | ↑ Excitability of dopaminergic neurons in VTA35 | ↓ LTD and LTP in PFC and hippocampus35,36*,39,60 |
| - | - | ↓ GABA release in the VTA35 | ↓ DSI in hippocampus41* |
| - | - | ↑ AMPA/NMDA ratio in VTA35 | Change in pyramidal neuronal excitability of PFC39,60 |
| - | - | ↓ Glutamatergic inputs (number and/or strength) onto dopaminergic neurons in VTA35 | ↓ mGlu5,TRPV1 and DAGL mRNA in PFC39*,60 |
| - | - | Change in long-term plasticity polarity35 | ↓ D2R mRNA in NAc26 |
| - | - | - | ↑ DOPAC/DA ratio in NAc and VTA58 |
| - | - | - | ↓ Glutamate levels (basal and evoked)36*,55 |
| - | - | - | Change in CB1R density in cortex and hippocampus59 |
| - | - | - | ↓ CB1R function in striatum and hippocampus63,153* |
| - | - | - | ↓ GABA levels (basal and evoked) in hippocampus63 |
The Δ9-tetrahydrocannabinol (THC) animal studies cited used low to moderate THC doses. CB1R, cannabinoid receptor type 1; DA, dopamine; DAGL, diacylglycerol lipase; DOPAC, dihydroxyphenylacetic acid; D2R, dopamine D2 receptor; DSI, depolarization- induced suppression of inhibition; GABA, γ-aminobutyric acid; GD, gestational day; LTP, long-term potentiation; LTD, long-term depression; MAGL, monoacylglycerol lipase; mGlu5, metabotropic glutamate receptor 5, NAc, nucleus accumbens; NMDAR, NMDA receptor; PFC, prefrontal cortex; PND, postnatal day; TRPV1, transient receptor potential vanilloid 1; VTA, ventral tegmental area.
The cannabinoid receptor agonist WIN-55,212–2 was used.